PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 23213191-6 2013 In salt-loaded rats continuously infused intracerebroventricularly with a Galphai(2) oligodeoxynucleotide, animals exhibited sodium and water retention, elevated plasma norepinephrine levels, and hypertension, despite suppression of plasma renin activity. galphai(2) oligodeoxynucleotide 74-105 renin Rattus norvegicus 240-245 20862299-10 2010 CONCLUSIONS: This study shows that TRPV(1) in brain is involved in the antinociceptive action of acetaminophen and provides a strategy for developing central nervous system active oral analgesics based on the coexpression of FAAH and TRPV(1) in the brain. Acetaminophen 97-110 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 234-241 20637792-0 2010 Role of caspase-1 and interleukin-1beta in acetaminophen-induced hepatic inflammation and liver injury. Acetaminophen 43-56 caspase 1 Mus musculus 8-17 20637792-0 2010 Role of caspase-1 and interleukin-1beta in acetaminophen-induced hepatic inflammation and liver injury. Acetaminophen 43-56 interleukin 1 beta Mus musculus 22-39 20637792-9 2010 To evaluate the potential of IL-1beta to increase injury, mice were given pharmacological doses of IL-1beta after APAP overdose. Acetaminophen 114-118 interleukin 1 beta Mus musculus 99-107 20637792-11 2010 We conclude that endogenous IL-1beta formation after APAP overdose is insufficient to activate and recruit neutrophils into the liver or cause liver injury. Acetaminophen 53-57 interleukin 1 beta Mus musculus 28-36 20713560-5 2010 Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency. Acetaminophen 28-39 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 93-96 20713560-6 2010 On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception. Acetaminophen 27-38 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 112-115 20542992-0 2010 Arylacetamide deacetylase is a determinant enzyme for the difference in hydrolase activities of phenacetin and acetaminophen. Acetaminophen 111-124 arylacetamide deacetylase Homo sapiens 0-25 20542992-15 2010 In conclusion, we found that AADAC is the principal enzyme responsible for the phenacetin hydrolysis, and the difference of hydrolase activity between phenacetin and APAP is largely due to the substrate specificity of AADAC. Acetaminophen 166-170 arylacetamide deacetylase Homo sapiens 29-34 20542992-15 2010 In conclusion, we found that AADAC is the principal enzyme responsible for the phenacetin hydrolysis, and the difference of hydrolase activity between phenacetin and APAP is largely due to the substrate specificity of AADAC. Acetaminophen 166-170 arylacetamide deacetylase Homo sapiens 218-223 20815767-0 2010 Molecular mechanisms of Id2 down-regulation in rat liver after acetaminophen overdose. Acetaminophen 63-76 inhibitor of DNA binding 2 Rattus norvegicus 24-27 20815767-4 2010 This study explored the molecular mechanisms for the modulation of Id2 expression elicited by GSH and oxidative stress in the liver of acetaminophen (APAP)-intoxicated rats. Acetaminophen 135-148 inhibitor of DNA binding 2 Rattus norvegicus 67-70 20815767-4 2010 This study explored the molecular mechanisms for the modulation of Id2 expression elicited by GSH and oxidative stress in the liver of acetaminophen (APAP)-intoxicated rats. Acetaminophen 150-154 inhibitor of DNA binding 2 Rattus norvegicus 67-70 20815767-5 2010 APAP-overdose induced GSH depletion, Id2 promoter hypoacetylation, RNApol-II released and, therefore, Id2 down-regulation. Acetaminophen 0-4 inhibitor of DNA binding 2 Rattus norvegicus 37-40 20815767-5 2010 APAP-overdose induced GSH depletion, Id2 promoter hypoacetylation, RNApol-II released and, therefore, Id2 down-regulation. Acetaminophen 0-4 inhibitor of DNA binding 2 Rattus norvegicus 102-105 20539006-10 2010 Acetaminophen-induced phosphorylation of JNK in the liver was also enhanced in KK-A(y) mice. Acetaminophen 0-13 mitogen-activated protein kinase 8 Mus musculus 41-44 20561950-3 2010 TQ supplementation dramatically reduced acetaminophen-induced hepatotoxicity, in a dose-dependent manner, as evidenced by decreased serum alanine aminotransferase (ALT) activities. Acetaminophen 40-53 glutamic pyruvic transaminase, soluble Mus musculus 138-162 20561950-6 2010 Interestingly, supplementation of TQ (2mg/kg/day) for 5 days before acetaminophen administration resulted in reversal of acetaminophen-induced increase in ALT, total nitrate/nitrite, lipid peroxide and a decrease in GSH and ATP. Acetaminophen 121-134 glutamic pyruvic transaminase, soluble Mus musculus 155-158 20683965-2 2010 This study seeks to further investigate the mechanisms involved in acetaminophen-induced hepatotoxicity and the role of chemokine (C-X-C motif) receptor 2 (CXCR2) receptor/ligand interactions in the liver"s response to and recovery from acetaminophen toxicity. Acetaminophen 237-250 chemokine (C-X-C motif) receptor 2 Mus musculus 120-154 20683965-2 2010 This study seeks to further investigate the mechanisms involved in acetaminophen-induced hepatotoxicity and the role of chemokine (C-X-C motif) receptor 2 (CXCR2) receptor/ligand interactions in the liver"s response to and recovery from acetaminophen toxicity. Acetaminophen 237-250 chemokine (C-X-C motif) receptor 2 Mus musculus 156-161 20683965-4 2010 CXCR2 knockout mice exposed to a median lethal dose of acetaminophen had a significantly lower mortality rate than wild-type mice. Acetaminophen 55-68 chemokine (C-X-C motif) receptor 2 Mus musculus 0-5 20628198-8 2010 Finally, adenoviral delivery of Adam17 prevented acetaminophen-induced liver failure in a clinically relevant model of Fas-dependent fulminant hepatitis. Acetaminophen 49-62 a disintegrin and metallopeptidase domain 17 Mus musculus 32-38 20573685-0 2010 Activation of the farnesoid X receptor provides protection against acetaminophen-induced hepatic toxicity. Acetaminophen 67-80 nuclear receptor subfamily 1, group H, member 4 Mus musculus 18-38 20573685-2 2010 In the current study, we provide evidence to support a role for FXR in hepatoprotection from acetaminophen (APAP)-induced toxicity. Acetaminophen 93-106 nuclear receptor subfamily 1, group H, member 4 Mus musculus 64-67 20573685-2 2010 In the current study, we provide evidence to support a role for FXR in hepatoprotection from acetaminophen (APAP)-induced toxicity. Acetaminophen 108-112 nuclear receptor subfamily 1, group H, member 4 Mus musculus 64-67 20573685-5 2010 Consistent with the observed transcriptional changes, FXR gene dosage is positively correlated with the degree of protection from APAP-induced hepatotoxicity in vivo. Acetaminophen 130-134 nuclear receptor subfamily 1, group H, member 4 Mus musculus 54-57 20573685-6 2010 Further, we demonstrate that pretreatment of wild-type mice with an FXR-specific agonist provides significant protection from APAP-induced hepatotoxicity. Acetaminophen 126-130 nuclear receptor subfamily 1, group H, member 4 Mus musculus 68-71 20653358-0 2010 Serum alanine aminotransferase elevation during 10 days of acetaminophen use in nondrinkers. Acetaminophen 59-72 glutamic--pyruvic transaminase Homo sapiens 6-30 20653358-1 2010 STUDY OBJECTIVE: To describe the changes in serum alanine aminotransferase (ALT) levels in nondrinkers receiving acetaminophen for 10 days. Acetaminophen 113-126 glutamic--pyruvic transaminase Homo sapiens 50-74 20650012-0 2010 PACE--the first placebo controlled trial of paracetamol for acute low back pain: design of a randomised controlled trial. Acetaminophen 44-55 furin, paired basic amino acid cleaving enzyme Homo sapiens 0-4 20551297-1 2010 BACKGROUND: Recurrent intake of 4 g/day or more of acetaminophen has been associated with elevation of serum alanine aminotransferase (ALT) levels in 30-40% of the exposed population and may result in hepatotoxicity. Acetaminophen 51-64 glutamic--pyruvic transaminase Homo sapiens 109-133 20300741-11 2010 CONCLUSIONS: Further research on differences in paracetamol pharmacokinetics between ICU and MCU patients is warranted, as these differences might result in differences in efficacy. Acetaminophen 48-59 mitochondrial calcium uniporter Homo sapiens 93-96 20503171-7 2010 The toxicity of APAP was determined by observing the survival of mice during 48 hours, by measuring concentration of alanine-aminotransferase (ALT) in plasma 20-22 hours after APAP administration and by liver histology. Acetaminophen 16-20 glutamic pyruvic transaminase, soluble Mus musculus 117-141 20503171-7 2010 The toxicity of APAP was determined by observing the survival of mice during 48 hours, by measuring concentration of alanine-aminotransferase (ALT) in plasma 20-22 hours after APAP administration and by liver histology. Acetaminophen 16-20 glutamic pyruvic transaminase, soluble Mus musculus 143-146 20039781-5 2010 The IL-17 levels were elevated in 60% of patients with IDILI, but also in a similar number of patients with acetaminophen-induced ALF and occasionally in patients with viral hepatitis. Acetaminophen 108-121 interleukin 17A Homo sapiens 4-9 20039781-6 2010 Levels of other cytokines, such as IL-21, that are also produced by T(H)17 cells were higher in patients with IDILI, but again, there was overlap with acetaminophen DILI. Acetaminophen 151-164 interleukin 21 Homo sapiens 35-40 20363854-0 2010 Human recombinant vascular endothelial growth factor reduces necrosis and enhances hepatocyte regeneration in a mouse model of acetaminophen toxicity. Acetaminophen 127-140 vascular endothelial growth factor A Mus musculus 18-52 20363854-1 2010 We reported previously that vascular endothelial growth factor (VEGF) was increased in acetaminophen (APAP) toxicity in mice and treatment with a VEGF receptor inhibitor reduced hepatocyte regeneration. Acetaminophen 87-100 vascular endothelial growth factor A Mus musculus 28-62 20363854-1 2010 We reported previously that vascular endothelial growth factor (VEGF) was increased in acetaminophen (APAP) toxicity in mice and treatment with a VEGF receptor inhibitor reduced hepatocyte regeneration. Acetaminophen 87-100 vascular endothelial growth factor A Mus musculus 64-68 20363854-1 2010 We reported previously that vascular endothelial growth factor (VEGF) was increased in acetaminophen (APAP) toxicity in mice and treatment with a VEGF receptor inhibitor reduced hepatocyte regeneration. Acetaminophen 87-100 vascular endothelial growth factor A Homo sapiens 146-150 20363854-1 2010 We reported previously that vascular endothelial growth factor (VEGF) was increased in acetaminophen (APAP) toxicity in mice and treatment with a VEGF receptor inhibitor reduced hepatocyte regeneration. Acetaminophen 102-106 vascular endothelial growth factor A Mus musculus 28-62 20363854-1 2010 We reported previously that vascular endothelial growth factor (VEGF) was increased in acetaminophen (APAP) toxicity in mice and treatment with a VEGF receptor inhibitor reduced hepatocyte regeneration. Acetaminophen 102-106 vascular endothelial growth factor A Mus musculus 64-68 20363854-1 2010 We reported previously that vascular endothelial growth factor (VEGF) was increased in acetaminophen (APAP) toxicity in mice and treatment with a VEGF receptor inhibitor reduced hepatocyte regeneration. Acetaminophen 102-106 vascular endothelial growth factor A Homo sapiens 146-150 20352459-0 2010 Heat shock protein 70 induction and its urinary excretion in a model of acetaminophen nephrotoxicity. Acetaminophen 72-85 heat shock protein family A (Hsp70) member 4 Homo sapiens 0-21 20352459-3 2010 We analyzed whether toxic doses of APAP could induce heat shock protein 70 (HSP70) in the kidney and whether HSP70 could be detected in urine. Acetaminophen 35-39 heat shock protein family A (Hsp70) member 4 Homo sapiens 53-74 20352459-3 2010 We analyzed whether toxic doses of APAP could induce heat shock protein 70 (HSP70) in the kidney and whether HSP70 could be detected in urine. Acetaminophen 35-39 heat shock protein family A (Hsp70) member 4 Homo sapiens 76-81 20352459-10 2010 HSP70 was detected in urine obtained from 4 to 24 h after APAP administration. Acetaminophen 58-62 heat shock protein family A (Hsp70) member 4 Homo sapiens 0-5 20352459-11 2010 HSP70 abundance in renal cortex was increased at early time points and 48 h after APAP administration. Acetaminophen 82-86 heat shock protein family A (Hsp70) member 4 Homo sapiens 0-5 20352459-13 2010 NAG would be a suitable early biomarker of APAP-induced nephrotoxicity. Acetaminophen 43-47 O-GlcNAcase Homo sapiens 0-3 20363829-7 2010 Furthermore, APAP treatment significantly upregulated jun oncogene (c-Jun) gene expression, which was confirmed by Western blotting for both the phosphorylated and the nonphosphorylated forms of c-Jun protein. Acetaminophen 13-17 jun proto-oncogene Mus musculus 68-73 20363829-7 2010 Furthermore, APAP treatment significantly upregulated jun oncogene (c-Jun) gene expression, which was confirmed by Western blotting for both the phosphorylated and the nonphosphorylated forms of c-Jun protein. Acetaminophen 13-17 jun proto-oncogene Mus musculus 195-200 20363829-8 2010 Transfection with JNK siRNA attenuated APAP toxicity after 24 h, suggesting that higher levels of APAP-induced activation of JNK were related to higher rates of cell death. Acetaminophen 39-43 mitogen-activated protein kinase 8 Mus musculus 18-21 20363829-8 2010 Transfection with JNK siRNA attenuated APAP toxicity after 24 h, suggesting that higher levels of APAP-induced activation of JNK were related to higher rates of cell death. Acetaminophen 39-43 mitogen-activated protein kinase 8 Mus musculus 125-128 20363829-8 2010 Transfection with JNK siRNA attenuated APAP toxicity after 24 h, suggesting that higher levels of APAP-induced activation of JNK were related to higher rates of cell death. Acetaminophen 98-102 mitogen-activated protein kinase 8 Mus musculus 18-21 20363829-8 2010 Transfection with JNK siRNA attenuated APAP toxicity after 24 h, suggesting that higher levels of APAP-induced activation of JNK were related to higher rates of cell death. Acetaminophen 98-102 mitogen-activated protein kinase 8 Mus musculus 125-128 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 90-113 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 115-118 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 15-19 mitogen-activated protein kinase 8 Homo sapiens 90-113 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 15-19 mitogen-activated protein kinase 8 Homo sapiens 115-118 20423716-11 2010 Our data suggest that the JNK inhibitor SP600125 protects against APAP-induced liver injury in part by attenuation of mitochondrial Bax translocation but mainly by preventing mitochondrial oxidant stress and peroxynitrite formation and thereby preventing the mitochondrial permeability transition pore opening, a key event in APAP-induced cell necrosis. Acetaminophen 66-70 mitogen-activated protein kinase 8 Homo sapiens 26-29 20423716-11 2010 Our data suggest that the JNK inhibitor SP600125 protects against APAP-induced liver injury in part by attenuation of mitochondrial Bax translocation but mainly by preventing mitochondrial oxidant stress and peroxynitrite formation and thereby preventing the mitochondrial permeability transition pore opening, a key event in APAP-induced cell necrosis. Acetaminophen 66-70 BCL2 associated X, apoptosis regulator Homo sapiens 132-135 20544007-0 2010 Acetaminophen modulates the transcriptional response to recombinant interferon-beta. Acetaminophen 0-13 interferon beta 1, fibroblast Mus musculus 68-83 20544007-4 2010 METHODOLOGY/PRINCIPAL FINDINGS: We tested whether the administration of acetaminophen causes a change in the response normally induced by interferon-beta treatment. Acetaminophen 72-85 interferon beta 1, fibroblast Mus musculus 138-153 20544007-12 2010 These results suggest that administration of acetaminophen has the potential to modify the efficacy of IFN-beta treatment. Acetaminophen 45-58 interferon beta 1, fibroblast Mus musculus 103-111 20404090-5 2010 We previously reported that hepatocyte-specific Keap1 knockout (Keap1(flox/-)::Albumin-Cre) mice are viable and more resistant to acute toxicity of acetaminophen (APAP). Acetaminophen 148-161 kelch-like ECH-associated protein 1 Mus musculus 48-53 20404090-5 2010 We previously reported that hepatocyte-specific Keap1 knockout (Keap1(flox/-)::Albumin-Cre) mice are viable and more resistant to acute toxicity of acetaminophen (APAP). Acetaminophen 148-161 kelch-like ECH-associated protein 1 Mus musculus 64-69 20404090-5 2010 We previously reported that hepatocyte-specific Keap1 knockout (Keap1(flox/-)::Albumin-Cre) mice are viable and more resistant to acute toxicity of acetaminophen (APAP). Acetaminophen 163-167 kelch-like ECH-associated protein 1 Mus musculus 48-53 20404090-5 2010 We previously reported that hepatocyte-specific Keap1 knockout (Keap1(flox/-)::Albumin-Cre) mice are viable and more resistant to acute toxicity of acetaminophen (APAP). Acetaminophen 163-167 kelch-like ECH-associated protein 1 Mus musculus 64-69 20493351-8 2010 Acetaminophen/hydrocodone-induced apoptosis of HEI-OC1 was evaluated by caspase 3-activation studies. Acetaminophen 0-13 one cut domain, family member 1 Mus musculus 51-54 20493351-8 2010 Acetaminophen/hydrocodone-induced apoptosis of HEI-OC1 was evaluated by caspase 3-activation studies. Acetaminophen 0-13 caspase 3 Mus musculus 72-81 20100502-0 2010 Potential role of caveolin-1 in acetaminophen-induced hepatotoxicity. Acetaminophen 32-45 caveolin 1, caveolae protein Mus musculus 18-28 20100502-5 2010 Acetaminophen-induced hepatotoxicity was significantly attenuated in Cav-1(-/-) mice, an effect that was independent of acetaminophen metabolism. Acetaminophen 0-13 caveolin 1, caveolae protein Mus musculus 69-74 20100502-6 2010 Acetaminophen administration resulted in increased hepatic expression of the oxidative stress marker, lipocalin 24p3, as well as hemeoxygenase-1, but decreased glutathione and superoxide dismutase-1; no differences were noted between the genotypes suggesting that reduced toxicity in Cav-1(-/-) mice is not due to alterations in antioxidant defense. Acetaminophen 0-13 caveolin 1, caveolae protein Mus musculus 284-289 20100502-7 2010 In wild-type mice, acetaminophen increased mRNA expression of the pro-inflammatory cytokines, interleukin-1beta, and monocyte chemoattractant protein-1 (MCP-1), as well as cyclooxygenase-2, while 15-lipoxygenase (15-LOX), which generates anti-inflammatory lipoxins, decreased. Acetaminophen 19-32 interleukin 1 beta Mus musculus 94-111 20100502-7 2010 In wild-type mice, acetaminophen increased mRNA expression of the pro-inflammatory cytokines, interleukin-1beta, and monocyte chemoattractant protein-1 (MCP-1), as well as cyclooxygenase-2, while 15-lipoxygenase (15-LOX), which generates anti-inflammatory lipoxins, decreased. Acetaminophen 19-32 chemokine (C-C motif) ligand 2 Mus musculus 117-151 20100502-7 2010 In wild-type mice, acetaminophen increased mRNA expression of the pro-inflammatory cytokines, interleukin-1beta, and monocyte chemoattractant protein-1 (MCP-1), as well as cyclooxygenase-2, while 15-lipoxygenase (15-LOX), which generates anti-inflammatory lipoxins, decreased. Acetaminophen 19-32 chemokine (C-C motif) ligand 2 Mus musculus 153-158 20100502-7 2010 In wild-type mice, acetaminophen increased mRNA expression of the pro-inflammatory cytokines, interleukin-1beta, and monocyte chemoattractant protein-1 (MCP-1), as well as cyclooxygenase-2, while 15-lipoxygenase (15-LOX), which generates anti-inflammatory lipoxins, decreased. Acetaminophen 19-32 prostaglandin-endoperoxide synthase 2 Mus musculus 172-188 20100502-7 2010 In wild-type mice, acetaminophen increased mRNA expression of the pro-inflammatory cytokines, interleukin-1beta, and monocyte chemoattractant protein-1 (MCP-1), as well as cyclooxygenase-2, while 15-lipoxygenase (15-LOX), which generates anti-inflammatory lipoxins, decreased. Acetaminophen 19-32 arachidonate 15-lipoxygenase Mus musculus 196-211 20100502-7 2010 In wild-type mice, acetaminophen increased mRNA expression of the pro-inflammatory cytokines, interleukin-1beta, and monocyte chemoattractant protein-1 (MCP-1), as well as cyclooxygenase-2, while 15-lipoxygenase (15-LOX), which generates anti-inflammatory lipoxins, decreased. Acetaminophen 19-32 arachidonate 15-lipoxygenase Mus musculus 213-219 20100502-8 2010 Acetaminophen-induced changes in MCP-1 and 15-LOX expression were greater in Cav-1(-/-) mice. Acetaminophen 0-13 chemokine (C-C motif) ligand 2 Mus musculus 33-38 20100502-8 2010 Acetaminophen-induced changes in MCP-1 and 15-LOX expression were greater in Cav-1(-/-) mice. Acetaminophen 0-13 arachidonate 15-lipoxygenase Mus musculus 43-49 20100502-8 2010 Acetaminophen-induced changes in MCP-1 and 15-LOX expression were greater in Cav-1(-/-) mice. Acetaminophen 0-13 caveolin 1, caveolae protein Mus musculus 77-82 20100502-9 2010 Although expression of tumor necrosis factor-alpha, a potent hepatocyte mitogen, was up-regulated in the liver of Cav-1(-/-) mice after acetaminophen, expression of proliferating cell nuclear antigen and survivin, markers of cellular proliferation, were delayed, which may reflect the reduced need for tissue repair. Acetaminophen 136-149 tumor necrosis factor Mus musculus 23-50 20100502-9 2010 Although expression of tumor necrosis factor-alpha, a potent hepatocyte mitogen, was up-regulated in the liver of Cav-1(-/-) mice after acetaminophen, expression of proliferating cell nuclear antigen and survivin, markers of cellular proliferation, were delayed, which may reflect the reduced need for tissue repair. Acetaminophen 136-149 caveolin 1, caveolae protein Mus musculus 114-119 20100502-10 2010 Taken together, these data demonstrate that Cav-1 plays a role in promoting inflammation and toxicity during the pathogenesis of acetaminophen-induced injury. Acetaminophen 129-142 caveolin 1, caveolae protein Mus musculus 44-49 20170747-1 2010 We used a green fluorescent kidney line, Tg(wt1b:GFP), as a model to access the acetaminophen (AAP)-induced nephrotoxicity dynamically. Acetaminophen 80-93 WT1 transcription factor b Danio rerio 44-48 20609067-8 2010 KEY FINDINGS: Increased activities of liver marker enzymes and elevated TNF-alpha and lipid peroxidation levels were observed in mice exposed to paracetamol (P < 0.05), whereas the antioxidant status was found to be depleted (P < 0.05) when compared with the control group. Acetaminophen 145-156 tumor necrosis factor Mus musculus 72-81 20456041-6 2010 However IL-10 outperfomed pro-inflammatory cytokines in the subgroups with ALF (0.80 vs 0.63 and 0.70) and acetaminophen-induced ALF (0.92 vs 0.67 and 0.81). Acetaminophen 107-120 interleukin 10 Homo sapiens 8-13 20175977-10 2010 TTMP was significantly better for tramadol/acetaminophen and naproxen than placebo (P<0.001 to P=0.015) for walks on Day 1 after a single dose and on Day 3. Acetaminophen 43-56 chromosome 3 open reading frame 52 Homo sapiens 0-4 20196639-3 2010 The potential for PKC-mediated inhibition of human UGT1A6, an isoform involved in the glucuronidation of drugs such as acetaminophen (paracetamol) and endogenous substrates including serotonin, was evaluated using various cell model systems. Acetaminophen 119-132 protein kinase C delta Homo sapiens 18-21 20196639-3 2010 The potential for PKC-mediated inhibition of human UGT1A6, an isoform involved in the glucuronidation of drugs such as acetaminophen (paracetamol) and endogenous substrates including serotonin, was evaluated using various cell model systems. Acetaminophen 119-132 UDP glucuronosyltransferase family 1 member A6 Homo sapiens 51-57 20196639-3 2010 The potential for PKC-mediated inhibition of human UGT1A6, an isoform involved in the glucuronidation of drugs such as acetaminophen (paracetamol) and endogenous substrates including serotonin, was evaluated using various cell model systems. Acetaminophen 134-145 protein kinase C delta Homo sapiens 18-21 20196639-3 2010 The potential for PKC-mediated inhibition of human UGT1A6, an isoform involved in the glucuronidation of drugs such as acetaminophen (paracetamol) and endogenous substrates including serotonin, was evaluated using various cell model systems. Acetaminophen 134-145 UDP glucuronosyltransferase family 1 member A6 Homo sapiens 51-57 19968966-0 2010 Acetaminophen (paracetamol) inhibits myeloperoxidase-catalyzed oxidant production and biological damage at therapeutically achievable concentrations. Acetaminophen 0-13 myeloperoxidase Homo sapiens 37-52 19968966-0 2010 Acetaminophen (paracetamol) inhibits myeloperoxidase-catalyzed oxidant production and biological damage at therapeutically achievable concentrations. Acetaminophen 15-26 myeloperoxidase Homo sapiens 37-52 19968966-3 2010 It is shown here that acetaminophen (paracetamol), a phenol-based drug with analgesic and antipyretic actions, is an efficient inhibitor of HOCl and HOBr generation by isolated MPO-H(2)O(2)-halide systems. Acetaminophen 22-35 myeloperoxidase Homo sapiens 177-180 19968966-3 2010 It is shown here that acetaminophen (paracetamol), a phenol-based drug with analgesic and antipyretic actions, is an efficient inhibitor of HOCl and HOBr generation by isolated MPO-H(2)O(2)-halide systems. Acetaminophen 37-48 myeloperoxidase Homo sapiens 177-180 19968966-9 2010 Inhibition of HOCl production was associated with the generation of fluorescent acetaminophen oxidation products, consistent with acetaminophen acting as a competitive substrate of MPO. Acetaminophen 130-143 myeloperoxidase Homo sapiens 181-184 19968966-10 2010 Inhibition by acetaminophen was maintained in the presence of heparan sulfate and extracellular matrix, materials implicated in the sequestration of MPO at sites of inflammation in vivo. Acetaminophen 14-27 myeloperoxidase Homo sapiens 149-152 19968966-11 2010 Overall, these data indicate that acetaminophen may be an important modulator of MPO activity in vivo. Acetaminophen 34-47 myeloperoxidase Homo sapiens 81-84 20234092-5 2010 In vivo analysis indicated that after instillation of thioglycollate to cause aseptic inflammation and after administration of acetaminophen to induce liver damage, endogenous HSCs/HPCs were actively recruited to the peritoneum and liver, respectively, in WT but not Ccr2-/- mice. Acetaminophen 127-140 chemokine (C-C motif) receptor 2 Mus musculus 267-271 20604837-0 2010 Up-regulation of the lysyl hydroxylase 2 gene by acetaminophen and isoniazid is modulated by transcription factor c-Myb. Acetaminophen 49-62 procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 Homo sapiens 21-40 20604837-0 2010 Up-regulation of the lysyl hydroxylase 2 gene by acetaminophen and isoniazid is modulated by transcription factor c-Myb. Acetaminophen 49-62 MYB proto-oncogene, transcription factor Homo sapiens 114-119 20604837-5 2010 KEY FINDINGS: The expression of LH2 was increased in HepG2 cells incubated with acetaminophen and isoniazid. Acetaminophen 80-93 procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 Homo sapiens 32-35 20371967-0 2010 Role of c-Jun N-terminal kinase (JNK) in regulating tumor necrosis factor-alpha (TNF-alpha) mediated increase of acetaminophen (APAP) and chlorpromazine (CPZ) toxicity in murine hepatocytes. Acetaminophen 113-126 mitogen-activated protein kinase 8 Mus musculus 33-36 20371967-0 2010 Role of c-Jun N-terminal kinase (JNK) in regulating tumor necrosis factor-alpha (TNF-alpha) mediated increase of acetaminophen (APAP) and chlorpromazine (CPZ) toxicity in murine hepatocytes. Acetaminophen 113-126 tumor necrosis factor Mus musculus 52-79 20371967-0 2010 Role of c-Jun N-terminal kinase (JNK) in regulating tumor necrosis factor-alpha (TNF-alpha) mediated increase of acetaminophen (APAP) and chlorpromazine (CPZ) toxicity in murine hepatocytes. Acetaminophen 113-126 tumor necrosis factor Mus musculus 81-90 20371967-0 2010 Role of c-Jun N-terminal kinase (JNK) in regulating tumor necrosis factor-alpha (TNF-alpha) mediated increase of acetaminophen (APAP) and chlorpromazine (CPZ) toxicity in murine hepatocytes. Acetaminophen 128-132 mitogen-activated protein kinase 8 Mus musculus 33-36 20371967-0 2010 Role of c-Jun N-terminal kinase (JNK) in regulating tumor necrosis factor-alpha (TNF-alpha) mediated increase of acetaminophen (APAP) and chlorpromazine (CPZ) toxicity in murine hepatocytes. Acetaminophen 128-132 tumor necrosis factor Mus musculus 52-79 20371967-0 2010 Role of c-Jun N-terminal kinase (JNK) in regulating tumor necrosis factor-alpha (TNF-alpha) mediated increase of acetaminophen (APAP) and chlorpromazine (CPZ) toxicity in murine hepatocytes. Acetaminophen 128-132 tumor necrosis factor Mus musculus 81-90 20371967-4 2010 Recent studies have shown that JNK can regulate the hepatotoxicity of the analgesic, acetaminophen (APAP). Acetaminophen 85-98 mitogen-activated protein kinase 8 Mus musculus 31-34 20371967-4 2010 Recent studies have shown that JNK can regulate the hepatotoxicity of the analgesic, acetaminophen (APAP). Acetaminophen 100-104 mitogen-activated protein kinase 8 Mus musculus 31-34 20371967-8 2010 We found that, pre-treatment with TNF-alpha resulted in approximately 50 to 60% increase in alanine aminotransferase (ALT) levels by APAP or CPZ, while interleukin-1beta (IL-1beta) or IL6 treatments showed only 15-20% increase in ALT release. Acetaminophen 133-137 tumor necrosis factor Mus musculus 34-43 20371967-8 2010 We found that, pre-treatment with TNF-alpha resulted in approximately 50 to 60% increase in alanine aminotransferase (ALT) levels by APAP or CPZ, while interleukin-1beta (IL-1beta) or IL6 treatments showed only 15-20% increase in ALT release. Acetaminophen 133-137 glutamic pyruvic transaminase, soluble Mus musculus 92-116 20371967-8 2010 We found that, pre-treatment with TNF-alpha resulted in approximately 50 to 60% increase in alanine aminotransferase (ALT) levels by APAP or CPZ, while interleukin-1beta (IL-1beta) or IL6 treatments showed only 15-20% increase in ALT release. Acetaminophen 133-137 glutamic pyruvic transaminase, soluble Mus musculus 118-121 20371967-11 2010 Pre-treatment with TNF-alpha resulted in prolonged activation of JNK (upto 2 hr) in the presence of APAP or CPZ. Acetaminophen 100-104 tumor necrosis factor Mus musculus 19-28 20371967-11 2010 Pre-treatment with TNF-alpha resulted in prolonged activation of JNK (upto 2 hr) in the presence of APAP or CPZ. Acetaminophen 100-104 mitogen-activated protein kinase 8 Mus musculus 65-68 20371967-12 2010 These results show that TNF-alpha is the major cytokine involved in sensitizing hepatocytes to APAP- or CPZ-induced hepatotoxicity, likely by a mechanism involving sustained activation of JNK. Acetaminophen 95-99 tumor necrosis factor Mus musculus 24-33 20371967-12 2010 These results show that TNF-alpha is the major cytokine involved in sensitizing hepatocytes to APAP- or CPZ-induced hepatotoxicity, likely by a mechanism involving sustained activation of JNK. Acetaminophen 95-99 mitogen-activated protein kinase 8 Mus musculus 188-191 20061376-0 2010 Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1. Acetaminophen 50-63 glycogen synthase kinase 3 beta Mus musculus 10-40 20061376-1 2010 Previously we demonstrated that c-Jun N-terminal kinase (JNK) plays a central role in acetaminophen (APAP)-induced liver injury. Acetaminophen 86-99 mitogen-activated protein kinase 8 Mus musculus 32-55 20061376-1 2010 Previously we demonstrated that c-Jun N-terminal kinase (JNK) plays a central role in acetaminophen (APAP)-induced liver injury. Acetaminophen 86-99 mitogen-activated protein kinase 8 Mus musculus 57-60 20061376-1 2010 Previously we demonstrated that c-Jun N-terminal kinase (JNK) plays a central role in acetaminophen (APAP)-induced liver injury. Acetaminophen 101-105 mitogen-activated protein kinase 8 Mus musculus 32-55 20061376-1 2010 Previously we demonstrated that c-Jun N-terminal kinase (JNK) plays a central role in acetaminophen (APAP)-induced liver injury. Acetaminophen 101-105 mitogen-activated protein kinase 8 Mus musculus 57-60 20061376-3 2010 APAP treatment to mice caused glycogen synthase kinase-3beta (GSK-3beta) activation and translocation to mitochondria during the initial phase of APAP-induced liver injury ( approximately 1 h). Acetaminophen 0-4 glycogen synthase kinase 3 beta Mus musculus 30-60 20061376-3 2010 APAP treatment to mice caused glycogen synthase kinase-3beta (GSK-3beta) activation and translocation to mitochondria during the initial phase of APAP-induced liver injury ( approximately 1 h). Acetaminophen 0-4 glycogen synthase kinase 3 beta Mus musculus 62-71 20061376-4 2010 The silencing of GSK-3beta, but not Akt-2 (protein kinase B) or glycogen synthase kinase-3alpha (GSK-3alpha), using antisense significantly protected mice from APAP-induced liver injury. Acetaminophen 160-164 glycogen synthase kinase 3 beta Mus musculus 17-26 20061376-5 2010 The silencing of GSK-3beta affected several key pathways important in conferring protection against APAP-induced liver injury. Acetaminophen 100-104 glycogen synthase kinase 3 beta Mus musculus 17-26 20061376-10 2010 The silencing of GSK-3beta reduced Mcl-1 degradation caused by APAP treatment. Acetaminophen 63-67 glycogen synthase kinase 3 beta Mus musculus 17-26 20061376-10 2010 The silencing of GSK-3beta reduced Mcl-1 degradation caused by APAP treatment. Acetaminophen 63-67 myeloid cell leukemia sequence 1 Mus musculus 35-40 20061376-11 2010 The silencing of GSK-3beta also resulted in an inhibition of the early phase (0-2 h), and blunted the late phase (after 4 h) of JNK activation and translocation to mitochondria in liver following APAP treatment. Acetaminophen 196-200 glycogen synthase kinase 3 beta Mus musculus 17-26 20079345-7 2010 Acetaminophen maintained mitochondrial cytochrome c content and reduced activation of caspase-9 and incidence of apoptosis. Acetaminophen 0-13 caspase 9 Rattus norvegicus 86-95 20335976-0 2010 The influence of alpha-, beta-, and gamma-melanocyte stimulating hormone on acetaminophen induced liver lesions in male CBA mice. Acetaminophen 76-89 pro-opiomelanocortin-alpha Mus musculus 17-72 20335976-2 2010 The purpose of the present paper is to compare protective effects of alpha-, beta-, and gamma-melanocyte stimulating hormone on acetaminophen induced liver lesions in male CBA mice. Acetaminophen 128-141 pro-opiomelanocortin-alpha Mus musculus 69-124 20166895-0 2010 Acetaminophen induced acute liver failure via oxidative stress and JNK activation: protective role of taurine by the suppression of cytochrome P450 2E1. Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 67-70 20166895-5 2010 APAP overdose caused injury in the hepatic tissue and hepatocytes via the upregulation of CYP2E1 and JNK. Acetaminophen 0-4 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 90-96 20166895-5 2010 APAP overdose caused injury in the hepatic tissue and hepatocytes via the upregulation of CYP2E1 and JNK. Acetaminophen 0-4 mitogen-activated protein kinase 8 Homo sapiens 101-104 20166895-7 2010 Results indicate that APAP overdose caused hepatic injury due to its metabolism to hepatotoxic NAPQI (N-acetyl-p-benzoquinone imine), usually catalysed by CYP2E1, and via the direct activation of JNK-dependent cell death pathway. Acetaminophen 22-26 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 155-161 20166895-7 2010 Results indicate that APAP overdose caused hepatic injury due to its metabolism to hepatotoxic NAPQI (N-acetyl-p-benzoquinone imine), usually catalysed by CYP2E1, and via the direct activation of JNK-dependent cell death pathway. Acetaminophen 22-26 mitogen-activated protein kinase 8 Homo sapiens 196-199 20099297-0 2010 Lactoferrin protects against acetaminophen-induced liver injury in mice. Acetaminophen 29-42 lactotransferrin Mus musculus 0-11 20099297-5 2010 Instead, Lac treatment significantly attenuated APAP-induced liver sinusoidal endothelial cell dysfunction and ameliorated hepatic microcirculation disorder. Acetaminophen 48-52 lactotransferrin Mus musculus 9-12 20346263-15 2010 When paracetamol, NSAIDs or COX-2 inhibitors were added to PCA morphine, there was a statistically significant reduction in morphine consumption: paracetamol (MD -6.34 mg; 95% CrI -9.02 to -3.65); NSAIDs (MD -10.18; 95% CrI -11.65 to -8.72); and COX-2 inhibitors (MD -10.92; 95% CrI -12.77 to -9.08). Acetaminophen 5-16 mitochondrially encoded cytochrome c oxidase II Homo sapiens 246-251 20346263-15 2010 When paracetamol, NSAIDs or COX-2 inhibitors were added to PCA morphine, there was a statistically significant reduction in morphine consumption: paracetamol (MD -6.34 mg; 95% CrI -9.02 to -3.65); NSAIDs (MD -10.18; 95% CrI -11.65 to -8.72); and COX-2 inhibitors (MD -10.92; 95% CrI -12.77 to -9.08). Acetaminophen 146-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-33 20071472-1 2010 BACKGROUND: Intravenous N-acetylcysteine (IV-NAC) is widely recognized as the antidote of choice for acetaminophen overdose. Acetaminophen 101-114 synuclein alpha Homo sapiens 45-48 20071472-3 2010 OBJECTIVE: The aim of this study was to investigate the type and incidence of ADR induced by IV-NAC in patients treated for acetaminophen overdose. Acetaminophen 124-137 synuclein alpha Homo sapiens 96-99 20071472-15 2010 CONCLUSION: ADR to IV-NAC were common among patients with acetaminophen overdose, but mostly minor and all reported adverse reactions were easily managed. Acetaminophen 58-71 synuclein alpha Homo sapiens 22-25 20160351-7 2010 Sat1-/- mice also displayed hypersulfaturia, hyposulfatemia, and enhanced acetaminophen-induced liver toxicity. Acetaminophen 74-87 solute carrier family 26 (sulfate transporter), member 1 Mus musculus 0-4 20035773-8 2010 Pre-treatment with AM251, a cannabinoid-1 receptor (CB1) antagonist, significantly diminished the antinociceptive effect of the acetaminophen + gabapentin combination. Acetaminophen 128-141 cannabinoid receptor 1 Rattus norvegicus 52-55 20067817-0 2010 Taurine protects acetaminophen-induced oxidative damage in mice kidney through APAP urinary excretion and CYP2E1 inactivation. Acetaminophen 17-30 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 106-112 19969075-8 2010 In addition, administration of arjunolic acid 4 h after acetaminophen intoxication reduced acetaminophen-induced JNK and downstream Bcl-2 and Bcl-xL phosphorylation, thus protecting against mitochondrial permeabilization, loss of mitochondrial membrane potential, and cytochrome c release. Acetaminophen 91-104 mitogen-activated protein kinase 8 Rattus norvegicus 113-116 19969075-8 2010 In addition, administration of arjunolic acid 4 h after acetaminophen intoxication reduced acetaminophen-induced JNK and downstream Bcl-2 and Bcl-xL phosphorylation, thus protecting against mitochondrial permeabilization, loss of mitochondrial membrane potential, and cytochrome c release. Acetaminophen 91-104 BCL2, apoptosis regulator Rattus norvegicus 132-137 19969075-8 2010 In addition, administration of arjunolic acid 4 h after acetaminophen intoxication reduced acetaminophen-induced JNK and downstream Bcl-2 and Bcl-xL phosphorylation, thus protecting against mitochondrial permeabilization, loss of mitochondrial membrane potential, and cytochrome c release. Acetaminophen 91-104 Bcl2-like 1 Rattus norvegicus 142-148 19931551-5 2010 ER redox alterations and early ER-stress-related signaling events induced by acetaminophen, such as ER glutathione depletion, phosphorylation of eIF2alpha and JNK and induction of the transcription factor GADD153, were not counteracted by co-treatment with BGP-15. Acetaminophen 77-90 eukaryotic translation initiation factor 2A Homo sapiens 145-154 19931551-5 2010 ER redox alterations and early ER-stress-related signaling events induced by acetaminophen, such as ER glutathione depletion, phosphorylation of eIF2alpha and JNK and induction of the transcription factor GADD153, were not counteracted by co-treatment with BGP-15. Acetaminophen 77-90 mitogen-activated protein kinase 8 Homo sapiens 159-162 19931551-5 2010 ER redox alterations and early ER-stress-related signaling events induced by acetaminophen, such as ER glutathione depletion, phosphorylation of eIF2alpha and JNK and induction of the transcription factor GADD153, were not counteracted by co-treatment with BGP-15. Acetaminophen 77-90 DNA damage inducible transcript 3 Homo sapiens 205-212 19932728-5 2010 Arsenic or acetaminophen increased serum ALT and AST activities and depleted CYP. Acetaminophen 11-24 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 77-80 19932728-6 2010 Arsenic decreased, but acetaminophen increased CYP-dependent enzyme activities. Acetaminophen 23-36 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 47-50 20039957-10 2010 RESULTS: Chronic paracetamol exposure led to an increase in CSD frequency and CSD-evoked Fos expression in cerebral cortex indicating the increase in neuronal excitability. Acetaminophen 17-28 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 89-92 19889793-7 2010 In addition to 4MUG, the PS(serosal) of the glucuronide conjugates of 7-ethyl-10-hydroxycamptothecin (SN-38) and acetaminophen in the jejunal everted sacs were also significantly reduced in Mrp3(-/-) mice compared with wild-type mice. Acetaminophen 113-126 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 190-194 21417014-0 2010 [COX-3: is it the target of acetaminophen? Acetaminophen 28-41 mitochondrially encoded cytochrome c oxidase III Homo sapiens 1-6 19922764-0 2010 Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acid. Acetaminophen 0-13 tumor necrosis factor Rattus norvegicus 60-69 19922764-9 2010 Our experimental evidence suggests that APAP-induced nephro-toxicity is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome C release. Acetaminophen 40-44 caspase 9 Rattus norvegicus 128-137 19922764-9 2010 Our experimental evidence suggests that APAP-induced nephro-toxicity is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome C release. Acetaminophen 40-44 caspase 3 Rattus norvegicus 142-151 20082487-0 2010 Gentiana manshurica Kitagawa prevents acetaminophen-induced acute hepatic injury in mice via inhibiting JNK/ERK MAPK pathway. Acetaminophen 38-51 mitogen-activated protein kinase 8 Mus musculus 104-107 20082487-0 2010 Gentiana manshurica Kitagawa prevents acetaminophen-induced acute hepatic injury in mice via inhibiting JNK/ERK MAPK pathway. Acetaminophen 38-51 mitogen-activated protein kinase 1 Mus musculus 108-111 20082487-0 2010 Gentiana manshurica Kitagawa prevents acetaminophen-induced acute hepatic injury in mice via inhibiting JNK/ERK MAPK pathway. Acetaminophen 38-51 mitogen-activated protein kinase 1 Mus musculus 112-116 20082487-3 2010 RESULTS: APAP treatment significantly depleted hepatic glutathione (GSH), increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and malonyldialdehyde (MDA) and 4-hydroxynonenal levels, and decreased hepatic activity of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD). Acetaminophen 9-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 90-116 20082487-3 2010 RESULTS: APAP treatment significantly depleted hepatic glutathione (GSH), increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and malonyldialdehyde (MDA) and 4-hydroxynonenal levels, and decreased hepatic activity of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD). Acetaminophen 9-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 118-121 20082487-3 2010 RESULTS: APAP treatment significantly depleted hepatic glutathione (GSH), increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and malonyldialdehyde (MDA) and 4-hydroxynonenal levels, and decreased hepatic activity of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD). Acetaminophen 9-13 glutamic pyruvic transaminase, soluble Mus musculus 124-148 20082487-3 2010 RESULTS: APAP treatment significantly depleted hepatic glutathione (GSH), increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and malonyldialdehyde (MDA) and 4-hydroxynonenal levels, and decreased hepatic activity of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD). Acetaminophen 9-13 glutamic pyruvic transaminase, soluble Mus musculus 150-153 20082487-4 2010 However, the pretreatment of GM significantly alleviated APAP-induced oxidative stress by increasing GSH content, decreasing serum ALT, AST and MDA, and retaining the activity of GSH-px and SOD in the liver. Acetaminophen 57-61 glutamic pyruvic transaminase, soluble Mus musculus 131-134 20082487-4 2010 However, the pretreatment of GM significantly alleviated APAP-induced oxidative stress by increasing GSH content, decreasing serum ALT, AST and MDA, and retaining the activity of GSH-px and SOD in the liver. Acetaminophen 57-61 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 136-139 19838684-11 2010 Acetaminophen exposure significantly increased hepatic LPO levels and inhibited AChE activity in gill (10-day NOEC and LOEC of 23 and 403 microg/L, respectively), whereas propranolol (11 microg/L) enhanced gill GST. Acetaminophen 0-13 acetylcholinesterase (Cartwright blood group) Homo sapiens 80-84 19838684-11 2010 Acetaminophen exposure significantly increased hepatic LPO levels and inhibited AChE activity in gill (10-day NOEC and LOEC of 23 and 403 microg/L, respectively), whereas propranolol (11 microg/L) enhanced gill GST. Acetaminophen 0-13 glutathione S-transferase kappa 1 Homo sapiens 211-214 19660437-0 2010 Role of cytochrome P450 2E1 in protein nitration and ubiquitin-mediated degradation during acetaminophen toxicity. Acetaminophen 91-104 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 8-27 19660437-1 2010 It is well established that following a toxic dose of acetaminophen (APAP), nitrotyrosine protein adducts (3-NT), a hallmark of peroxynitrite production, were colocalized with necrotic hepatic centrilobular regions where cytochrome P450 2E1 (CYP2E1) is highly expressed, suggesting that 3-NT formation may be essential in APAP-mediated toxicity. Acetaminophen 54-67 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 221-240 19660437-1 2010 It is well established that following a toxic dose of acetaminophen (APAP), nitrotyrosine protein adducts (3-NT), a hallmark of peroxynitrite production, were colocalized with necrotic hepatic centrilobular regions where cytochrome P450 2E1 (CYP2E1) is highly expressed, suggesting that 3-NT formation may be essential in APAP-mediated toxicity. Acetaminophen 54-67 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 242-248 19660437-1 2010 It is well established that following a toxic dose of acetaminophen (APAP), nitrotyrosine protein adducts (3-NT), a hallmark of peroxynitrite production, were colocalized with necrotic hepatic centrilobular regions where cytochrome P450 2E1 (CYP2E1) is highly expressed, suggesting that 3-NT formation may be essential in APAP-mediated toxicity. Acetaminophen 69-73 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 221-240 19660437-1 2010 It is well established that following a toxic dose of acetaminophen (APAP), nitrotyrosine protein adducts (3-NT), a hallmark of peroxynitrite production, were colocalized with necrotic hepatic centrilobular regions where cytochrome P450 2E1 (CYP2E1) is highly expressed, suggesting that 3-NT formation may be essential in APAP-mediated toxicity. Acetaminophen 69-73 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 242-248 19660437-6 2010 For instance, cytosolic superoxide dismutase (SOD1) levels were clearly decreased and immunoprecipitated SOD1 was nitrated and ubiquitinated, likely leading to its accelerated degradation in APAP-exposed wild-type mice. Acetaminophen 191-195 superoxide dismutase 1, soluble Mus musculus 46-50 19660437-6 2010 For instance, cytosolic superoxide dismutase (SOD1) levels were clearly decreased and immunoprecipitated SOD1 was nitrated and ubiquitinated, likely leading to its accelerated degradation in APAP-exposed wild-type mice. Acetaminophen 191-195 superoxide dismutase 1, soluble Mus musculus 105-109 19782400-9 2010 Arsenic or acetaminophen given alone depleted GSH and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and these effects remained mostly unaffected after co-exposure. Acetaminophen 11-24 catalase Rattus norvegicus 104-112 19782400-9 2010 Arsenic or acetaminophen given alone depleted GSH and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and these effects remained mostly unaffected after co-exposure. Acetaminophen 11-24 glutathione-disulfide reductase Rattus norvegicus 138-159 19782400-9 2010 Arsenic or acetaminophen given alone depleted GSH and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and these effects remained mostly unaffected after co-exposure. Acetaminophen 11-24 hematopoietic prostaglandin D synthase Rattus norvegicus 164-189 19923254-0 2010 An integrative genomic analysis identifies Bhmt2 as a diet-dependent genetic factor protecting against acetaminophen-induced liver toxicity. Acetaminophen 103-116 betaine-homocysteine methyltransferase 2 Mus musculus 43-48 19923254-2 2010 An integrative genetic, transcriptional, and two-dimensional NMR-based metabolomic analysis performed using multiple inbred mouse strains, along with knowledge-based filtering of these data, identified betaine-homocysteine methyltransferase 2 (Bhmt2) as a diet-dependent genetic factor that affected susceptibility to acetaminophen-induced liver toxicity in mice. Acetaminophen 318-331 betaine-homocysteine methyltransferase 2 Mus musculus 202-242 19923254-2 2010 An integrative genetic, transcriptional, and two-dimensional NMR-based metabolomic analysis performed using multiple inbred mouse strains, along with knowledge-based filtering of these data, identified betaine-homocysteine methyltransferase 2 (Bhmt2) as a diet-dependent genetic factor that affected susceptibility to acetaminophen-induced liver toxicity in mice. Acetaminophen 318-331 betaine-homocysteine methyltransferase 2 Mus musculus 244-249 19923254-3 2010 Through an effect on methionine and glutathione biosynthesis, Bhmt2 could utilize its substrate (S-methylmethionine [SMM]) to confer protection against acetaminophen-induced injury in vivo. Acetaminophen 152-165 betaine-homocysteine methyltransferase 2 Mus musculus 62-67 20020266-4 2010 In acetaminophen (APAP)-induced liver injury, hepatocyte death requires the sustained activation of c-Jun kinase (JNK), a kinase important in mediating apoptotic and necrotic death. Acetaminophen 3-16 mitogen-activated protein kinase 8 Mus musculus 100-112 20020266-4 2010 In acetaminophen (APAP)-induced liver injury, hepatocyte death requires the sustained activation of c-Jun kinase (JNK), a kinase important in mediating apoptotic and necrotic death. Acetaminophen 3-16 mitogen-activated protein kinase 8 Mus musculus 114-117 20020266-4 2010 In acetaminophen (APAP)-induced liver injury, hepatocyte death requires the sustained activation of c-Jun kinase (JNK), a kinase important in mediating apoptotic and necrotic death. Acetaminophen 18-22 mitogen-activated protein kinase 8 Mus musculus 100-112 20020266-4 2010 In acetaminophen (APAP)-induced liver injury, hepatocyte death requires the sustained activation of c-Jun kinase (JNK), a kinase important in mediating apoptotic and necrotic death. Acetaminophen 18-22 mitogen-activated protein kinase 8 Mus musculus 114-117 20020266-11 2010 The inhibition of NF-kappaB by subtoxic doses of APAP sensitizes hepatocyte to the cytotoxic actions of tumor necrosis factor (TNF). Acetaminophen 49-53 tumor necrosis factor Mus musculus 104-125 20020266-11 2010 The inhibition of NF-kappaB by subtoxic doses of APAP sensitizes hepatocyte to the cytotoxic actions of tumor necrosis factor (TNF). Acetaminophen 49-53 tumor necrosis factor Mus musculus 127-130 20802454-0 2010 Effects of URB597, an inhibitor of fatty acid amide hydrolase (FAAH), on analgesic activity of paracetamol. Acetaminophen 95-106 fatty acid amide hydrolase Mus musculus 46-61 20802454-0 2010 Effects of URB597, an inhibitor of fatty acid amide hydrolase (FAAH), on analgesic activity of paracetamol. Acetaminophen 95-106 fatty acid amide hydrolase Mus musculus 63-67 20802454-1 2010 OBJECTIVES: Paracetamol is converted to an active metabolite AM404 via fatty acid amide hydrolase (FAAH). Acetaminophen 12-23 fatty acid amide hydrolase Mus musculus 82-97 20802454-1 2010 OBJECTIVES: Paracetamol is converted to an active metabolite AM404 via fatty acid amide hydrolase (FAAH). Acetaminophen 12-23 fatty acid amide hydrolase Mus musculus 99-103 20802454-2 2010 The aim of the present study was to ascertain whether a FAAH inhibitor URB597 antagonizes paracetamol analgesic activity (and to asses by this way the role of FAAH in analgesic activity of paracetamol). Acetaminophen 90-101 fatty acid amide hydrolase Mus musculus 56-60 20802454-2 2010 The aim of the present study was to ascertain whether a FAAH inhibitor URB597 antagonizes paracetamol analgesic activity (and to asses by this way the role of FAAH in analgesic activity of paracetamol). Acetaminophen 189-200 fatty acid amide hydrolase Mus musculus 159-163 20802454-3 2010 METHODS: The interaction between a FAAH inhibitor URB597 and paracetamol was investigated in the writhing test in mice using an isobolographic analysis. Acetaminophen 61-72 fatty acid amide hydrolase Mus musculus 35-39 20032874-5 2009 L-alpha-MSH exhibited potent hepatoprotective effect in the experimental model of acetaminophen induced hepatotoxicity in male CBA mice, while its D-mirror image was inefficient. Acetaminophen 82-95 pro-opiomelanocortin-alpha Mus musculus 2-11 20120521-3 2009 The aim of this study was to determine whether PGI2 is playing a role in host defense to toxic effect of acetaminophen (APAP). Acetaminophen 105-118 prostaglandin I receptor (IP) Mus musculus 47-51 20120521-3 2009 The aim of this study was to determine whether PGI2 is playing a role in host defense to toxic effect of acetaminophen (APAP). Acetaminophen 120-124 prostaglandin I receptor (IP) Mus musculus 47-51 20120521-7 2009 The toxicity of APAP was determined by observing the survival of mice during 48 hours, by measuring the concentration of alanine-aminotransferase (ALT) in plasma 20-24 hours after APAP administration, and by liver histology. Acetaminophen 16-20 glutamic pyruvic transaminase, soluble Mus musculus 121-145 20120521-7 2009 The toxicity of APAP was determined by observing the survival of mice during 48 hours, by measuring the concentration of alanine-aminotransferase (ALT) in plasma 20-24 hours after APAP administration, and by liver histology. Acetaminophen 16-20 glutamic pyruvic transaminase, soluble Mus musculus 147-150 19934368-2 2009 The objective of this experiment was to compare the temporal impacts of knockouts of GPX1 and SOD1 alone or together on mouse susceptibility to an injection of a low dose of APAP (300 mg/kg). Acetaminophen 174-178 glutathione peroxidase 1 Mus musculus 85-89 19934368-2 2009 The objective of this experiment was to compare the temporal impacts of knockouts of GPX1 and SOD1 alone or together on mouse susceptibility to an injection of a low dose of APAP (300 mg/kg). Acetaminophen 174-178 superoxide dismutase 1, soluble Mus musculus 94-98 19934368-5 2009 Knockout of SOD1 prevented the APAP-induced hepatic GPX inactivation (P < 0.05), whereas knockout of GPX1 aggravated the APAP-induced hepatic SOD activity loss (P < 0.05). Acetaminophen 31-35 superoxide dismutase 1, soluble Mus musculus 12-16 19934368-5 2009 Knockout of SOD1 prevented the APAP-induced hepatic GPX inactivation (P < 0.05), whereas knockout of GPX1 aggravated the APAP-induced hepatic SOD activity loss (P < 0.05). Acetaminophen 31-35 peroxiredoxin 6 pseudogene 2 Mus musculus 52-55 19934368-5 2009 Knockout of SOD1 prevented the APAP-induced hepatic GPX inactivation (P < 0.05), whereas knockout of GPX1 aggravated the APAP-induced hepatic SOD activity loss (P < 0.05). Acetaminophen 124-128 glutathione peroxidase 1 Mus musculus 104-108 19934368-7 2009 In conclusion, knockout of GPX1 or SOD1 exerted differential impact on mouse susceptibility to this low dose of APAP, but neither shifted urinary APAP-cysteine formation. Acetaminophen 112-116 glutathione peroxidase 1 Mus musculus 27-31 19934368-7 2009 In conclusion, knockout of GPX1 or SOD1 exerted differential impact on mouse susceptibility to this low dose of APAP, but neither shifted urinary APAP-cysteine formation. Acetaminophen 112-116 superoxide dismutase 1, soluble Mus musculus 35-39 25206247-2 2009 Paracetamol (2gm/kg, po) significantly elevated the serum levels of biochemical markers like SGPT, SGOT, ALP, bilirubin (total and direct), total cholesterol, triglycerides and depleted tissue GSH and increased the lipid peroxidation. Acetaminophen 0-11 PDZ and LIM domain 3 Rattus norvegicus 105-108 19783637-0 2009 High-mobility group box-1 protein and keratin-18, circulating serum proteins informative of acetaminophen-induced necrosis and apoptosis in vivo. Acetaminophen 92-105 high mobility group box 1 Mus musculus 0-25 19783637-0 2009 High-mobility group box-1 protein and keratin-18, circulating serum proteins informative of acetaminophen-induced necrosis and apoptosis in vivo. Acetaminophen 92-105 keratin 18 Mus musculus 38-48 20099654-5 2009 Comparative analysis of the characteristics of the agents showed that paracetamol produced a more powerful antistress defense, as confirmed by the time course of changes in the levels of TNF-alpha and CRP. Acetaminophen 70-81 tumor necrosis factor Homo sapiens 187-196 20099654-5 2009 Comparative analysis of the characteristics of the agents showed that paracetamol produced a more powerful antistress defense, as confirmed by the time course of changes in the levels of TNF-alpha and CRP. Acetaminophen 70-81 C-reactive protein Homo sapiens 201-204 19821601-0 2009 Mechanism of acetaminophen oxidation by the peroxidase-like activity of methemoglobin. Acetaminophen 13-26 hemoglobin subunit gamma 2 Homo sapiens 72-85 19821601-1 2009 Oxidation of acetaminophen by human methemoglobin in the presence of H(2)O(2) has been kinetically studied in the present paper. Acetaminophen 13-26 hemoglobin subunit gamma 2 Homo sapiens 36-49 19881208-13 2009 Metabolism by CYP and GSH conjugation are common metabolic pathways for many drugs such as APAP. Acetaminophen 91-95 peptidyl-prolyl isomerase G (cyclophilin G) Mus musculus 14-17 19801828-4 2009 As a result, pretreated with ASE prior to the administration of APAP significantly prevented the increases of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-alpha) levels in serum, and glutathione (GSH) depletion, malondialdehyde (MDA) accumulation in liver tissue. Acetaminophen 64-68 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 110-136 19801828-4 2009 As a result, pretreated with ASE prior to the administration of APAP significantly prevented the increases of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-alpha) levels in serum, and glutathione (GSH) depletion, malondialdehyde (MDA) accumulation in liver tissue. Acetaminophen 64-68 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 138-141 19801828-4 2009 As a result, pretreated with ASE prior to the administration of APAP significantly prevented the increases of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-alpha) levels in serum, and glutathione (GSH) depletion, malondialdehyde (MDA) accumulation in liver tissue. Acetaminophen 64-68 glutamic pyruvic transaminase, soluble Mus musculus 144-168 19801828-4 2009 As a result, pretreated with ASE prior to the administration of APAP significantly prevented the increases of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-alpha) levels in serum, and glutathione (GSH) depletion, malondialdehyde (MDA) accumulation in liver tissue. Acetaminophen 64-68 glutamic pyruvic transaminase, soluble Mus musculus 170-173 19801828-4 2009 As a result, pretreated with ASE prior to the administration of APAP significantly prevented the increases of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-alpha) levels in serum, and glutathione (GSH) depletion, malondialdehyde (MDA) accumulation in liver tissue. Acetaminophen 64-68 tumor necrosis factor Mus musculus 180-207 19799668-5 2009 Acetaminophen treatment significantly depleted hepatic GSH and ascorbic acid levels, increased hepatic level of malonyldialdehyde (MDA), reactive oxygen species (ROS), and oxidized glutathione (GSSG), as well as decreased hepatic activity of glutathione peroxidase (GPX), catalase, and superoxide dismutase (SOD) (P < 0.05). Acetaminophen 0-13 catalase Mus musculus 272-280 19799668-6 2009 However, the pre-intake of carnosine or histidine significantly alleviated acetaminophen-induced oxidative stress by increasing GSH content, decreasing MDA, ROS, and GSSG formations, and retaining activity of GPX, catalase, and SOD in liver (P < 0.05). Acetaminophen 75-88 catalase Mus musculus 214-222 19799668-7 2009 The pre-intake of these compounds also significantly retarded subsequent acetaminophen-induced increase of cytochrome P450 2E1 activity (P < 0.05). Acetaminophen 73-86 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 107-126 19799668-8 2009 Acetaminophen treatment increased the hepatic levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha, and monocyte chemoattractant protein (MCP)-1 (P < 0.05). Acetaminophen 0-13 interleukin 10 Mus musculus 76-81 19799668-8 2009 Acetaminophen treatment increased the hepatic levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha, and monocyte chemoattractant protein (MCP)-1 (P < 0.05). Acetaminophen 0-13 tumor necrosis factor Mus musculus 83-116 19799668-8 2009 Acetaminophen treatment increased the hepatic levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha, and monocyte chemoattractant protein (MCP)-1 (P < 0.05). Acetaminophen 0-13 chemokine (C-C motif) ligand 2 Mus musculus 122-162 19834287-1 2009 Our previous studies showed that administration of a subtoxic dose of acetaminophen (APAP) to female rats increased generation of carbon monoxide from dichloromethane, a metabolic reaction catalyzed mainly by cytochrome P450 (CYP) 2E1. Acetaminophen 70-83 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 209-234 19834287-1 2009 Our previous studies showed that administration of a subtoxic dose of acetaminophen (APAP) to female rats increased generation of carbon monoxide from dichloromethane, a metabolic reaction catalyzed mainly by cytochrome P450 (CYP) 2E1. Acetaminophen 85-89 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 209-234 19580839-0 2009 Endocannabinoids mediate anxiolytic-like effect of acetaminophen via CB1 receptors. Acetaminophen 51-64 cannabinoid receptor 1 (brain) Mus musculus 69-72 19580839-1 2009 Acetaminophen (Paracetamol), a most commonly used antipyretic/analgesic agent, is metabolized to AM404 (N-arachidonoylphenolamine) that inhibits uptake and degradation of anandamide which is reported to mediate the analgesic action of acetaminophen via CB1 receptor. Acetaminophen 0-13 cannabinoid receptor 1 (brain) Mus musculus 253-256 19580839-1 2009 Acetaminophen (Paracetamol), a most commonly used antipyretic/analgesic agent, is metabolized to AM404 (N-arachidonoylphenolamine) that inhibits uptake and degradation of anandamide which is reported to mediate the analgesic action of acetaminophen via CB1 receptor. Acetaminophen 15-26 cannabinoid receptor 1 (brain) Mus musculus 253-256 19647030-6 2009 Serum AST and ALT were significantly increased by single oral administration of acetaminophen (1000 mg/kg) to these SOD2-knockdown rats without fasting compared with the control adenovirus infected groups. Acetaminophen 80-93 superoxide dismutase 2 Rattus norvegicus 116-120 19647030-7 2009 Heme oxygenase-1 protein, known to be induced by oxidative stress, was detected in SOD2-knockdown rats administered acetaminophen. Acetaminophen 116-129 heme oxygenase 1 Rattus norvegicus 0-16 19647030-7 2009 Heme oxygenase-1 protein, known to be induced by oxidative stress, was detected in SOD2-knockdown rats administered acetaminophen. Acetaminophen 116-129 superoxide dismutase 2 Rattus norvegicus 83-87 19762092-5 2009 This can be investigated using whole blood assays, an approach used recently to show that acetaminophen (paracetamol) is a COX-2-selective inhibitor. Acetaminophen 90-103 mitochondrially encoded cytochrome c oxidase II Homo sapiens 123-128 19762092-5 2009 This can be investigated using whole blood assays, an approach used recently to show that acetaminophen (paracetamol) is a COX-2-selective inhibitor. Acetaminophen 105-116 mitochondrially encoded cytochrome c oxidase II Homo sapiens 123-128 19446955-6 2009 After the 7-day exposure, the activity of peroxidase and superoxide dismutase in wheat leaves increased with an increase in the concentration of paracetamol in order to eliminate the peroxides produced and maintain the function of cells. Acetaminophen 145-156 peroxidase-like Triticum aestivum 42-52 19446955-7 2009 However, the activity of peroxidase in wheat roots decreased significantly after the 14-day exposure, which indicated the antioxidative defensive system in wheat roots was damaged by paracetamol. Acetaminophen 183-194 peroxidase-like Triticum aestivum 25-35 19576946-7 2009 Elevation of serum ALT and AST activities, decrease of reduced glutathione levels and histopathological liver changes were observed to the same extents in both APAP-treated groups. Acetaminophen 160-164 glutamic pyruvic transaminase, soluble Mus musculus 19-22 19576946-7 2009 Elevation of serum ALT and AST activities, decrease of reduced glutathione levels and histopathological liver changes were observed to the same extents in both APAP-treated groups. Acetaminophen 160-164 transmembrane protease, serine 11d Mus musculus 27-30 19679878-0 2009 Beta-catenin activation promotes liver regeneration after acetaminophen-induced injury. Acetaminophen 58-71 catenin beta 1 Homo sapiens 0-12 19679878-6 2009 A nonlethal dose of acetaminophen, which induces liver regeneration, led to stabilization and activation of beta-catenin for 1 to 12 hours. Acetaminophen 20-33 catenin beta 1 Homo sapiens 108-120 19679878-9 2009 These observations were next substantiated in beta-catenin conditional-null mice (beta-catenin-null), which show dampened regeneration after acetaminophen injury following induction of CYP2e1/1a2 expression. Acetaminophen 141-154 catenin (cadherin associated protein), beta 1 Mus musculus 46-58 19679878-9 2009 These observations were next substantiated in beta-catenin conditional-null mice (beta-catenin-null), which show dampened regeneration after acetaminophen injury following induction of CYP2e1/1a2 expression. Acetaminophen 141-154 catenin (cadherin associated protein), beta 1 Mus musculus 82-94 19679878-12 2009 Retrospective analysis of liver samples from acetaminophen-overdose patients demonstrated a positive correlation between nuclear beta-catenin, proliferation, and spontaneous liver regeneration. Acetaminophen 45-58 catenin beta 1 Homo sapiens 129-141 19679878-13 2009 Thus, our studies demonstrate early activation of beta-catenin signaling during acetaminophen-induced injury, which contributes to hepatic regeneration. Acetaminophen 80-93 catenin beta 1 Homo sapiens 50-62 19700751-9 2009 Eventually, the protective effect of orally administered glucose on liver injury induced by LPS, overdose of acetaminophen, or alpha-amanitin was shown to be mediated by the anti-inflammatory cytokine interleukin-10. Acetaminophen 109-122 interleukin 10 Mus musculus 201-215 19487254-3 2009 The hypothesis that sex-dependent Bcrp expression influences the hepatobiliary disposition of phase II metabolites was tested in the present study using acetaminophen (APAP) and the generated APAP glucuronide (AG) and sulfate (AS) metabolites in single-pass in situ perfused livers from male and female wild-type and Abcg(-/-) (Bcrp-deficient) mice. Acetaminophen 153-166 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 34-38 19487254-3 2009 The hypothesis that sex-dependent Bcrp expression influences the hepatobiliary disposition of phase II metabolites was tested in the present study using acetaminophen (APAP) and the generated APAP glucuronide (AG) and sulfate (AS) metabolites in single-pass in situ perfused livers from male and female wild-type and Abcg(-/-) (Bcrp-deficient) mice. Acetaminophen 168-172 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 34-38 19487254-3 2009 The hypothesis that sex-dependent Bcrp expression influences the hepatobiliary disposition of phase II metabolites was tested in the present study using acetaminophen (APAP) and the generated APAP glucuronide (AG) and sulfate (AS) metabolites in single-pass in situ perfused livers from male and female wild-type and Abcg(-/-) (Bcrp-deficient) mice. Acetaminophen 192-196 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 34-38 19928578-3 2009 The most pronounced chondroprotective effect of paracetamol was observed in doses of 1/4 MTD and 1/8 MTD (10 and 5 mg/kg, respectively), but not in the case of MTD. Acetaminophen 48-59 WD repeat and HMG-box DNA binding protein 1 Homo sapiens 85-104 19928578-3 2009 The most pronounced chondroprotective effect of paracetamol was observed in doses of 1/4 MTD and 1/8 MTD (10 and 5 mg/kg, respectively), but not in the case of MTD. Acetaminophen 48-59 metallothionein 1E Homo sapiens 89-92 19416960-0 2009 Mouse population-guided resequencing reveals that variants in CD44 contribute to acetaminophen-induced liver injury in humans. Acetaminophen 81-94 CD44 molecule (Indian blood group) Homo sapiens 62-66 19416960-9 2009 Finally, we demonstrated that variation in the orthologous human gene, CD44, is associated with susceptibility to acetaminophen in two independent cohorts. Acetaminophen 114-127 CD44 molecule (Indian blood group) Homo sapiens 71-75 19416960-10 2009 Our results indicate a role for CD44 in modulation of susceptibility to acetaminophen hepatotoxicity. Acetaminophen 72-85 CD44 molecule (Indian blood group) Homo sapiens 32-36 19394078-3 2009 Primary hepatocytes cultured for 7 days with the in situ controlled released TGF-beta1 exhibited up to four-fold higher albumin secretion and two-fold higher phase I/II enzymatic activities, significantly improving the sensitivity of hepatocytes to acetaminophen-mediated hepatotoxicity, compared to hepatocytes cultured with directly perfused TGF-beta1 or without TGF-beta1. Acetaminophen 249-262 transforming growth factor beta 1 Homo sapiens 77-86 19460945-0 2009 Rifampicin-activated human pregnane X receptor and CYP3A4 induction enhance acetaminophen-induced toxicity. Acetaminophen 76-89 nuclear receptor subfamily 1 group I member 2 Homo sapiens 27-46 19460945-0 2009 Rifampicin-activated human pregnane X receptor and CYP3A4 induction enhance acetaminophen-induced toxicity. Acetaminophen 76-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 nuclear receptor subfamily 1 group I member 2 Homo sapiens 6-9 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 glutamic--pyruvic transaminase Homo sapiens 102-126 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 glutamic pyruvic transaminase, soluble Mus musculus 128-131 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 solute carrier family 17 member 5 Homo sapiens 137-163 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 solute carrier family 17 member 5 Homo sapiens 165-168 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 262-266 nuclear receptor subfamily 1 group I member 2 Homo sapiens 6-9 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 262-266 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 262-266 nuclear receptor subfamily 1 group I member 2 Homo sapiens 6-9 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 262-266 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19460945-4 2009 In contrast, hPXR mice, wild-type mice, and Pxr-null mice exhibited significantly lower ALT/AST levels compared with TgCYP3A4/hPXR mice after APAP administration. Acetaminophen 142-146 nuclear receptor subfamily 1, group I, member 2 Mus musculus 44-47 19460945-4 2009 In contrast, hPXR mice, wild-type mice, and Pxr-null mice exhibited significantly lower ALT/AST levels compared with TgCYP3A4/hPXR mice after APAP administration. Acetaminophen 142-146 glutamic pyruvic transaminase, soluble Mus musculus 88-91 19460945-4 2009 In contrast, hPXR mice, wild-type mice, and Pxr-null mice exhibited significantly lower ALT/AST levels compared with TgCYP3A4/hPXR mice after APAP administration. Acetaminophen 142-146 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 92-95 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 72-76 nuclear receptor subfamily 1 group I member 2 Homo sapiens 39-42 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 72-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 72-76 nuclear receptor subfamily 1 group I member 2 Homo sapiens 164-167 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 140-144 nuclear receptor subfamily 1 group I member 2 Homo sapiens 39-42 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 140-144 nuclear receptor subfamily 1 group I member 2 Homo sapiens 164-167 19308365-11 2009 CONCLUSIONS: Our study revealed significant inhibition in the O-demethylation of codeine to morphine in homozygous EM of CYP2D6 treated with low-dose levomepromazine and codeine/paracetamol, compared to treatment with codeine/paracetamol only. Acetaminophen 178-189 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 121-127 19308365-11 2009 CONCLUSIONS: Our study revealed significant inhibition in the O-demethylation of codeine to morphine in homozygous EM of CYP2D6 treated with low-dose levomepromazine and codeine/paracetamol, compared to treatment with codeine/paracetamol only. Acetaminophen 226-237 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 121-127 19409413-0 2009 Molecular interaction of human serum albumin with paracetamol: spectroscopic and molecular modeling studies. Acetaminophen 50-61 albumin Homo sapiens 31-44 19409413-1 2009 The interaction between paracetamol and human serum albumin (HSA) under physiological conditions has been investigated by fluorescence, circular dichroism (CD) and docking. Acetaminophen 24-35 albumin Homo sapiens 46-59 19641606-0 2009 Aging-associated dysfunction of Akt/protein kinase B: S-nitrosylation and acetaminophen intervention. Acetaminophen 74-87 AKT serine/threonine kinase 1 Rattus norvegicus 32-35 19641606-4 2009 Here we report a novel dysfunction of Akt in aging muscle, which may relate to S-nitrosylation and can be prevented by acetaminophen intervention. Acetaminophen 119-132 AKT serine/threonine kinase 1 Rattus norvegicus 38-41 19641606-10 2009 CONCLUSIONS: These data demonstrate that Akt dysfunction and increased S-nitrosylation of Akt may contribute to age-associated disorders in skeletal muscle and that acetaminophen may be efficacious for the treatment of age-related muscle dysfunction. Acetaminophen 165-178 AKT serine/threonine kinase 1 Rattus norvegicus 41-44 19446244-4 2009 After a 23.5h recovery period, the PAP fraction that did penetrate was completely N-acetylated to acetaminophen (APAP). Acetaminophen 98-111 poly(A) polymerase alpha Homo sapiens 35-38 19446244-4 2009 After a 23.5h recovery period, the PAP fraction that did penetrate was completely N-acetylated to acetaminophen (APAP). Acetaminophen 113-117 poly(A) polymerase alpha Homo sapiens 35-38 19527004-4 2009 The utility of this methodology was evaluated through analysis of NAC conjugates of acetaminophen in human urine after an oral dose. Acetaminophen 84-97 X-linked Kx blood group Homo sapiens 66-69 19513568-4 2009 It was also found that APAP selectively caused escalation in reactive oxygen species (ROS) formation and intracellular GSH (ICG) depletion in melanocytic human SK-MEL-28 and murine B16-F0 melanoma cells that express functional tyrosinase whereas it lacked significant effects on ROS formation and ICG in amelanotic C32 melanoma cells that do not express functional tyrosinase. Acetaminophen 23-27 tyrosinase Mus musculus 227-237 19513568-4 2009 It was also found that APAP selectively caused escalation in reactive oxygen species (ROS) formation and intracellular GSH (ICG) depletion in melanocytic human SK-MEL-28 and murine B16-F0 melanoma cells that express functional tyrosinase whereas it lacked significant effects on ROS formation and ICG in amelanotic C32 melanoma cells that do not express functional tyrosinase. Acetaminophen 23-27 tyrosinase Mus musculus 365-375 19219624-4 2009 This induction was delayed compared to COX-2 induced by LPS and paracetamol selectively inhibited activity of this protein. Acetaminophen 64-75 prostaglandin-endoperoxide synthase 2 Mus musculus 39-44 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 241-244 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 interleukin 6 signal transducer Mus musculus 250-281 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 interleukin 6 signal transducer Mus musculus 283-288 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 oncostatin M receptor Mus musculus 355-376 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 oncostatin M receptor Mus musculus 378-382 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 MLX interacting protein-like Mus musculus 388-416 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 157-170 MLX interacting protein-like Mus musculus 418-424 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 241-244 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 interleukin 6 signal transducer Mus musculus 250-281 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 interleukin 6 signal transducer Mus musculus 283-288 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 oncostatin M receptor Mus musculus 355-376 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 oncostatin M receptor Mus musculus 378-382 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 MLX interacting protein-like Mus musculus 388-416 19420014-7 2009 Importantly, most of these biomarker genes are part of the intracellular signaling involved in hepatocyte death and include genes previously associated with acetaminophen-induced hepatotoxicity, such as cyclin-dependent kinase inhibitor 1A (p21) and interleukin 6 signal transducer (Il6st), and genes not previously associated with acetaminophen, such as oncostatin M receptor (Osmr) and MLX interacting protein like (Mlxipl). Acetaminophen 332-345 MLX interacting protein-like Mus musculus 418-424 19109935-5 2009 A significant elevation (p<0.001) of the levels of AST and ALT was observed in mice toxicated with APAP. Acetaminophen 102-106 transmembrane protease, serine 11d Mus musculus 54-57 19109935-5 2009 A significant elevation (p<0.001) of the levels of AST and ALT was observed in mice toxicated with APAP. Acetaminophen 102-106 glutamic pyruvic transaminase, soluble Mus musculus 62-65 19109935-7 2009 However, a significant inhibition (p<0.05) in the elevation of AST and ALT was observed in mice that received UBG and GIBG compared with APAP-treated mice. Acetaminophen 140-144 transmembrane protease, serine 11d Mus musculus 66-69 19109935-7 2009 However, a significant inhibition (p<0.05) in the elevation of AST and ALT was observed in mice that received UBG and GIBG compared with APAP-treated mice. Acetaminophen 140-144 glutamic pyruvic transaminase, soluble Mus musculus 74-77 19589095-2 2009 We investigated the effect of subtoxic concentrations of acetaminophen in conjunction with bacterial lipopolysaccharide (LPS) on the expression of the pro-inflammatory cytokines TNFalpha and IL-1beta using the mouse macrophage cell line RAW264.7 as a model. Acetaminophen 57-70 tumor necrosis factor Mus musculus 178-186 19589095-2 2009 We investigated the effect of subtoxic concentrations of acetaminophen in conjunction with bacterial lipopolysaccharide (LPS) on the expression of the pro-inflammatory cytokines TNFalpha and IL-1beta using the mouse macrophage cell line RAW264.7 as a model. Acetaminophen 57-70 interleukin 1 beta Mus musculus 191-199 19589095-3 2009 APAP alone induced in a dose-dependent manner the production of TNFalpha and IL-1beta in this cell line. Acetaminophen 0-4 tumor necrosis factor Mus musculus 64-72 19589095-3 2009 APAP alone induced in a dose-dependent manner the production of TNFalpha and IL-1beta in this cell line. Acetaminophen 0-4 interleukin 1 beta Mus musculus 77-85 19589095-4 2009 When LPS was added to APAP-treated cells, the increase in TNFalpha and IL-1beta production observed was higher than the sum of cytokine amounts produced with each agent alone, suggesting a synergistic mechanism. Acetaminophen 22-26 tumor necrosis factor Mus musculus 58-66 19589095-4 2009 When LPS was added to APAP-treated cells, the increase in TNFalpha and IL-1beta production observed was higher than the sum of cytokine amounts produced with each agent alone, suggesting a synergistic mechanism. Acetaminophen 22-26 interleukin 1 beta Mus musculus 71-79 19589095-5 2009 Moreover, we found that p38MAPK, JNK, and ERK were activated by APAP or LPS alone or in association. Acetaminophen 64-68 mitogen-activated protein kinase 14 Mus musculus 24-31 19589095-5 2009 Moreover, we found that p38MAPK, JNK, and ERK were activated by APAP or LPS alone or in association. Acetaminophen 64-68 mitogen-activated protein kinase 8 Mus musculus 33-36 19589095-5 2009 Moreover, we found that p38MAPK, JNK, and ERK were activated by APAP or LPS alone or in association. Acetaminophen 64-68 mitogen-activated protein kinase 1 Mus musculus 42-45 19589095-7 2009 When inhibiting MAPKs using pharmacological inhibitors, we showed that p38MAPK inhibition abrogated the synergistic effect of APAP and LPS found for TNFalpha production but not for IL-1beta production. Acetaminophen 126-130 mitogen-activated protein kinase 14 Mus musculus 71-78 19589095-7 2009 When inhibiting MAPKs using pharmacological inhibitors, we showed that p38MAPK inhibition abrogated the synergistic effect of APAP and LPS found for TNFalpha production but not for IL-1beta production. Acetaminophen 126-130 tumor necrosis factor Mus musculus 149-157 19589095-9 2009 Furafylline, a CYP1A inhibitor, and indomethacin, a PGHS inhibitor, exhibited a significant inhibitory effect on TNFalpha and IL-1beta production induced by the APAP and LPS combination. Acetaminophen 161-165 tumor necrosis factor Mus musculus 113-121 19589095-9 2009 Furafylline, a CYP1A inhibitor, and indomethacin, a PGHS inhibitor, exhibited a significant inhibitory effect on TNFalpha and IL-1beta production induced by the APAP and LPS combination. Acetaminophen 161-165 interleukin 1 beta Mus musculus 126-134 19589095-10 2009 This work suggests that in macrophages, APAP and LPS can synergistically provoke the induction of pro-inflammatory cytokines, an effect involving the MAPK pathway and APAP bioactivation by CYP and PGHS. Acetaminophen 40-44 mitogen-activated protein kinase 1 Mus musculus 150-154 19155536-6 2009 RESULTS: The progression rate for regular users of acetaminophen was slower than that for non-regular users (regular users progressed 0.93 mL/min/1.73 m(2) per year slower than non-regular users; 95% CI 0.03, 1.8). Acetaminophen 51-64 CD59 molecule (CD59 blood group) Homo sapiens 142-147 19519048-0 2009 Spin-density wave fermi surface reconstruction in underdoped YBa2Cu3O6+x. Acetaminophen 71-72 spindlin 1 Homo sapiens 0-4 19426699-7 2009 APAP pre-treatment induced a partial shift from biliary to urinary elimination of APAP-Glu after administration with the toxic dose, and decreased hepatic content and increased serum content of this conjugate, consistent with a marked up-regulation of its basolateral transporter Mrp3 relative to apical Mrp2. Acetaminophen 0-4 ATP binding cassette subfamily C member 3 Rattus norvegicus 280-284 19426699-7 2009 APAP pre-treatment induced a partial shift from biliary to urinary elimination of APAP-Glu after administration with the toxic dose, and decreased hepatic content and increased serum content of this conjugate, consistent with a marked up-regulation of its basolateral transporter Mrp3 relative to apical Mrp2. Acetaminophen 0-4 ATP binding cassette subfamily C member 2 Rattus norvegicus 304-308 19014921-0 2009 Th1/Th2 cytokine balance as a determinant of acetaminophen-induced liver injury. Acetaminophen 45-58 negative elongation factor complex member C/D, Th1l Mus musculus 0-3 19014921-0 2009 Th1/Th2 cytokine balance as a determinant of acetaminophen-induced liver injury. Acetaminophen 45-58 heart and neural crest derivatives expressed 2 Mus musculus 4-7 19014921-4 2009 Acetaminophen-induced liver injury was investigated in two mouse strains, C57BL/6 and BALB/c, which develop predominantly Th1 and Th2 responses, respectively. Acetaminophen 0-13 negative elongation factor complex member C/D, Th1l Mus musculus 122-125 19014921-4 2009 Acetaminophen-induced liver injury was investigated in two mouse strains, C57BL/6 and BALB/c, which develop predominantly Th1 and Th2 responses, respectively. Acetaminophen 0-13 heart and neural crest derivatives expressed 2 Mus musculus 130-133 19014921-8 2009 TNF-alpha was highly induced 24 h after administration of acetaminophen in C57BL/6 mice, whereas no change in BALB/c mice. Acetaminophen 58-71 tumor necrosis factor Mus musculus 0-9 19014921-10 2009 In addition, treatment of CD-1 mice, another susceptible strain, with an anti-inflammatory polyphenol, resveratrol, protected mice against the acetaminophen-induced liver injury, and the mice with attenuated toxicity revealed lower expression of TNF-alpha and higher expression of IL-6. Acetaminophen 143-156 CD1 antigen complex Mus musculus 26-30 19014921-11 2009 It is therefore suggested that acetaminophen-induced liver injury is associated with Th1-dominant response in Th1/Th2 cytokine balance, and TNF-alpha may play a pathological role in the toxicity. Acetaminophen 31-44 negative elongation factor complex member C/D, Th1l Mus musculus 85-88 19014921-11 2009 It is therefore suggested that acetaminophen-induced liver injury is associated with Th1-dominant response in Th1/Th2 cytokine balance, and TNF-alpha may play a pathological role in the toxicity. Acetaminophen 31-44 negative elongation factor complex member C/D, Th1l Mus musculus 110-113 19014921-11 2009 It is therefore suggested that acetaminophen-induced liver injury is associated with Th1-dominant response in Th1/Th2 cytokine balance, and TNF-alpha may play a pathological role in the toxicity. Acetaminophen 31-44 heart and neural crest derivatives expressed 2 Mus musculus 114-117 19675387-11 2009 RESULTS: PCM toxicity significantly increased ALT, AST and ALP (321.00 +/- 87.93, 273.17 +/- 45.68, 257.50 +/- 17.64 IU/l vs normal control, 33.33 +/- 0.61, 89.33 +/- 9.50, 152.17 +/- 11.40 IU/l respectively, P<0.05), prolonged phenobarbitone induced sleeping time (from 277.50 +/- 8.04 min to 335.83 +/- 7.00 min, P<0.05). Acetaminophen 9-12 glutamic pyruvic transaminase, soluble Mus musculus 46-49 19675387-11 2009 RESULTS: PCM toxicity significantly increased ALT, AST and ALP (321.00 +/- 87.93, 273.17 +/- 45.68, 257.50 +/- 17.64 IU/l vs normal control, 33.33 +/- 0.61, 89.33 +/- 9.50, 152.17 +/- 11.40 IU/l respectively, P<0.05), prolonged phenobarbitone induced sleeping time (from 277.50 +/- 8.04 min to 335.83 +/- 7.00 min, P<0.05). Acetaminophen 9-12 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 51-54 19265712-9 2009 In addition, we document, for the first time, that acetaminophen increases expression of the anti-apoptotic protein Bcl2. Acetaminophen 51-64 BCL2 apoptosis regulator Homo sapiens 116-120 19265712-10 2009 Suppressing Bcl2 with siRNA blocks the pro-survival effect of acetaminophen. Acetaminophen 62-75 BCL2 apoptosis regulator Homo sapiens 12-16 19246624-0 2009 Altered disposition of acetaminophen in Nrf2-null and Keap1-knockdown mice. Acetaminophen 23-36 nuclear factor, erythroid derived 2, like 2 Mus musculus 40-44 19246624-0 2009 Altered disposition of acetaminophen in Nrf2-null and Keap1-knockdown mice. Acetaminophen 23-36 kelch-like ECH-associated protein 1 Mus musculus 54-59 19370779-0 2009 Protective effect of tea polyphenols against paracetamol-induced hepatotoxicity in mice is significantly correlated with cytochrome P450 suppression. Acetaminophen 45-56 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 Mus musculus 21-24 19370779-0 2009 Protective effect of tea polyphenols against paracetamol-induced hepatotoxicity in mice is significantly correlated with cytochrome P450 suppression. Acetaminophen 45-56 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 121-136 19283895-0 2009 Oleanolic acid activates Nrf2 and protects from acetaminophen hepatotoxicity via Nrf2-dependent and Nrf2-independent processes. Acetaminophen 48-61 nuclear factor, erythroid derived 2, like 2 Mus musculus 81-85 19283895-0 2009 Oleanolic acid activates Nrf2 and protects from acetaminophen hepatotoxicity via Nrf2-dependent and Nrf2-independent processes. Acetaminophen 48-61 nuclear factor, erythroid derived 2, like 2 Mus musculus 81-85 19283895-8 2009 Oleanolic acid-mediated Nrf2-independent protection from acetaminophen is, in part, due to induction of Nrf2-independent cytoprotective genes, such as metallothionein. Acetaminophen 57-70 nuclear factor, erythroid derived 2, like 2 Mus musculus 24-28 19283895-8 2009 Oleanolic acid-mediated Nrf2-independent protection from acetaminophen is, in part, due to induction of Nrf2-independent cytoprotective genes, such as metallothionein. Acetaminophen 57-70 nuclear factor, erythroid derived 2, like 2 Mus musculus 104-108 19283895-9 2009 Collectively, the present study demonstrates that oleanolic acid facilitates Nrf2 nuclear accumulation, causing induction of Nrf2-dependent genes, which contributes to protection from acetaminophen hepatotoxicity. Acetaminophen 184-197 nuclear factor, erythroid derived 2, like 2 Mus musculus 77-81 19283895-9 2009 Collectively, the present study demonstrates that oleanolic acid facilitates Nrf2 nuclear accumulation, causing induction of Nrf2-dependent genes, which contributes to protection from acetaminophen hepatotoxicity. Acetaminophen 184-197 nuclear factor, erythroid derived 2, like 2 Mus musculus 125-129 19256530-0 2009 Serum metabolomics reveals irreversible inhibition of fatty acid beta-oxidation through the suppression of PPARalpha activation as a contributing mechanism of acetaminophen-induced hepatotoxicity. Acetaminophen 159-172 peroxisome proliferator activated receptor alpha Mus musculus 107-116 19256530-3 2009 In this study, serum metabolomes of control and APAP-treated wild-type and Cyp2e1-null mice were examined by liquid chromatography-mass spectrometry (LC-MS) and multivariate data analysis. Acetaminophen 48-52 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 75-81 19256530-6 2009 A time-course study further indicated that both wild-type and Cyp2e1-null mice had their serum acylcarnitine levels markedly elevated within the early hours of APAP treatment. Acetaminophen 160-164 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 62-68 19256530-10 2009 The upregulation of PPARalpha activity following APAP treatment was transient in wild-type mice but was much more prolonged in Cyp2e1-null mice. Acetaminophen 49-53 peroxisome proliferator activated receptor alpha Mus musculus 20-29 19256530-10 2009 The upregulation of PPARalpha activity following APAP treatment was transient in wild-type mice but was much more prolonged in Cyp2e1-null mice. Acetaminophen 49-53 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 127-133 19256530-11 2009 Overall, serum metabolomics of APAP-induced hepatotoxicity revealed that the CYP2E1-mediated metabolic activation and oxidative stress following APAP treatment can cause irreversible inhibition of fatty acid oxidation, potentially through suppression of PPARalpha-regulated pathways. Acetaminophen 31-35 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 77-83 19256530-11 2009 Overall, serum metabolomics of APAP-induced hepatotoxicity revealed that the CYP2E1-mediated metabolic activation and oxidative stress following APAP treatment can cause irreversible inhibition of fatty acid oxidation, potentially through suppression of PPARalpha-regulated pathways. Acetaminophen 31-35 peroxisome proliferator activated receptor alpha Mus musculus 254-263 19256530-11 2009 Overall, serum metabolomics of APAP-induced hepatotoxicity revealed that the CYP2E1-mediated metabolic activation and oxidative stress following APAP treatment can cause irreversible inhibition of fatty acid oxidation, potentially through suppression of PPARalpha-regulated pathways. Acetaminophen 145-149 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 77-83 19256530-11 2009 Overall, serum metabolomics of APAP-induced hepatotoxicity revealed that the CYP2E1-mediated metabolic activation and oxidative stress following APAP treatment can cause irreversible inhibition of fatty acid oxidation, potentially through suppression of PPARalpha-regulated pathways. Acetaminophen 145-149 peroxisome proliferator activated receptor alpha Mus musculus 254-263 19459732-8 2009 These results suggest that AF protects against APAP-induced hepatotoxicity by blocking CYP2E1-mediated APAP bioactivation, by up-regulating hepatic GSH levels, and by acting as a free radical scavenger. Acetaminophen 47-51 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 87-93 19459732-8 2009 These results suggest that AF protects against APAP-induced hepatotoxicity by blocking CYP2E1-mediated APAP bioactivation, by up-regulating hepatic GSH levels, and by acting as a free radical scavenger. Acetaminophen 103-107 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 87-93 19167421-6 2009 The synergism was: COX-3>COX-2>COX-1 inhibitors, this is particularly interesting since the inhibitor of COX-3, paracetamol, displayed a robust anti-inflammatory activity in an assay of acute and inflammatory pain that mimics inflammatory pain in humans. Acetaminophen 118-129 mitochondrially encoded cytochrome c oxidase III Homo sapiens 19-24 19167421-6 2009 The synergism was: COX-3>COX-2>COX-1 inhibitors, this is particularly interesting since the inhibitor of COX-3, paracetamol, displayed a robust anti-inflammatory activity in an assay of acute and inflammatory pain that mimics inflammatory pain in humans. Acetaminophen 118-129 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-33 19167421-6 2009 The synergism was: COX-3>COX-2>COX-1 inhibitors, this is particularly interesting since the inhibitor of COX-3, paracetamol, displayed a robust anti-inflammatory activity in an assay of acute and inflammatory pain that mimics inflammatory pain in humans. Acetaminophen 118-129 mitochondrially encoded cytochrome c oxidase I Homo sapiens 37-42 19167421-6 2009 The synergism was: COX-3>COX-2>COX-1 inhibitors, this is particularly interesting since the inhibitor of COX-3, paracetamol, displayed a robust anti-inflammatory activity in an assay of acute and inflammatory pain that mimics inflammatory pain in humans. Acetaminophen 118-129 mitochondrially encoded cytochrome c oxidase III Homo sapiens 111-116 19371622-1 2009 During APAP toxicity, activation of Kupffer cells is critical for protection from hepatotoxicity and up-regulation of multidrug resistance-associated protein 4 (Mrp4) in centrilobular hepatocytes. Acetaminophen 7-11 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 118-159 19371622-1 2009 During APAP toxicity, activation of Kupffer cells is critical for protection from hepatotoxicity and up-regulation of multidrug resistance-associated protein 4 (Mrp4) in centrilobular hepatocytes. Acetaminophen 7-11 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 161-165 19371629-0 2009 CDDO-Im protects from acetaminophen hepatotoxicity through induction of Nrf2-dependent genes. Acetaminophen 22-35 nuclear factor, erythroid derived 2, like 2 Mus musculus 72-76 19291322-11 2009 In addition, we document, for the first time, that acetaminophen increases expression of the anti-apoptotic protein Bcl2 in brain neurons and decreases the menadione-induced elevation of the proapoptotic protein, cleaved caspase 3. Acetaminophen 51-64 BCL2 apoptosis regulator Homo sapiens 116-120 19291322-12 2009 We show that blocking acetaminophen-induced expression of Bcl2 reduces the pro-survival effect of the drug. Acetaminophen 22-35 BCL2 apoptosis regulator Homo sapiens 58-62 19041234-6 2009 Also, HS-PDPA-GOx electrode shows high selectivity towards glucose in the presence of ascorbic acid, uric acid and acetaminophen at their maximum physiological concentrations. Acetaminophen 115-128 hydroxyacid oxidase 1 Homo sapiens 14-17 19177471-0 2009 Acetaminophen prevents aging-associated hyperglycemia in aged rats: effect of aging-associated hyperactivation of p38-MAPK and ERK1/2. Acetaminophen 0-13 mitogen activated protein kinase 14 Rattus norvegicus 114-117 19177471-0 2009 Acetaminophen prevents aging-associated hyperglycemia in aged rats: effect of aging-associated hyperactivation of p38-MAPK and ERK1/2. Acetaminophen 0-13 mitogen activated protein kinase 3 Rattus norvegicus 127-133 19177471-5 2009 Chronic acetaminophen treatment attenuated age-associated increase in blood glucose by 61.3% (p<0.05) and increased soleus Glut4 protein by 157.2% (p<0.05). Acetaminophen 8-21 solute carrier family 2 member 4 Rattus norvegicus 126-131 21783944-3 2009 HEK 293 cells were cultured in 96-well plates and then pretreated with or without 20muM acetaminophen (IC(50) value: 17.5+-1.9) for 1h. Acetaminophen 88-101 latexin Homo sapiens 84-87 21783952-6 2009 Hemin attenuated the acetaminophen-induced elevations in renal tumor necrosis factor-alpha and nitric oxide levels, and caspase-3 activity. Acetaminophen 21-34 tumor necrosis factor Rattus norvegicus 63-90 21783952-6 2009 Hemin attenuated the acetaminophen-induced elevations in renal tumor necrosis factor-alpha and nitric oxide levels, and caspase-3 activity. Acetaminophen 21-34 caspase 3 Rattus norvegicus 120-129 19280152-5 2009 After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 mug/kg). Acetaminophen 202-206 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 87-113 19280152-5 2009 After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 mug/kg). Acetaminophen 315-319 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 87-113 19028810-7 2009 A combination of CIH and APAP caused liver injury, with marked increases in serum alanine aminotransferase, aspartate aminotransferase (AST), gamma-glutamyl transferase and total bilirubin levels, whereas CIH alone induced only elevation in serum AST levels. Acetaminophen 25-29 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 108-134 19028810-7 2009 A combination of CIH and APAP caused liver injury, with marked increases in serum alanine aminotransferase, aspartate aminotransferase (AST), gamma-glutamyl transferase and total bilirubin levels, whereas CIH alone induced only elevation in serum AST levels. Acetaminophen 25-29 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 136-139 19028810-7 2009 A combination of CIH and APAP caused liver injury, with marked increases in serum alanine aminotransferase, aspartate aminotransferase (AST), gamma-glutamyl transferase and total bilirubin levels, whereas CIH alone induced only elevation in serum AST levels. Acetaminophen 25-29 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 247-250 19028810-12 2009 A combination of CIH and APAP caused marked increases in pro-inflammatory chemokines, monocyte chemoattractant protein-1 and macrophage inflammatory protein-2, which were not observed in mice exposed to CIH or APAP alone. Acetaminophen 25-29 chemokine (C-C motif) ligand 2 Mus musculus 86-120 19028810-12 2009 A combination of CIH and APAP caused marked increases in pro-inflammatory chemokines, monocyte chemoattractant protein-1 and macrophage inflammatory protein-2, which were not observed in mice exposed to CIH or APAP alone. Acetaminophen 25-29 chemokine (C-X-C motif) ligand 2 Mus musculus 125-158 19085960-9 2009 CONCLUSION: Using animal models of hepatoxicity induced by carbon tetrachloride and acetaminophen, we found that both serum ALT1 and ALT2 protein levels were significantly elevated and correlated with ALT activity, providing, for the first time, the molecular basis for the elevated total serum ALT activity. Acetaminophen 84-97 glutamic--pyruvic transaminase Rattus norvegicus 124-128 19085960-9 2009 CONCLUSION: Using animal models of hepatoxicity induced by carbon tetrachloride and acetaminophen, we found that both serum ALT1 and ALT2 protein levels were significantly elevated and correlated with ALT activity, providing, for the first time, the molecular basis for the elevated total serum ALT activity. Acetaminophen 84-97 glutamic--pyruvic transaminase 2 Rattus norvegicus 133-137 19164858-0 2009 Acetaminophen-induced hepatotoxicity in mice is dependent on Tlr9 and the Nalp3 inflammasome. Acetaminophen 0-13 toll-like receptor 9 Mus musculus 61-65 19164858-0 2009 Acetaminophen-induced hepatotoxicity in mice is dependent on Tlr9 and the Nalp3 inflammasome. Acetaminophen 0-13 NLR family, pyrin domain containing 3 Mus musculus 74-79 19164858-6 2009 By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Acetaminophen 248-261 caspase 1 Mus musculus 14-23 19164858-6 2009 By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Acetaminophen 248-261 interleukin 1 beta Mus musculus 70-78 19164858-6 2009 By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Acetaminophen 248-261 interleukin 18 Mus musculus 83-88 19164858-6 2009 By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Acetaminophen 248-261 interleukin 1 beta Mus musculus 98-106 19164858-6 2009 By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Acetaminophen 248-261 interleukin 18 Mus musculus 115-120 19164858-6 2009 By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Acetaminophen 248-261 NLR family, pyrin domain containing 3 Mus musculus 140-145 19164858-7 2009 Tlr9 antagonists and aspirin reduced mortality from acetaminophen hepatotoxicity. Acetaminophen 52-65 toll-like receptor 9 Mus musculus 0-4 19164858-9 2009 In summary, we have identified a 2-signal requirement (Tlr9 and the Nalp3 inflammasome) for acetaminophen-induced hepatotoxicity and some potential therapeutic approaches. Acetaminophen 92-105 toll-like receptor 9 Mus musculus 55-59 19164858-9 2009 In summary, we have identified a 2-signal requirement (Tlr9 and the Nalp3 inflammasome) for acetaminophen-induced hepatotoxicity and some potential therapeutic approaches. Acetaminophen 92-105 NLR family, pyrin domain containing 3 Mus musculus 68-73 19179955-1 2009 In this second article we describe the more interesting pharmacological interactions in dental practice based on the prescription of analgesic narcotics, paracetamol and non-selective non-steroid anti-inflammatory drugs (NSAI) (which inhibit cyclooxigenase 1 -COX 1- and cyclooxigenase 2 -COX 2-) and selective NSAIs (COX 2 inhibitors). Acetaminophen 154-165 mitochondrially encoded cytochrome c oxidase I Homo sapiens 260-265 19179955-1 2009 In this second article we describe the more interesting pharmacological interactions in dental practice based on the prescription of analgesic narcotics, paracetamol and non-selective non-steroid anti-inflammatory drugs (NSAI) (which inhibit cyclooxigenase 1 -COX 1- and cyclooxigenase 2 -COX 2-) and selective NSAIs (COX 2 inhibitors). Acetaminophen 154-165 mitochondrially encoded cytochrome c oxidase II Homo sapiens 289-294 19179955-1 2009 In this second article we describe the more interesting pharmacological interactions in dental practice based on the prescription of analgesic narcotics, paracetamol and non-selective non-steroid anti-inflammatory drugs (NSAI) (which inhibit cyclooxigenase 1 -COX 1- and cyclooxigenase 2 -COX 2-) and selective NSAIs (COX 2 inhibitors). Acetaminophen 154-165 mitochondrially encoded cytochrome c oxidase II Homo sapiens 318-323 19332662-2 2009 Therefore, we evaluated the reproducibility of troglitazone-induced liver injury in Sod2+/- mice, as well as their validity as an animal model with higher sensitivity to mitochondrial toxicity by single-dose treatment with acetaminophen in Sod2+/- mice. Acetaminophen 223-236 superoxide dismutase 2, mitochondrial Mus musculus 240-244 19332662-4 2009 On the other hand, six hours and twenty-four hours after an administration of 300 mg/kg acetaminophen, plasma ALT activity was significantly increased in Sod2+/- mice, compared to wild-type mice. Acetaminophen 88-101 glutamic pyruvic transaminase, soluble Mus musculus 110-113 19332662-4 2009 On the other hand, six hours and twenty-four hours after an administration of 300 mg/kg acetaminophen, plasma ALT activity was significantly increased in Sod2+/- mice, compared to wild-type mice. Acetaminophen 88-101 superoxide dismutase 2, mitochondrial Mus musculus 154-158 18835260-0 2009 Protection of acetaminophen induced mitochondrial dysfunctions and hepatic necrosis via Akt-NF-kappaB pathway: role of a novel plant protein. Acetaminophen 14-27 thymoma viral proto-oncogene 1 Mus musculus 88-91 18835260-4 2009 Treatment of mice with the protein before administration of acetaminophen also reduced serum nitrite and TNF-alpha formation. Acetaminophen 60-73 tumor necrosis factor Mus musculus 105-114 19107278-4 2009 To validate the feasibility of drug metabolism study on the microfluidic chip, UDP-glucuronosyltransferase (UGT) metabolism of acetaminophen (AP) and its effect on hepG2 cytotoxicity were studied first. Acetaminophen 127-140 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 79-106 19107278-4 2009 To validate the feasibility of drug metabolism study on the microfluidic chip, UDP-glucuronosyltransferase (UGT) metabolism of acetaminophen (AP) and its effect on hepG2 cytotoxicity were studied first. Acetaminophen 127-140 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 108-111 19238980-1 2009 The role of primary active species (ecb(-), hvb(+), *OH, HO2*, O2*(-), and H2O2) during photocatalytic degradation of paracetamol (acetaminophen) using TiO2 catalyst was systematically investigated. Acetaminophen 118-129 heme oxygenase 2 Homo sapiens 57-60 19090677-5 2009 It had previously been shown that the acetaminophen metabolite, N-acetyl-p-benzoquinone imine (NAPQI), covalently binds to the active site of MIF. Acetaminophen 38-51 macrophage migration inhibitory factor Homo sapiens 142-145 19090677-7 2009 The structure of MIF cocrystallized with NAPQI reveals that the NAPQI has undergone a chemical alteration forming an acetaminophen dimer (bi-APAP) and binds noncovalently to MIF at the mouth of the active site. Acetaminophen 117-130 macrophage migration inhibitory factor Homo sapiens 17-20 19007345-1 2009 OBJECTIVES: The objective was to evaluate the effectiveness of intravenous N-acetylcysteine (IV NAC; 300 mg/kg over 21 hours) in early acute acetaminophen (APAP) overdose patients. Acetaminophen 141-154 synuclein alpha Homo sapiens 96-99 19007345-1 2009 OBJECTIVES: The objective was to evaluate the effectiveness of intravenous N-acetylcysteine (IV NAC; 300 mg/kg over 21 hours) in early acute acetaminophen (APAP) overdose patients. Acetaminophen 156-160 synuclein alpha Homo sapiens 96-99 19526678-5 2009 The use of "DockingServer" is illustrated by the formation of acetaminophene (paracetamol)-CYP2E1 complex. Acetaminophen 62-76 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 91-97 19526678-5 2009 The use of "DockingServer" is illustrated by the formation of acetaminophene (paracetamol)-CYP2E1 complex. Acetaminophen 78-89 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 91-97 19345936-5 2009 Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). Acetaminophen 83-90 mitochondrially encoded cytochrome c oxidase I Homo sapiens 31-36 19345936-5 2009 Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). Acetaminophen 83-90 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 21791392-4 2009 Administration of APAP significantly increased the release of serum transaminases, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin and serum proteins, whereas concomitantly decreased hemoglobin, blood sugar and albumin. Acetaminophen 18-22 gamma-glutamyltransferase 1 Rattus norvegicus 128-157 19462927-4 2009 For this reason we undertook a study of the effects of these extracts alone and in combination with paracetamol, along with the action of paracetamol alone, on the activity of the antioxidant enzymes GSHPx, CAT, Px, XOD, GSHR, glutathione content, LPx intensity, as well as activities of AST and ALT. Acetaminophen 100-111 catalase Mus musculus 207-210 19462927-7 2009 In combination with paracetamol, extracts of both Magnum and Aroma varieties reduced significantly the LPx intensity, activities of CAT and GSHPx, as well as GSH content in the liver homogenate. Acetaminophen 20-31 catalase Mus musculus 132-135 19002106-0 2009 Reduced acetaminophen-induced liver injury in mice by genetic disruption of IL-1 receptor antagonist. Acetaminophen 8-21 interleukin 1 receptor antagonist Mus musculus 76-100 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 0-13 interleukin 1 alpha Mus musculus 69-93 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 0-13 interleukin 1 beta Mus musculus 95-104 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 0-13 interleukin 1 receptor antagonist Mus musculus 110-134 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 0-13 interleukin 1 receptor antagonist Mus musculus 136-142 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 15-19 interleukin 1 alpha Mus musculus 69-93 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 15-19 interleukin 1 beta Mus musculus 95-104 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 15-19 interleukin 1 receptor antagonist Mus musculus 110-134 19002106-1 2009 Acetaminophen (APAP) induced increases in intrahepatic expression of interleukin (IL)-1 alpha, IL-1 beta, and IL-1 receptor antagonist (IL-1ra), when administered intraperitoneally. Acetaminophen 15-19 interleukin 1 receptor antagonist Mus musculus 136-142 19002106-3 2009 Compared with wild-type (WT) mouse-derived hepatocytes, IL-1ra-deficient (IL-1ra KO)-derived hepatocytes exhibited more resistance against APAP but not APAP-derived major toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 139-143 interleukin 1 receptor antagonist Mus musculus 56-62 19002106-3 2009 Compared with wild-type (WT) mouse-derived hepatocytes, IL-1ra-deficient (IL-1ra KO)-derived hepatocytes exhibited more resistance against APAP but not APAP-derived major toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 139-143 interleukin 1 receptor antagonist Mus musculus 74-80 19002106-8 2009 Moreover, when mice were intraperitoneally administered APAP (200 mg/kg), IL-1ra KO mice exhibited attenuated APAP-induced liver injury as evidenced by reductions in serum alanine transferase levels and histopathological changes such as centrilobular necrosis, hemorrhages, and leukocyte infiltration. Acetaminophen 56-60 interleukin 1 receptor antagonist Mus musculus 74-80 19002106-8 2009 Moreover, when mice were intraperitoneally administered APAP (200 mg/kg), IL-1ra KO mice exhibited attenuated APAP-induced liver injury as evidenced by reductions in serum alanine transferase levels and histopathological changes such as centrilobular necrosis, hemorrhages, and leukocyte infiltration. Acetaminophen 110-114 interleukin 1 receptor antagonist Mus musculus 74-80 19002106-9 2009 Finally, when given 12 h before APAP challenge, IL-1 alpha repressed the intrahepatic expression of CYP1A2, CYP2E1, and CYP3A11, eventually reducing APAP-induced liver injury, along with reduction in APAP adducts. Acetaminophen 32-36 interleukin 1 alpha Mus musculus 48-58 19002106-9 2009 Finally, when given 12 h before APAP challenge, IL-1 alpha repressed the intrahepatic expression of CYP1A2, CYP2E1, and CYP3A11, eventually reducing APAP-induced liver injury, along with reduction in APAP adducts. Acetaminophen 149-153 interleukin 1 alpha Mus musculus 48-58 19002106-9 2009 Finally, when given 12 h before APAP challenge, IL-1 alpha repressed the intrahepatic expression of CYP1A2, CYP2E1, and CYP3A11, eventually reducing APAP-induced liver injury, along with reduction in APAP adducts. Acetaminophen 149-153 interleukin 1 alpha Mus musculus 48-58 19002106-10 2009 Collectively, NF-kappaB was activated without any stimuli by the genetic disruption of IL-1ra, and suppressed cytochrome P450 enzyme expression, thereby reducing APAP-induced liver injury. Acetaminophen 162-166 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 14-23 18751681-0 2009 Ruthenium red protects HepG2 cells overexpressing CYP2E1 against acetaminophen cytotoxicity. Acetaminophen 65-78 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 50-56 19168428-7 2009 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP) and decrease in total protein. Acetaminophen 0-13 gamma-glutamyltransferase 1 Rattus norvegicus 157-187 19168428-7 2009 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP) and decrease in total protein. Acetaminophen 0-13 gamma-glutamyltransferase 1 Rattus norvegicus 189-193 18380536-9 2009 GR activity was decreased already after 3 h of incubation and remained also decreased in cells treated with 2.5, 5, 10 and 20 mM AAP during further incubation. Acetaminophen 129-132 glutathione-disulfide reductase Rattus norvegicus 0-2 19219744-0 2009 Acetaminophen bioactivation by human cytochrome P450 enzymes and animal microsomes. Acetaminophen 0-13 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 37-52 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 161-164 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 174-180 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 182-188 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 190-196 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 198-204 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 206-212 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 214-221 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 223-229 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 231-237 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 243-249 19219744-9 2009 This study suggests that CYP3A4 is the major CYP enzyme form catalysing acetaminophen oxidation to NAPQI in human liver. Acetaminophen 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19219744-9 2009 This study suggests that CYP3A4 is the major CYP enzyme form catalysing acetaminophen oxidation to NAPQI in human liver. Acetaminophen 72-85 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 25-28 18713872-6 2008 Furthermore, in the absence of the IMs, the resolution of hepatic damage following APAP-induced hepatotoxicity was delayed in CCR2(-/-) mice compared with wild-type mice. Acetaminophen 83-87 chemokine (C-C motif) receptor 2 Mus musculus 126-130 18818195-3 2008 In the process, CYP2E1 can generate toxic or carcinogenic compounds, as occurs with acetaminophen overdose, nitrosamines in cigarette smoke, and reactive oxygen species from uncoupled catalysis. Acetaminophen 84-97 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 16-22 19002085-5 2008 Some investigation have shown that a low concentration of Gc-globulin may be used as a prognostic factor in patients with fulminant hepatic failure, acetaminophen (paracetamol) overdose, multiple trauma or multiple organ dysfunction syndrome (MODS), or sepsis. Acetaminophen 149-162 GC vitamin D binding protein Homo sapiens 58-69 19002085-5 2008 Some investigation have shown that a low concentration of Gc-globulin may be used as a prognostic factor in patients with fulminant hepatic failure, acetaminophen (paracetamol) overdose, multiple trauma or multiple organ dysfunction syndrome (MODS), or sepsis. Acetaminophen 164-175 GC vitamin D binding protein Homo sapiens 58-69 18983661-4 2008 The purpose of this study is to assess whether treatment with acetaminophen for 3 days will result in improved functional outcome through a modest reduction in body temperature and prevention of fever.The previously planned statistical analysis based on a dichotomization of the scores on the modified Rankin Scale (mRS) may not make the most efficient use of the available baseline information. Acetaminophen 62-75 sterile alpha motif domain containing 11 Mus musculus 316-319 18373199-0 2008 Green-tea polyphenols downregulate cyclooxygenase and Bcl-2 activity in acetaminophen-induced hepatotoxicity. Acetaminophen 72-85 B cell leukemia/lymphoma 2 Mus musculus 54-59 18373199-1 2008 Acetaminophen (APAP) elicits hepatotoxicity via multifactorial pathways, including increased apoptosis, cyclooxygenase (Cox-2) generation, reactive metabolite release, and glutathione (GSH) depletion. Acetaminophen 0-13 cytochrome c oxidase II, mitochondrial Mus musculus 120-125 18373199-1 2008 Acetaminophen (APAP) elicits hepatotoxicity via multifactorial pathways, including increased apoptosis, cyclooxygenase (Cox-2) generation, reactive metabolite release, and glutathione (GSH) depletion. Acetaminophen 15-19 cytochrome c oxidase II, mitochondrial Mus musculus 120-125 18373199-5 2008 APAP administration upregulated Cox-2 and B-cell lymphoma-2 (Bcl-2) production and had an effect, albeit minor, on Cox-1 and Fas expression in hepatic tissue. Acetaminophen 0-4 cytochrome c oxidase II, mitochondrial Mus musculus 32-37 18373199-5 2008 APAP administration upregulated Cox-2 and B-cell lymphoma-2 (Bcl-2) production and had an effect, albeit minor, on Cox-1 and Fas expression in hepatic tissue. Acetaminophen 0-4 B cell leukemia/lymphoma 2 Mus musculus 42-59 18373199-5 2008 APAP administration upregulated Cox-2 and B-cell lymphoma-2 (Bcl-2) production and had an effect, albeit minor, on Cox-1 and Fas expression in hepatic tissue. Acetaminophen 0-4 B cell leukemia/lymphoma 2 Mus musculus 61-66 18373199-5 2008 APAP administration upregulated Cox-2 and B-cell lymphoma-2 (Bcl-2) production and had an effect, albeit minor, on Cox-1 and Fas expression in hepatic tissue. Acetaminophen 0-4 cytochrome c oxidase I, mitochondrial Mus musculus 115-120 18579547-0 2008 The relation between paracetamol use and asthma: a GA2LEN European case-control study. Acetaminophen 21-32 electron transfer flavoprotein subunit alpha Homo sapiens 51-54 18435715-8 2008 WLP-S-10 inhibited mitochondrial swelling, breakdown of membrane potential and depletion of mitochondrial ATP, and also reduced release of cytochrome C and AIF from mitochondria induced by acetaminophen. Acetaminophen 189-202 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 156-159 18579359-4 2008 Acetaminophen treatment significantly elevated both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; however, the pre-intake of G. amboinense significantly and dose-dependently protected liver against the subsequent acetaminophen-induced elevation of ALT and AST activities. Acetaminophen 0-13 glutamic pyruvic transaminase, soluble Mus musculus 52-76 18579359-4 2008 Acetaminophen treatment significantly elevated both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; however, the pre-intake of G. amboinense significantly and dose-dependently protected liver against the subsequent acetaminophen-induced elevation of ALT and AST activities. Acetaminophen 0-13 glutamic pyruvic transaminase, soluble Mus musculus 78-81 18579359-4 2008 Acetaminophen treatment significantly elevated both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; however, the pre-intake of G. amboinense significantly and dose-dependently protected liver against the subsequent acetaminophen-induced elevation of ALT and AST activities. Acetaminophen 0-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 87-113 18579359-4 2008 Acetaminophen treatment significantly elevated both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; however, the pre-intake of G. amboinense significantly and dose-dependently protected liver against the subsequent acetaminophen-induced elevation of ALT and AST activities. Acetaminophen 0-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 115-118 18579359-4 2008 Acetaminophen treatment significantly elevated both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; however, the pre-intake of G. amboinense significantly and dose-dependently protected liver against the subsequent acetaminophen-induced elevation of ALT and AST activities. Acetaminophen 0-13 glutamic pyruvic transaminase, soluble Mus musculus 282-285 18579359-4 2008 Acetaminophen treatment significantly elevated both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; however, the pre-intake of G. amboinense significantly and dose-dependently protected liver against the subsequent acetaminophen-induced elevation of ALT and AST activities. Acetaminophen 0-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 290-293 18579359-5 2008 Acetaminophen treatment also caused significant GSH depletion, malondialdehyde (MDA) and reactive oxygen species (ROS) increase, and activity reduction of glutathione peroxidase (GPX) and catalase. Acetaminophen 0-13 catalase Mus musculus 188-196 18684486-4 2008 Levels of acetaminophen and caffeine in STP effluents were very low compared to the influent concentrations. Acetaminophen 10-23 thyroid hormone receptor interactor 10 Homo sapiens 40-43 18780337-0 2008 Prostate-specific antigen levels in relation to consumption of nonsteroidal anti-inflammatory drugs and acetaminophen: results from the 2001-2002 National Health and Nutrition Examination Survey. Acetaminophen 104-117 kallikrein related peptidase 3 Homo sapiens 0-25 18780337-3 2008 To further characterize this association, the authors evaluated serum PSA levels with regard to NSAID and acetaminophen consumption in a large cross-sectional study of men in the US. Acetaminophen 106-119 kallikrein related peptidase 3 Homo sapiens 70-73 18780337-5 2008 Linear regressions were performed on log-transformed PSA levels, accounting for the complex survey design, to evaluate the relations between PSA and the use of NSAIDs and acetaminophen after adjusting for the effects of age, race, educational level, smoking status, body mass index, coexisting inflammatory conditions, and heart disease. Acetaminophen 171-184 kallikrein related peptidase 3 Homo sapiens 141-144 18780337-6 2008 RESULTS: NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. Acetaminophen 19-32 kallikrein related peptidase 3 Homo sapiens 83-86 18780337-6 2008 RESULTS: NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. Acetaminophen 19-32 kallikrein related peptidase 3 Homo sapiens 193-196 18780337-6 2008 RESULTS: NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. Acetaminophen 152-165 kallikrein related peptidase 3 Homo sapiens 83-86 18780337-6 2008 RESULTS: NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. Acetaminophen 152-165 kallikrein related peptidase 3 Homo sapiens 193-196 18780337-6 2008 RESULTS: NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. Acetaminophen 152-165 kallikrein related peptidase 3 Homo sapiens 83-86 18780337-6 2008 RESULTS: NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. Acetaminophen 152-165 kallikrein related peptidase 3 Homo sapiens 193-196 18780337-7 2008 PSA levels among NSAID users were 0.9 times the levels among nondrug takers (P = .038), whereas PSA levels among acetaminophen users were 0.76 times the levels in nondrug takers (P = .14). Acetaminophen 113-126 kallikrein related peptidase 3 Homo sapiens 96-99 18780337-8 2008 Individuals who stated they took both NSAIDs and acetaminophen (0.99%) on a regular basis had higher PSA levels (1.8 times greater), although not statistically significantly so (P = .24), than individuals who stated they did not take either of these drugs regularly. Acetaminophen 49-62 kallikrein related peptidase 3 Homo sapiens 101-104 21886711-4 2008 In this case of a patient who needs life-long therapy, we demonstrated the value of the IFN-gamma release test, which showed positive reactivity to 3 out of 9 suspicious drugs: paracetamol, phenytoin and dypirone, allowing for more therapeutic options. Acetaminophen 177-188 interferon gamma Homo sapiens 88-97 19230593-4 2008 For this reason we undertook a study of the effects of these extracts alone and in combination with paracetamol, along with the action of paracetamol alone, on the activity of the antioxidant enzymes GSHPx, CAT, Px, XOD, GSHR, glutathione content, LPx intensity, as well as activities of AST and ALT. Acetaminophen 100-111 catalase Mus musculus 207-210 19230593-7 2008 In combination with paracetamol, extracts of both Magnum and Aroma varieties reduced significantly the LPx intensity, activities of CAT and GSHPx, as well as GSH content in the liver homogenate. Acetaminophen 20-31 catalase Mus musculus 132-135 18700144-0 2008 Deletion of apoptosis signal-regulating kinase 1 attenuates acetaminophen-induced liver injury by inhibiting c-Jun N-terminal kinase activation. Acetaminophen 60-73 mitogen-activated protein kinase kinase kinase 5 Mus musculus 12-48 18700144-0 2008 Deletion of apoptosis signal-regulating kinase 1 attenuates acetaminophen-induced liver injury by inhibiting c-Jun N-terminal kinase activation. Acetaminophen 60-73 mitogen-activated protein kinase 8 Mus musculus 109-132 18785192-0 2008 The hepatotoxic metabolite of acetaminophen directly activates the Keap1-Nrf2 cell defense system. Acetaminophen 30-43 kelch-like ECH-associated protein 1 Mus musculus 67-72 18785192-0 2008 The hepatotoxic metabolite of acetaminophen directly activates the Keap1-Nrf2 cell defense system. Acetaminophen 30-43 nuclear factor, erythroid derived 2, like 2 Mus musculus 73-77 18785192-2 2008 We have demonstrated previously that acetaminophen activates Nrf2 in mouse liver following administration of non-hepatotoxic and hepatotoxic doses in vivo, implying that Nrf2 may have an important role in the protection against drug-induced liver injury. Acetaminophen 37-50 nuclear factor, erythroid derived 2, like 2 Mus musculus 61-65 18785192-2 2008 We have demonstrated previously that acetaminophen activates Nrf2 in mouse liver following administration of non-hepatotoxic and hepatotoxic doses in vivo, implying that Nrf2 may have an important role in the protection against drug-induced liver injury. Acetaminophen 37-50 nuclear factor, erythroid derived 2, like 2 Mus musculus 170-174 18785192-4 2008 We hypothesized that acetaminophen activates Nrf2 via the formation of its reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI), which may disrupt the repression of Nrf2 through the modification of cysteine residues within Keap1. Acetaminophen 21-34 nuclear factor, erythroid derived 2, like 2 Mus musculus 45-49 18785192-4 2008 We hypothesized that acetaminophen activates Nrf2 via the formation of its reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI), which may disrupt the repression of Nrf2 through the modification of cysteine residues within Keap1. Acetaminophen 21-34 nuclear factor, erythroid derived 2, like 2 Mus musculus 169-173 18785192-4 2008 We hypothesized that acetaminophen activates Nrf2 via the formation of its reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI), which may disrupt the repression of Nrf2 through the modification of cysteine residues within Keap1. Acetaminophen 21-34 kelch-like ECH-associated protein 1 Mus musculus 227-232 18785192-10 2008 It is possible that both of these mechanisms contribute to the activation of Nrf2 by acetaminophen. Acetaminophen 85-98 nuclear factor, erythroid derived 2, like 2 Mus musculus 77-81 18485596-5 2008 Accordingly with these results, we also demonstrated that the inhibition of FAAH, an enzyme involved in the cerebral metabolism of acetaminophen into AM404, known to reinforce the activity of the endocannabinoid system, suppressed the antinociceptive effect of acetaminophen. Acetaminophen 131-144 fatty acid amide hydrolase Mus musculus 76-80 18485596-5 2008 Accordingly with these results, we also demonstrated that the inhibition of FAAH, an enzyme involved in the cerebral metabolism of acetaminophen into AM404, known to reinforce the activity of the endocannabinoid system, suppressed the antinociceptive effect of acetaminophen. Acetaminophen 261-274 fatty acid amide hydrolase Mus musculus 76-80 18485596-7 2008 We therefore propose that acetaminophen-induced analgesia could involve the following sequence: (1) FAAH-dependent metabolism of acetaminophen into AM404; (2) indirect involvement of CB(1) receptors by this metabolite; (3) endocannabinoid-dependent reinforcement of the serotonergic bulbospinal pathways, and (4) involvement of spinal pain-suppressing serotonergic receptors. Acetaminophen 26-39 fatty acid amide hydrolase Mus musculus 100-104 18485596-7 2008 We therefore propose that acetaminophen-induced analgesia could involve the following sequence: (1) FAAH-dependent metabolism of acetaminophen into AM404; (2) indirect involvement of CB(1) receptors by this metabolite; (3) endocannabinoid-dependent reinforcement of the serotonergic bulbospinal pathways, and (4) involvement of spinal pain-suppressing serotonergic receptors. Acetaminophen 129-142 fatty acid amide hydrolase Mus musculus 100-104 18586006-0 2008 Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury. Acetaminophen 48-61 mitogen-activated protein kinase 9 Mus musculus 19-44 18586006-1 2008 Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). Acetaminophen 121-134 mitogen-activated protein kinase 9 Mus musculus 53-86 18586006-1 2008 Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). Acetaminophen 121-134 mitogen-activated protein kinase 9 Mus musculus 88-92 18586006-1 2008 Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). Acetaminophen 136-140 mitogen-activated protein kinase 9 Mus musculus 53-86 18586006-1 2008 Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). Acetaminophen 136-140 mitogen-activated protein kinase 9 Mus musculus 88-92 18586006-3 2008 When male C57BL/6J wild type (WT) and JNK2(-/-) mice were treated with 300mg APAP/kg, 90% of JNK2(-/-) mice died of ALF compared to 20% of WT mice within 48h. Acetaminophen 77-81 mitogen-activated protein kinase 9 Mus musculus 38-42 18586006-3 2008 When male C57BL/6J wild type (WT) and JNK2(-/-) mice were treated with 300mg APAP/kg, 90% of JNK2(-/-) mice died of ALF compared to 20% of WT mice within 48h. Acetaminophen 77-81 mitogen-activated protein kinase 9 Mus musculus 93-97 18392951-5 2008 The cytoprotective effect of HSP27/70 induced by bicyclol against hepatotoxicity of acetaminophen (AP) was assessed in mice. Acetaminophen 84-97 heat shock protein 1 Mus musculus 29-34 18573333-2 2008 Our objective was to determine if SOD1 catalyzes murine liver protein nitration induced by acetaminophen (APAP) and lipopolysaccharide (LPS). Acetaminophen 91-104 superoxide dismutase 1, soluble Mus musculus 34-38 18573333-2 2008 Our objective was to determine if SOD1 catalyzes murine liver protein nitration induced by acetaminophen (APAP) and lipopolysaccharide (LPS). Acetaminophen 106-110 superoxide dismutase 1, soluble Mus musculus 34-38 18573333-9 2008 In conclusion, the diminished hepatic protein nitration mediated by APAP or LPS in the SOD1-/- mice is due to the lack of SOD1 activity per se. Acetaminophen 68-72 superoxide dismutase 1, soluble Mus musculus 87-91 18588957-7 2008 When APAP and LEF were incubated with human recombinant P450 enzymes, CYP1A2 was found to be the isozyme responsible for the inhibition of APAP bioactivation. Acetaminophen 5-9 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 70-76 18556419-0 2008 Hepatic Mrp4 induction following acetaminophen exposure is dependent on Kupffer cell function. Acetaminophen 33-46 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 8-12 18556419-1 2008 During acetaminophen (APAP) hepatotoxicity, increased expression of multidrug resistance-associated proteins 2, 3, and 4 (Mrp2-4) occurs. Acetaminophen 7-20 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 68-120 18556419-1 2008 During acetaminophen (APAP) hepatotoxicity, increased expression of multidrug resistance-associated proteins 2, 3, and 4 (Mrp2-4) occurs. Acetaminophen 7-20 ATP-binding cassette, sub-family C (CFTR/MRP), member 2 Mus musculus 122-128 18556419-1 2008 During acetaminophen (APAP) hepatotoxicity, increased expression of multidrug resistance-associated proteins 2, 3, and 4 (Mrp2-4) occurs. Acetaminophen 22-26 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 68-120 18556419-1 2008 During acetaminophen (APAP) hepatotoxicity, increased expression of multidrug resistance-associated proteins 2, 3, and 4 (Mrp2-4) occurs. Acetaminophen 22-26 ATP-binding cassette, sub-family C (CFTR/MRP), member 2 Mus musculus 122-128 18556419-9 2008 At 48 and 72 h after APAP dosing, Mrp4 levels were increased by 10- and 33-fold, respectively, in mice receiving empty liposomes. Acetaminophen 21-25 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 34-38 18556419-11 2008 Remarkably, Kupffer cell depletion completely prevented Mrp4 induction by APAP. Acetaminophen 74-78 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 56-60 18816295-2 2008 UGT1A9 is a UGT that catalyses the conjugation of endogenous oestrogenic and thyroid hormones, acetaminophen, SN-38 (an active metabolite of irinotecan) and phenols. Acetaminophen 95-108 UDP glucuronosyltransferase family 1 member A9 Homo sapiens 0-6 19232164-5 2008 In patients admitted with acetaminophen (paracetamol) overdose, Gc-globulin concentrations were lower in patients with hepatic encephalopathy than in those without and the levels nadired at approximately 60-72 hours after acetaminophen ingestion, corresponding with the peak in aminotransferese levels (and thus, hepatic necrosis). Acetaminophen 26-39 GC vitamin D binding protein Homo sapiens 64-75 19232164-5 2008 In patients admitted with acetaminophen (paracetamol) overdose, Gc-globulin concentrations were lower in patients with hepatic encephalopathy than in those without and the levels nadired at approximately 60-72 hours after acetaminophen ingestion, corresponding with the peak in aminotransferese levels (and thus, hepatic necrosis). Acetaminophen 41-52 GC vitamin D binding protein Homo sapiens 64-75 19232164-5 2008 In patients admitted with acetaminophen (paracetamol) overdose, Gc-globulin concentrations were lower in patients with hepatic encephalopathy than in those without and the levels nadired at approximately 60-72 hours after acetaminophen ingestion, corresponding with the peak in aminotransferese levels (and thus, hepatic necrosis). Acetaminophen 222-235 GC vitamin D binding protein Homo sapiens 64-75 18468992-0 2008 Acquired resistance to acetaminophen hepatotoxicity is associated with induction of multidrug resistance-associated protein 4 (Mrp4) in proliferating hepatocytes. Acetaminophen 23-36 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 84-125 18468992-0 2008 Acquired resistance to acetaminophen hepatotoxicity is associated with induction of multidrug resistance-associated protein 4 (Mrp4) in proliferating hepatocytes. Acetaminophen 23-36 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 127-131 18468992-4 2008 We hypothesized that upregulation of Mrp3 and Mrp4 is one mechanism by which hepatocytes become resistant to a subsequent higher dose of APAP by limiting accumulation of xeno-, endobiotics, and byproducts of hepatocellular injury. Acetaminophen 137-141 prolactin family 2, subfamily c, member 4 Mus musculus 37-41 18468992-4 2008 We hypothesized that upregulation of Mrp3 and Mrp4 is one mechanism by which hepatocytes become resistant to a subsequent higher dose of APAP by limiting accumulation of xeno-, endobiotics, and byproducts of hepatocellular injury. Acetaminophen 137-141 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 46-50 18468992-7 2008 Maximal Mrp3 and Mrp4 induction occurred 48 h after APAP. Acetaminophen 52-56 prolactin family 2, subfamily c, member 4 Mus musculus 8-12 18468992-7 2008 Maximal Mrp3 and Mrp4 induction occurred 48 h after APAP. Acetaminophen 52-56 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 17-21 18468992-12 2008 Interestingly, mice pretreated and challenged with APAP had dramatic increases in Mrp4 expression as well as enhanced hepatocyte proliferation. Acetaminophen 51-55 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 82-86 18469330-0 2008 Plasminogen activator inhibitor-1 limits liver injury and facilitates regeneration after acetaminophen overdose. Acetaminophen 89-102 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 0-33 18501395-0 2008 Nonalcoholic steatohepatitic (NASH) mice are protected from higher hepatotoxicity of acetaminophen upon induction of PPARalpha with clofibrate. Acetaminophen 85-98 peroxisome proliferator activated receptor alpha Mus musculus 117-126 18501395-1 2008 The objective was to investigate if the hepatotoxic sensitivity in nonalcoholic steatohepatitic mice to acetaminophen (APAP) is due to downregulation of nuclear receptor PPARalpha via lower cell division and tissue repair. Acetaminophen 104-117 peroxisome proliferator activated receptor alpha Mus musculus 170-179 18501395-1 2008 The objective was to investigate if the hepatotoxic sensitivity in nonalcoholic steatohepatitic mice to acetaminophen (APAP) is due to downregulation of nuclear receptor PPARalpha via lower cell division and tissue repair. Acetaminophen 119-123 peroxisome proliferator activated receptor alpha Mus musculus 170-179 18501395-5 2008 Liver injury progressed only in steatohepatitic livers between 6 and 24 h. Cell division and tissue repair assessed by (3)H-thymidine incorporation and PCNA were inhibited only in the steatohepatitic mice given APAP suggesting that higher sensitivity of NASH liver to APAP-induced hepatotoxicity was due to lower tissue repair. Acetaminophen 211-215 proliferating cell nuclear antigen Mus musculus 152-156 18501395-11 2008 These findings suggest that inadequate PPARalpha expression in steatohepatitic mice sensitizes them to APAP hepatotoxicity. Acetaminophen 103-107 peroxisome proliferator activated receptor alpha Mus musculus 39-48 18597458-3 2008 A tetraalkylammonium salt of the CuX 2 (-) anion in which X = phthalimidate was also isolated. Acetaminophen 58-61 cut like homeobox 2 Homo sapiens 33-38 18467506-0 2008 Stem cell factor and c-kit are involved in hepatic recovery after acetaminophen-induced liver injury in mice. Acetaminophen 66-79 kit ligand Mus musculus 0-16 18467506-0 2008 Stem cell factor and c-kit are involved in hepatic recovery after acetaminophen-induced liver injury in mice. Acetaminophen 66-79 KIT proto-oncogene receptor tyrosine kinase Mus musculus 21-26 18467506-4 2008 In the current study, we further examined the expression of SCF and c-kit in acetaminophen (APAP)-induced liver injury in C57BL/6J mice or SCF-deficient sl-sld mice and their appropriate wild-type controls. Acetaminophen 77-90 kit ligand Mus musculus 60-63 18467506-4 2008 In the current study, we further examined the expression of SCF and c-kit in acetaminophen (APAP)-induced liver injury in C57BL/6J mice or SCF-deficient sl-sld mice and their appropriate wild-type controls. Acetaminophen 77-90 KIT proto-oncogene receptor tyrosine kinase Mus musculus 68-73 18467506-4 2008 In the current study, we further examined the expression of SCF and c-kit in acetaminophen (APAP)-induced liver injury in C57BL/6J mice or SCF-deficient sl-sld mice and their appropriate wild-type controls. Acetaminophen 92-96 kit ligand Mus musculus 60-63 18467506-4 2008 In the current study, we further examined the expression of SCF and c-kit in acetaminophen (APAP)-induced liver injury in C57BL/6J mice or SCF-deficient sl-sld mice and their appropriate wild-type controls. Acetaminophen 92-96 KIT proto-oncogene receptor tyrosine kinase Mus musculus 68-73 18467506-7 2008 The mortality rate in SCF-deficient mice treated with APAP was significantly higher than that of wild-type mice; furthermore, administration of exogenous SCF significantly reduced the mortality of APAP-treated wild-type mice. Acetaminophen 54-58 kit ligand Mus musculus 22-25 18467506-8 2008 Bromodeoxyuridine incorporation experiments showed that SCF significantly increased hepatocyte proliferation at 48 and 72 h in APAP-treated mice. Acetaminophen 127-131 kit ligand Mus musculus 56-59 18467506-10 2008 In summary, SCF and c-kit expression was increased after APAP-induced liver injury. Acetaminophen 57-61 kit ligand Mus musculus 12-15 18467506-10 2008 In summary, SCF and c-kit expression was increased after APAP-induced liver injury. Acetaminophen 57-61 KIT proto-oncogene receptor tyrosine kinase Mus musculus 20-25 18467506-11 2008 Administration of exogenous SCF reduces mortality in APAP-treated mice, increases hepatocyte proliferation, and prevents hepatocyte apoptosis induced by APAP, suggesting that these molecules are important in the liver"s recovery from these injuries. Acetaminophen 53-57 kit ligand Mus musculus 28-31 18467506-11 2008 Administration of exogenous SCF reduces mortality in APAP-treated mice, increases hepatocyte proliferation, and prevents hepatocyte apoptosis induced by APAP, suggesting that these molecules are important in the liver"s recovery from these injuries. Acetaminophen 153-157 kit ligand Mus musculus 28-31 18648099-3 2008 APAP administration produced a decrease in hepatic SOD, CAT, and GSH-Px activities, and coadministration of erdosteine (150 and 300 mg/kg) resulted in increases in the activities. Acetaminophen 0-4 catalase Rattus norvegicus 56-59 18648099-5 2008 Significant elevations in serum AST and ALT levels were observed in the APAP group, and when erdosteine and APAP were coadministered, their serum levels were close to those in the control group. Acetaminophen 72-76 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 32-35 18541126-7 2008 In line with the significant alleviation of pain, from Days 0 to 2 of treatment, subjects in the NSPN group also needed significantly less escape aanalgesica therapy (paracetamol tablets) than those in the placebo group. Acetaminophen 167-178 sarcospan Homo sapiens 97-101 18346862-7 2008 Although N-acetylbenzoquinoneimine, a minor metabolite of APAP, which is mainly formed by CYP2E1 at high APAP concentration in every species studied, is thought to initiate the toxic processes, no correlation was found between CYP2E1 activities and hepatocyte sensitivity of different species. Acetaminophen 58-62 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 90-96 18337250-0 2008 Role of JNK translocation to mitochondria leading to inhibition of mitochondria bioenergetics in acetaminophen-induced liver injury. Acetaminophen 97-110 mitogen-activated protein kinase 8 Mus musculus 8-11 18337250-3 2008 JNK inhibitor (SP600125) was observed to significantly protect against APAP-induced liver injury. Acetaminophen 71-75 mitogen-activated protein kinase 8 Mus musculus 0-3 18337250-4 2008 Increased mitochondria-derived reactive oxygen species were implicated in APAP-induced JNK activation based on the following: 1) mitochondrial GSH depletion (maximal at 2 h) caused increased H2O2 release from mitochondria, which preceded JNK activation (maximal at 4 h); 2) treatment of isolated hepatocytes with H2O2 or inhibitors (e.g. antimycin) that cause increased H2O2 release from mitochondria-activated JNK. Acetaminophen 74-78 mitogen-activated protein kinase 8 Mus musculus 87-90 18337250-4 2008 Increased mitochondria-derived reactive oxygen species were implicated in APAP-induced JNK activation based on the following: 1) mitochondrial GSH depletion (maximal at 2 h) caused increased H2O2 release from mitochondria, which preceded JNK activation (maximal at 4 h); 2) treatment of isolated hepatocytes with H2O2 or inhibitors (e.g. antimycin) that cause increased H2O2 release from mitochondria-activated JNK. Acetaminophen 74-78 mitogen-activated protein kinase 8 Mus musculus 238-241 18337250-4 2008 Increased mitochondria-derived reactive oxygen species were implicated in APAP-induced JNK activation based on the following: 1) mitochondrial GSH depletion (maximal at 2 h) caused increased H2O2 release from mitochondria, which preceded JNK activation (maximal at 4 h); 2) treatment of isolated hepatocytes with H2O2 or inhibitors (e.g. antimycin) that cause increased H2O2 release from mitochondria-activated JNK. Acetaminophen 74-78 mitogen-activated protein kinase 8 Mus musculus 238-241 18337250-5 2008 An important downstream target of JNK following activation was mitochondria based on the following: 1) JNK translocated to mitochondria following activation; 2) JNK inhibitor treatment partially protected against a decline in mitochondria respiration caused by APAP treatment; and 3) addition of purified active JNK to mitochondria isolated from mice treated with APAP plus JNK inhibitor (mitochondria with severe GSH depletion, covalent binding) directly inhibited respiration. Acetaminophen 261-265 mitogen-activated protein kinase 8 Mus musculus 34-37 18337250-5 2008 An important downstream target of JNK following activation was mitochondria based on the following: 1) JNK translocated to mitochondria following activation; 2) JNK inhibitor treatment partially protected against a decline in mitochondria respiration caused by APAP treatment; and 3) addition of purified active JNK to mitochondria isolated from mice treated with APAP plus JNK inhibitor (mitochondria with severe GSH depletion, covalent binding) directly inhibited respiration. Acetaminophen 261-265 mitogen-activated protein kinase 8 Mus musculus 103-106 18337250-5 2008 An important downstream target of JNK following activation was mitochondria based on the following: 1) JNK translocated to mitochondria following activation; 2) JNK inhibitor treatment partially protected against a decline in mitochondria respiration caused by APAP treatment; and 3) addition of purified active JNK to mitochondria isolated from mice treated with APAP plus JNK inhibitor (mitochondria with severe GSH depletion, covalent binding) directly inhibited respiration. Acetaminophen 261-265 mitogen-activated protein kinase 8 Mus musculus 103-106 18337250-5 2008 An important downstream target of JNK following activation was mitochondria based on the following: 1) JNK translocated to mitochondria following activation; 2) JNK inhibitor treatment partially protected against a decline in mitochondria respiration caused by APAP treatment; and 3) addition of purified active JNK to mitochondria isolated from mice treated with APAP plus JNK inhibitor (mitochondria with severe GSH depletion, covalent binding) directly inhibited respiration. Acetaminophen 261-265 mitogen-activated protein kinase 8 Mus musculus 103-106 18337250-5 2008 An important downstream target of JNK following activation was mitochondria based on the following: 1) JNK translocated to mitochondria following activation; 2) JNK inhibitor treatment partially protected against a decline in mitochondria respiration caused by APAP treatment; and 3) addition of purified active JNK to mitochondria isolated from mice treated with APAP plus JNK inhibitor (mitochondria with severe GSH depletion, covalent binding) directly inhibited respiration. Acetaminophen 261-265 mitogen-activated protein kinase 8 Mus musculus 103-106 18337250-5 2008 An important downstream target of JNK following activation was mitochondria based on the following: 1) JNK translocated to mitochondria following activation; 2) JNK inhibitor treatment partially protected against a decline in mitochondria respiration caused by APAP treatment; and 3) addition of purified active JNK to mitochondria isolated from mice treated with APAP plus JNK inhibitor (mitochondria with severe GSH depletion, covalent binding) directly inhibited respiration. Acetaminophen 364-368 mitogen-activated protein kinase 8 Mus musculus 34-37 18337250-6 2008 Cyclosporin A blocked the inhibitory effect of JNK on mitochondria respiration, suggesting JNK was directly inducing mitochondrial permeability transition in isolated mitochondria from mice treated with APAP plus JNK inhibitor. Acetaminophen 203-207 mitogen-activated protein kinase 8 Mus musculus 47-50 18337250-6 2008 Cyclosporin A blocked the inhibitory effect of JNK on mitochondria respiration, suggesting JNK was directly inducing mitochondrial permeability transition in isolated mitochondria from mice treated with APAP plus JNK inhibitor. Acetaminophen 203-207 mitogen-activated protein kinase 8 Mus musculus 91-94 18337250-6 2008 Cyclosporin A blocked the inhibitory effect of JNK on mitochondria respiration, suggesting JNK was directly inducing mitochondrial permeability transition in isolated mitochondria from mice treated with APAP plus JNK inhibitor. Acetaminophen 203-207 mitogen-activated protein kinase 8 Mus musculus 91-94 18337250-8 2008 Our results suggests that APAP-induced liver injury involves JNK activation, due to increased reactive oxygen species generated by GSH-depleted mitochondria, and translocation of activated JNK to mitochondria where JNK induces mitochondrial permeability transition and inhibits mitochondria bioenergetics. Acetaminophen 26-30 mitogen-activated protein kinase 8 Mus musculus 61-64 18337250-8 2008 Our results suggests that APAP-induced liver injury involves JNK activation, due to increased reactive oxygen species generated by GSH-depleted mitochondria, and translocation of activated JNK to mitochondria where JNK induces mitochondrial permeability transition and inhibits mitochondria bioenergetics. Acetaminophen 26-30 mitogen-activated protein kinase 8 Mus musculus 189-192 18337250-8 2008 Our results suggests that APAP-induced liver injury involves JNK activation, due to increased reactive oxygen species generated by GSH-depleted mitochondria, and translocation of activated JNK to mitochondria where JNK induces mitochondrial permeability transition and inhibits mitochondria bioenergetics. Acetaminophen 26-30 mitogen-activated protein kinase 8 Mus musculus 189-192 18715889-12 2008 Compared with AAP group, the levels of ALT were lower after AAP ingestion in AAP-NAC, AAP-Se, and AAP-Se-NAC groups at the 8th hour. Acetaminophen 14-17 glutamic pyruvic transaminase, soluble Mus musculus 39-42 18715889-12 2008 Compared with AAP group, the levels of ALT were lower after AAP ingestion in AAP-NAC, AAP-Se, and AAP-Se-NAC groups at the 8th hour. Acetaminophen 60-63 glutamic pyruvic transaminase, soluble Mus musculus 39-42 18715889-12 2008 Compared with AAP group, the levels of ALT were lower after AAP ingestion in AAP-NAC, AAP-Se, and AAP-Se-NAC groups at the 8th hour. Acetaminophen 60-63 glutamic pyruvic transaminase, soluble Mus musculus 39-42 18715889-12 2008 Compared with AAP group, the levels of ALT were lower after AAP ingestion in AAP-NAC, AAP-Se, and AAP-Se-NAC groups at the 8th hour. Acetaminophen 60-63 glutamic pyruvic transaminase, soluble Mus musculus 39-42 18345653-4 2008 The elongation of the X-Hal bond length is caused by the electron-density transfer to the X-Hal sigma* antibonding orbital. Acetaminophen 22-23 histidine ammonia-lyase Homo sapiens 24-27 18345653-4 2008 The elongation of the X-Hal bond length is caused by the electron-density transfer to the X-Hal sigma* antibonding orbital. Acetaminophen 22-23 histidine ammonia-lyase Homo sapiens 92-95 18630824-5 2008 AST/ALT levels are measured on admission, 12 hours after, and according to outcome every 12-24 h. N-acetylcysteine (NAC) administration within 8-10 hours protects against acetaminophen-induced hepatotoxicity. Acetaminophen 171-184 solute carrier family 17 member 5 Homo sapiens 0-3 18043697-0 2008 Upregulation of multidrug resistance-associated protein 3 by acetaminophen may help to increase its own clearance. Acetaminophen 61-74 ATP binding cassette subfamily C member 3 Homo sapiens 16-57 17934819-3 2008 The present study has been conducted to evaluate the eventual role of the platelet activating factor in post-acetaminophen intoxication of liver, using ginkgolide B, BN52021, a selective PAF receptor antagonist. Acetaminophen 109-122 PCNA clamp associated factor Rattus norvegicus 74-100 17934819-8 2008 APAP was found to cause an acute hepatic injury, evident by alterations of biochemical (serum enzymes: ALT, AST and ALP) and liver histopathological (degree of inflammation and apoptosis) indices, which was followed by liver regeneration evident by three independent indices ([3H] thymidine incorporation into hepatic DNA, liver thymidine kinase activity and hepatocyte mitotic index). Acetaminophen 0-4 PDZ and LIM domain 3 Rattus norvegicus 116-119 18379447-10 2008 When the ingestion of alcohol is stopped, CYP2E1 is greatly increased and only metabolises the paracetamol giving rise to high quantities of hepatotoxic metabolites so that the hepatic glutathione is unable to detoxify resulting in irreversible hepatic damage. Acetaminophen 95-106 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 42-48 18313239-0 2008 Mitochondrial protein thiol modifications in acetaminophen hepatotoxicity: effect on HMG-CoA synthase. Acetaminophen 45-58 3-hydroxy-3-methylglutaryl-CoA synthase 2 Homo sapiens 85-101 18313239-5 2008 APAP caused a significant increase in liver toxicity 3h post-APAP administration as measured by increased serum alanine aminotransferase (ALT) levels. Acetaminophen 0-4 glutamic--pyruvic transaminase Homo sapiens 112-136 18313239-7 2008 However, 3-hydroxy-3-methylglutaryl coenzyme A synthase 2 (HMG-CoA synthase) had significantly decreased levels of reduced thiols and activity after APAP treatment. Acetaminophen 149-153 3-hydroxy-3-methylglutaryl-CoA synthase 2 Homo sapiens 59-75 18237725-11 2008 To conclude suppression of IFN-gamma and increase in alpha-class GSTs expression may exert a protective role in acute hepatotoxicity of APAP and 5 kGy GIHA showed comparable protective effect to that of UIHA. Acetaminophen 136-140 interferon gamma Mus musculus 27-36 18237725-11 2008 To conclude suppression of IFN-gamma and increase in alpha-class GSTs expression may exert a protective role in acute hepatotoxicity of APAP and 5 kGy GIHA showed comparable protective effect to that of UIHA. Acetaminophen 136-140 glutathione S-transferase cluster Mus musculus 65-69 18313080-2 2008 While carbon tetrachloride (CCl4), thioacetamide (TAA) and chloroform (CHCl3) inflict liver damage by producing free radicals, acetaminophen (AAP) and bromobenzene (BB) exert their effects by severe glutathione depletion. Acetaminophen 127-140 C-C motif chemokine ligand 4 Homo sapiens 28-32 18313080-2 2008 While carbon tetrachloride (CCl4), thioacetamide (TAA) and chloroform (CHCl3) inflict liver damage by producing free radicals, acetaminophen (AAP) and bromobenzene (BB) exert their effects by severe glutathione depletion. Acetaminophen 142-145 C-C motif chemokine ligand 4 Homo sapiens 28-32 18232020-7 2008 CONCLUSIONS: The results of this study lead to the hypothesis that genetic variation in SULT1A3/4 represents a risk factor for the development of gastroschisis in the offspring of mothers exposed to APAP early in pregnancy. Acetaminophen 199-203 sulfotransferase family 1A member 3 Homo sapiens 88-95 18096675-13 2008 We demonstrate a more efficient hepatic synthesis and basolateral excretion of APAP-GLU followed by its urinary elimination in BDL group, the latter two processes consistent with up-regulation of liver Mrp3 and renal Mrp2. Acetaminophen 79-84 ATP binding cassette subfamily C member 3 Rattus norvegicus 202-206 18096675-13 2008 We demonstrate a more efficient hepatic synthesis and basolateral excretion of APAP-GLU followed by its urinary elimination in BDL group, the latter two processes consistent with up-regulation of liver Mrp3 and renal Mrp2. Acetaminophen 79-84 ATP binding cassette subfamily C member 2 Rattus norvegicus 217-221 18054472-1 2008 Paracetamol (acetaminophen, PCM) is widely used as an over-the-counter analgesic and antipyretic drug. Acetaminophen 0-11 solute carrier family 40 (iron-regulated transporter), member 1 Mus musculus 28-31 18054472-7 2008 Paracetamol caused liver damage as evident by statistically significant (P<0.05) increased in plasma activities of AST and ALT. Acetaminophen 0-11 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 118-121 18054472-7 2008 Paracetamol caused liver damage as evident by statistically significant (P<0.05) increased in plasma activities of AST and ALT. Acetaminophen 0-11 glutamic pyruvic transaminase, soluble Mus musculus 126-129 18054472-8 2008 There were general statistically significant losses in the activities of SOD, GPx, CAT, and delta-ALA-D and an increase in TBARS in the liver of paracetamol-treated group compared with the control group. Acetaminophen 145-156 catalase Mus musculus 83-86 18338302-3 2008 The pathophysiology of renal toxicity in acetaminophen poisoning has been attributed to cytochrome P-450 mixed function oxidase isoenzymes present in the kidney, although other mechanisms have been elucidated, including the role of prostaglandin synthetase and N-deacetylase enzymes. Acetaminophen 41-54 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 88-104 18093979-0 2008 Identification of novel toxicity-associated metabolites by metabolomics and mass isotopomer analysis of acetaminophen metabolism in wild-type and Cyp2e1-null mice. Acetaminophen 104-117 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 146-152 18093979-1 2008 CYP2E1 is recognized as the most important enzyme for initiation of acetaminophen (APAP)-induced toxicity. Acetaminophen 68-81 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 0-6 18093979-1 2008 CYP2E1 is recognized as the most important enzyme for initiation of acetaminophen (APAP)-induced toxicity. Acetaminophen 83-87 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 0-6 18093979-3 2008 However, unexpectedly, profiling of major known APAP metabolites in urine and serum revealed that the contribution of CYP2E1 to APAP metabolism decreased with increasing APAP doses administered. Acetaminophen 48-52 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 118-124 18197691-6 2008 These nanoporous PtPb electrodes are also highly resistant toward poisoning by chloride ions and capable of sensing glucose amperometrically at a very low potential, -80 mV (Ag/AgCl), where the interference from the oxidation of common interfering species such as ascorbic acid, acetamidophenol, and uric acid is effectively avoided. Acetaminophen 279-294 protein tyrosine phosphatase receptor type B Homo sapiens 17-21 18068290-11 2008 APAP induced centrilobular necrosis, increased liver weight and alanine transaminase (ALT) levels, depressed total hepatic glutathione (GSH), increased protein carbonyls and 4-hydroxynonenal (4-HNE) adducted proteins. Acetaminophen 0-4 glutamic pyruvic transaminase, soluble Mus musculus 64-84 18068290-11 2008 APAP induced centrilobular necrosis, increased liver weight and alanine transaminase (ALT) levels, depressed total hepatic glutathione (GSH), increased protein carbonyls and 4-hydroxynonenal (4-HNE) adducted proteins. Acetaminophen 0-4 glutamic pyruvic transaminase, soluble Mus musculus 86-89 18068290-13 2008 Treatment with SAMe or NAC 1h after APAP was sufficient to return total hepatic glutathione (GSH) to levels comparable to the VEH group. Acetaminophen 36-40 nucleus accumbens associated 1, BEN and BTB (POZ) domain containing Mus musculus 23-28 18157167-1 2008 BACKGROUND AND PURPOSE: The analgesics, paracetamol and dipyrone are weak inhibitors of the cyclooxygenase isoforms 1 or 2 (COX-1, COX-2) but more potent on COX-3. Acetaminophen 40-51 cytochrome c oxidase I, mitochondrial Rattus norvegicus 124-129 18157167-1 2008 BACKGROUND AND PURPOSE: The analgesics, paracetamol and dipyrone are weak inhibitors of the cyclooxygenase isoforms 1 or 2 (COX-1, COX-2) but more potent on COX-3. Acetaminophen 40-51 cytochrome c oxidase II, mitochondrial Rattus norvegicus 131-136 18157167-1 2008 BACKGROUND AND PURPOSE: The analgesics, paracetamol and dipyrone are weak inhibitors of the cyclooxygenase isoforms 1 or 2 (COX-1, COX-2) but more potent on COX-3. Acetaminophen 40-51 cytochrome c oxidase III, mitochondrial Rattus norvegicus 157-162 17884974-0 2008 Acetaminophen (paracetamol) is a selective cyclooxygenase-2 inhibitor in man. Acetaminophen 0-13 prostaglandin-endoperoxide synthase 2 Homo sapiens 43-59 17884974-0 2008 Acetaminophen (paracetamol) is a selective cyclooxygenase-2 inhibitor in man. Acetaminophen 15-26 prostaglandin-endoperoxide synthase 2 Homo sapiens 43-59 17884974-3 2008 The fact that acetaminophen acts functionally as a selective COX-2 inhibitor led us to investigate the hypothesis of whether it works via preferential COX-2 blockade. Acetaminophen 14-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 61-66 17884974-6 2008 In vitro, acetaminophen elicited a 4.4-fold selectivity toward COX-2 inhibition (IC(50)=113.7 micromol/L for COX-1; IC(50)=25.8 micromol/L for COX-2). Acetaminophen 10-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 17884974-6 2008 In vitro, acetaminophen elicited a 4.4-fold selectivity toward COX-2 inhibition (IC(50)=113.7 micromol/L for COX-1; IC(50)=25.8 micromol/L for COX-2). Acetaminophen 10-23 mitochondrially encoded cytochrome c oxidase I Homo sapiens 109-114 17884974-6 2008 In vitro, acetaminophen elicited a 4.4-fold selectivity toward COX-2 inhibition (IC(50)=113.7 micromol/L for COX-1; IC(50)=25.8 micromol/L for COX-2). Acetaminophen 10-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 143-148 17884974-8 2008 Acetaminophen plasma concentrations remained above the in vitro IC(50) for COX-2 for at least 5 h postadministration. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 75-80 17884974-9 2008 Ex vivo IC(50) values (COX-1: 105.2 micromol/L; COX-2: 26.3 micromol/L) of acetaminophen compared favorably with its in vitro IC(50) values. Acetaminophen 75-88 mitochondrially encoded cytochrome c oxidase I Homo sapiens 23-28 17884974-9 2008 Ex vivo IC(50) values (COX-1: 105.2 micromol/L; COX-2: 26.3 micromol/L) of acetaminophen compared favorably with its in vitro IC(50) values. Acetaminophen 75-88 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 17884974-10 2008 In contrast to previous concepts, acetaminophen inhibited COX-2 by more than 80%, i.e., to a degree comparable to nonsteroidal antiinflammatory drugs (NSAIDs) and selective COX-2 inhibitors. Acetaminophen 34-47 mitochondrially encoded cytochrome c oxidase II Homo sapiens 58-63 17884974-13 2008 In view of its substantial COX-2 inhibition, recently defined cardiovascular warnings for use of COX-2 inhibitors should also be considered for acetaminophen. Acetaminophen 144-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-102 18183605-2 2008 Transaldolase exchange was quantified in five healthy, fed subjects following an oral bolus of [1,2,3-(13)C(3)]glycerol (25-30 mg/kg) and paracetamol (10-12 mg/kg). Acetaminophen 138-149 transaldolase 1 Homo sapiens 0-13 18078705-2 2008 Recent studies by our group using paracetamol (APAP), diethylmaleate and buthionine sulphoximine have shown that for a given xenobiotic molecule, Nrf2 induction in the murine liver is associated with protein reactivity and glutathione depletion. Acetaminophen 34-45 nuclear factor, erythroid derived 2, like 2 Mus musculus 146-150 18078705-2 2008 Recent studies by our group using paracetamol (APAP), diethylmaleate and buthionine sulphoximine have shown that for a given xenobiotic molecule, Nrf2 induction in the murine liver is associated with protein reactivity and glutathione depletion. Acetaminophen 47-51 nuclear factor, erythroid derived 2, like 2 Mus musculus 146-150 18078705-6 2008 Each compound elicited significant serum ALT increases after 24h (ALT U/L: APAP, 3036+/-1462; BB, 5308+/-2210; CCl4, 5089+/-1665; FS, 2301+/-1053), accompanied by centrilobular damage as assessed by histopathology. Acetaminophen 75-79 glutamic pyruvic transaminase, soluble Mus musculus 41-44 18078705-6 2008 Each compound elicited significant serum ALT increases after 24h (ALT U/L: APAP, 3036+/-1462; BB, 5308+/-2210; CCl4, 5089+/-1665; FS, 2301+/-1053), accompanied by centrilobular damage as assessed by histopathology. Acetaminophen 75-79 glutamic pyruvic transaminase, soluble Mus musculus 66-69 18078705-7 2008 Treatment with APAP also elicited toxicity at a much earlier time point (5h) than the other hepatotoxins (ALT U/L: APAP, 1780+/-661; BB, 161+/-15; CCl4, 90+/-23; FS, 136+/-27). Acetaminophen 15-19 glutamic pyruvic transaminase, soluble Mus musculus 106-109 18078705-7 2008 Treatment with APAP also elicited toxicity at a much earlier time point (5h) than the other hepatotoxins (ALT U/L: APAP, 1780+/-661; BB, 161+/-15; CCl4, 90+/-23; FS, 136+/-27). Acetaminophen 15-19 chemokine (C-C motif) ligand 4 Mus musculus 147-151 18078705-9 2008 Western Blot analysis revealed an increase in nuclear Nrf2, 1h after administration of BB (209+/-10% control), CCl4 (146+/-3% control) and FS (254+/-41% control), however this was significantly lower than the levels observed in the APAP-treated mice (462+/-36% control). Acetaminophen 232-236 nuclear factor, erythroid derived 2, like 2 Mus musculus 54-58 18078705-11 2008 Treatment with APAP for 1h caused a significant increase in the levels of haem oxygenase-1 (HO-1; 2.85-fold) and glutamate cysteine ligase (GCLC; 1.62-fold) mRNA. Acetaminophen 15-19 heme oxygenase 1 Mus musculus 74-90 18078705-11 2008 Treatment with APAP for 1h caused a significant increase in the levels of haem oxygenase-1 (HO-1; 2.85-fold) and glutamate cysteine ligase (GCLC; 1.62-fold) mRNA. Acetaminophen 15-19 heme oxygenase 1 Mus musculus 92-96 18078705-11 2008 Treatment with APAP for 1h caused a significant increase in the levels of haem oxygenase-1 (HO-1; 2.85-fold) and glutamate cysteine ligase (GCLC; 1.62-fold) mRNA. Acetaminophen 15-19 glutamate-cysteine ligase, catalytic subunit Mus musculus 140-144 18642143-4 2008 Gclm null mice exhibit low GSH levels and enhanced sensitivity to acetaminophen. Acetaminophen 66-79 glutamate-cysteine ligase, modifier subunit Mus musculus 0-4 17724253-3 2008 Whereas the prevailing concept assumes a direct reduction of the active, oxidized enzyme by acetaminophen, here we show that acetaminophen is a potent scavenger of peroxynitrite (peroxynitrite-mediated phenol nitration, IC50 approximately 72 microM; Sin-1-mediated DHR123 oxidation, IC50 approximately 11 microM) and thus inhibits PGHS by eliminating the peroxide tone. Acetaminophen 125-138 MAPK associated protein 1 Homo sapiens 250-255 17906064-0 2008 Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity. Acetaminophen 101-114 BCL2-associated X protein Mus musculus 14-17 17906064-3 2008 APAP overdose induced Bax translocation from the cytosol to the mitochondria as early as 1 h after APAP injection. Acetaminophen 0-4 BCL2-associated X protein Mus musculus 22-25 17906064-3 2008 APAP overdose induced Bax translocation from the cytosol to the mitochondria as early as 1 h after APAP injection. Acetaminophen 99-103 BCL2-associated X protein Mus musculus 22-25 18354249-2 2008 We, and others, have previously reported that thyrotropin-releasing hormone (TRH, pGlu-His-Pro-NH(2)) and TRH-like peptides with the general structure pGlu-X-Pro-NH(2), where "X" can be any amino acid residue, have neuroprotective, antidepressant, analeptic, arousal, and anti-epileptic effects that could mediate the neuropsychiatric and therapeutic effects of a variety of neurotropic agents. Acetaminophen 156-157 thyrotropin releasing hormone Rattus norvegicus 77-80 18354249-2 2008 We, and others, have previously reported that thyrotropin-releasing hormone (TRH, pGlu-His-Pro-NH(2)) and TRH-like peptides with the general structure pGlu-X-Pro-NH(2), where "X" can be any amino acid residue, have neuroprotective, antidepressant, analeptic, arousal, and anti-epileptic effects that could mediate the neuropsychiatric and therapeutic effects of a variety of neurotropic agents. Acetaminophen 156-157 thyrotropin releasing hormone Rattus norvegicus 106-109 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 gamma-glutamyltransferase 1 Rattus norvegicus 157-187 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 gamma-glutamyltransferase 1 Rattus norvegicus 189-193 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 lactoperoxidase Rattus norvegicus 196-212 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 lactoperoxidase Rattus norvegicus 214-217 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 catalase Rattus norvegicus 282-290 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 hematopoietic prostaglandin D synthase Rattus norvegicus 325-350 18166521-4 2008 Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Acetaminophen 0-13 hematopoietic prostaglandin D synthase Rattus norvegicus 352-355 18583171-4 2008 This unexpected finding suggested that the CYP2E1-null mice compensate with other isozymes as already described for acetaminophen-induced liver damage. Acetaminophen 116-129 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 43-49 18203258-3 2008 Here, human GST pi (GSTP) was exploited as a model target protein to determine the chemical, biochemical and functional consequences of exposure to the hepatotoxic CRM of paracetamol (APAP), N-acetyl-p-benzoquinoneimine (NAPQI). Acetaminophen 171-182 glutathione S-transferase pi 1 Homo sapiens 12-18 18203258-3 2008 Here, human GST pi (GSTP) was exploited as a model target protein to determine the chemical, biochemical and functional consequences of exposure to the hepatotoxic CRM of paracetamol (APAP), N-acetyl-p-benzoquinoneimine (NAPQI). Acetaminophen 171-182 glutathione S-transferase pi 1 Homo sapiens 20-24 18203258-3 2008 Here, human GST pi (GSTP) was exploited as a model target protein to determine the chemical, biochemical and functional consequences of exposure to the hepatotoxic CRM of paracetamol (APAP), N-acetyl-p-benzoquinoneimine (NAPQI). Acetaminophen 184-188 glutathione S-transferase pi 1 Homo sapiens 12-18 18203258-3 2008 Here, human GST pi (GSTP) was exploited as a model target protein to determine the chemical, biochemical and functional consequences of exposure to the hepatotoxic CRM of paracetamol (APAP), N-acetyl-p-benzoquinoneimine (NAPQI). Acetaminophen 184-188 glutathione S-transferase pi 1 Homo sapiens 20-24 17935745-0 2008 Induction of Mrp3 and Mrp4 transporters during acetaminophen hepatotoxicity is dependent on Nrf2. Acetaminophen 47-60 prolactin family 2, subfamily c, member 4 Mus musculus 13-17 17935745-0 2008 Induction of Mrp3 and Mrp4 transporters during acetaminophen hepatotoxicity is dependent on Nrf2. Acetaminophen 47-60 prolactin family 2, subfamily c, member 5 Mus musculus 22-26 17935745-0 2008 Induction of Mrp3 and Mrp4 transporters during acetaminophen hepatotoxicity is dependent on Nrf2. Acetaminophen 47-60 nuclear factor, erythroid derived 2, like 2 Mus musculus 92-96 17935745-2 2008 Mice deficient in Nrf2 (Nrf2-null) are highly susceptible to acetaminophen (APAP) hepatotoxicity and exhibit lower basal and inducible expression of cytoprotective genes, including NADPH quinone oxidoreductase 1 (Nqo1) and glutamate cysteine ligase (catalytic subunit, or Gclc). Acetaminophen 61-74 nuclear factor, erythroid derived 2, like 2 Mus musculus 18-22 17935745-2 2008 Mice deficient in Nrf2 (Nrf2-null) are highly susceptible to acetaminophen (APAP) hepatotoxicity and exhibit lower basal and inducible expression of cytoprotective genes, including NADPH quinone oxidoreductase 1 (Nqo1) and glutamate cysteine ligase (catalytic subunit, or Gclc). Acetaminophen 61-74 nuclear factor, erythroid derived 2, like 2 Mus musculus 24-28 18710030-4 2008 A high-fat diet enhanced reactions of biotransformation of amidopyrine, acetanilide, toluene, sulfadimezine, were catalyzed with CYP2E1, CYP3A and enzymes of conjugation, simultaneously it increased the hepatotoxicity of paracetamol. Acetaminophen 221-232 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 129-135 18710030-4 2008 A high-fat diet enhanced reactions of biotransformation of amidopyrine, acetanilide, toluene, sulfadimezine, were catalyzed with CYP2E1, CYP3A and enzymes of conjugation, simultaneously it increased the hepatotoxicity of paracetamol. Acetaminophen 221-232 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 137-142 20525116-4 2007 The recently elucidated mechanism of action of acetaminophen may explain some occurrences of adverse reactions in patients with cross-reactive NSAID hypersensitivity on the basis of its inhibitory activity on the newly described enzyme, cyclooxygenase (COX)-3. Acetaminophen 47-60 mitochondrially encoded cytochrome c oxidase III Homo sapiens 237-259 17967565-10 2007 High levels of sFas and HGF might help to confirm a diagnosis of drug-induced liver injury or acetaminophen-related ALF. Acetaminophen 94-107 hepatocyte growth factor Homo sapiens 24-27 18028081-5 2007 Use of paracetamol-containing medicines was overtaken by NSAIDs in 1999/2000, corresponding to the introduction of the Cox-2-selective agents. Acetaminophen 7-18 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 18047802-12 2007 In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Acetaminophen 13-26 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 40-55 17929948-5 2007 cITP-NMR was used in this work to isolate and detect 4-aminophenol (PAP) in an acetaminophen sample spiked at the 0.1% level, with no interference from the parent compound. Acetaminophen 79-92 regenerating family member 3 alpha Homo sapiens 68-71 18058324-0 2007 A cross-performance relationship between Carr"s index and dissolution rate constant: the study of acetaminophen batches. Acetaminophen 98-111 arrestin 3 Homo sapiens 41-45 18058324-4 2007 It was found that the Carr"s Index, C, an overall manifestation of particle size distribution, of only a few grams of the dry blended acetaminophen was good enough to be linearly related to the dissolution rate constant, k, of the formulated granules by ln k = alpha ln C + ln A (or exponentially by a power law of k = AC(alpha)) where A was the exponential factor and alpha was the power index. Acetaminophen 134-147 arrestin 3 Homo sapiens 22-26 17934960-7 2007 It was determined that plasma ALT activity was elevated at 24 and 48 h after APAP administration. Acetaminophen 77-81 glutamic pyruvic transaminase, soluble Mus musculus 30-33 17711562-10 2007 Both paracetamol (P < 0.01) and diclofenac (P < 0.005) inhibited the release of thromboxane B(2) at 1 h but they did not affect serum aminotransferase and GSTA1-1 levels. Acetaminophen 5-16 glutathione S-transferase alpha 1 Homo sapiens 161-168 17711562-11 2007 One patient given paracetamol displayed a transient increase in GSTA1-1 and liver aminotransferases. Acetaminophen 18-29 glutathione S-transferase alpha 1 Homo sapiens 64-71 17431590-0 2007 VEGF isoforms and receptors expression throughout acute acetaminophen-induced liver injury and regeneration. Acetaminophen 56-69 vascular endothelial growth factor A Rattus norvegicus 0-4 17894645-5 2007 In fact, NCX-701 has been shown to be effective in acute nociception as well as in neuropathic pain, situations in which paracetamol and other COX inhibitors are devoid of any effect. Acetaminophen 121-132 T cell leukemia homeobox 2 Homo sapiens 9-12 17705945-2 2007 OBJECTIVE: To provide descriptive data on the safety and efficacy of intravenous N-acetylcysteine (IV-NAC) in the treatment of APAP toxicity, based on information in the Hunter Area Toxicology Service (HATS) database involving residents of the Greater Newcastle Area of New South Wales, Australia. Acetaminophen 127-131 synuclein alpha Homo sapiens 102-105 17705945-10 2007 A total of 26 patients (15.6%) receiving IV-NAC treatment within 8 hours after APAP ingestion had hospitalization stays > 48 hours compared with 70 (33.3%) receiving IV-NAC > 8 hours after ingestion (p < 0.0001). Acetaminophen 79-83 synuclein alpha Homo sapiens 44-47 17705945-11 2007 CONCLUSIONS: For patients with APAP overdose seen in the HATS database of New South Wales, Australia, in-hospital death was infrequent (< 1%) and hepatotoxicity was significantly less likely when IV-NAC was administered within 8 hours after APAP ingestion compared with longer intervals (p < 0.01). Acetaminophen 31-35 synuclein alpha Homo sapiens 202-205 17979661-2 2007 In particular, cytochrome P450 2E1 (CYP2E1) is implicated in the oxidative bioactivation of a variety of small hydrophobic chemicals including a number of epoxide-forming drugs and environmentally important toxicants including urethane, acrylamide, acrylonitrile, benzene, vinyl chloride, styrene, 1-bromopropane, trichloroethylene, dichloroethylene, acetaminophen, and butadiene. Acetaminophen 351-364 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 15-34 17979661-2 2007 In particular, cytochrome P450 2E1 (CYP2E1) is implicated in the oxidative bioactivation of a variety of small hydrophobic chemicals including a number of epoxide-forming drugs and environmentally important toxicants including urethane, acrylamide, acrylonitrile, benzene, vinyl chloride, styrene, 1-bromopropane, trichloroethylene, dichloroethylene, acetaminophen, and butadiene. Acetaminophen 351-364 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 36-42 17410443-0 2007 Platelet-activating factor inactivator (rPAF-AH) enhances liver"s recovery after paracetamol intoxication. Acetaminophen 81-92 PCNA clamp associated factor Rattus norvegicus 0-26 17410443-2 2007 The aim of this study was to investigate the effects of PAF inactivator, recombinant PAF acetylhydrolase (rPAF-AH) on post-paracetamol treatment functional outcome of the liver in the rat. Acetaminophen 123-134 PCNA clamp associated factor Rattus norvegicus 56-59 17410443-2 2007 The aim of this study was to investigate the effects of PAF inactivator, recombinant PAF acetylhydrolase (rPAF-AH) on post-paracetamol treatment functional outcome of the liver in the rat. Acetaminophen 123-134 PCNA clamp associated factor Rattus norvegicus 85-88 17410443-5 2007 APAP was found to cause acute hepatic injury, evident by alterations of biochemical (serum enzymes: ALT, AST, and ALP) and liver histopathological (degree of inflammation and apoptosis) indexes, which was followed by liver regeneration evident by three independent indexes ([(3)H]thymidine incorporation into hepatic DNA, liver thymidine kinase activity, and hepatocyte mitotic index). Acetaminophen 0-4 PDZ and LIM domain 3 Rattus norvegicus 114-117 17410443-8 2007 These results suggest that PAF plays an important role in paracetamol-induced liver injury and regeneration. Acetaminophen 58-69 PCNA clamp associated factor Rattus norvegicus 27-30 17410443-9 2007 Furthermore, PAF inactivator enhances liver"s recovery and attenuates the severity of experimental liver injury, providing important means of improving liver function following paracetamol intoxication. Acetaminophen 177-188 PCNA clamp associated factor Rattus norvegicus 13-16 17620348-0 2007 Induction of hepatic CYP2E1 by a subtoxic dose of acetaminophen in rats: increase in dichloromethane metabolism and carboxyhemoglobin elevation. Acetaminophen 50-63 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 21-27 17620348-7 2007 Hepatic CYP2E1-mediated activities measured with chlorzoxazone, p-nitrophenol, and p-nitroanisole as substrates were all induced markedly in microsomes of rats treated with APAP. Acetaminophen 173-177 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 8-14 17620348-11 2007 The results indicate that, contrary to the well known hepatotoxic effects of this drug at large doses, a subtoxic dose of APAP may induce CYP2E1, and to a lesser degree, CYP3A expression. Acetaminophen 122-126 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 138-144 17620348-11 2007 The results indicate that, contrary to the well known hepatotoxic effects of this drug at large doses, a subtoxic dose of APAP may induce CYP2E1, and to a lesser degree, CYP3A expression. Acetaminophen 122-126 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 170-175 17627974-5 2007 Compared with normal liver specimens, MRP1 and MRP4 mRNA levels were elevated after APAP overdose and in PBC. Acetaminophen 84-88 ATP binding cassette subfamily C member 1 Homo sapiens 38-42 17627974-5 2007 Compared with normal liver specimens, MRP1 and MRP4 mRNA levels were elevated after APAP overdose and in PBC. Acetaminophen 84-88 ATP binding cassette subfamily C member 4 Homo sapiens 47-51 17627974-8 2007 Increased P-gp protein was confirmed immunohistochemically and was found to localize to areas of PCNA-positive hepatocytes, which were detected in APAP overdose and PBC livers. Acetaminophen 147-151 phosphoglycolate phosphatase Homo sapiens 10-14 17627974-8 2007 Increased P-gp protein was confirmed immunohistochemically and was found to localize to areas of PCNA-positive hepatocytes, which were detected in APAP overdose and PBC livers. Acetaminophen 147-151 proliferating cell nuclear antigen Homo sapiens 97-101 17916057-7 2007 Important work has elucidated the relationship between CYP2E1-mediated formation of the hepatotoxic metabolite of acetaminophen and alcohol consumption. Acetaminophen 114-127 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 55-61 17654741-11 2007 Mice lacking PAR-1 developed less injury and hepatic fibrin deposits at 6 hours in response to APAP than control mice. Acetaminophen 95-99 coagulation factor II (thrombin) receptor Mus musculus 13-18 17652633-8 2007 To further investigate this effect, we tested and showed that the antipyretic, acetaminophen, suppressed the hyperthermia caused by TRPV1 blockade. Acetaminophen 79-92 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 132-137 17584759-0 2007 Glutamate cysteine ligase modifier subunit deficiency and gender as determinants of acetaminophen-induced hepatotoxicity in mice. Acetaminophen 84-97 glutamate-cysteine ligase, modifier subunit Mus musculus 0-42 17526808-0 2007 High-dose acetaminophen inhibits the lethal effect of doxorubicin in HepG2 cells: the role of P-glycoprotein and mitogen-activated protein kinase p44/42 pathway. Acetaminophen 10-23 ATP binding cassette subfamily B member 1 Homo sapiens 94-108 17526808-0 2007 High-dose acetaminophen inhibits the lethal effect of doxorubicin in HepG2 cells: the role of P-glycoprotein and mitogen-activated protein kinase p44/42 pathway. Acetaminophen 10-23 interferon induced protein 44 Homo sapiens 146-149 17533171-2 2007 We found Tsc-22 downregulation in livers from B6C3F1 mice following treatment for 2 weeks with carcinogenic doses of the antianxiety drug oxazepam (2500 ppm) or the peroxisome proliferator Wyeth-14,643 (500 ppm) but not with two other carcinogens such as o-nitrotoluene or methyleugenol or three noncarcinogens including p-nitrotoluene, eugenol, or acetaminophen. Acetaminophen 349-362 TSC22 domain family, member 1 Mus musculus 9-15 17573345-0 2007 Knock down of gamma-glutamylcysteine synthetase in rat causes acetaminophen-induced hepatotoxicity. Acetaminophen 62-75 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 14-47 17593074-0 2007 A randomized trial to determine the change in alanine aminotransferase during 10 days of paracetamol (acetaminophen) administration in subjects who consume moderate amounts of alcohol. Acetaminophen 89-100 glutamic--pyruvic transaminase Homo sapiens 46-70 17593074-0 2007 A randomized trial to determine the change in alanine aminotransferase during 10 days of paracetamol (acetaminophen) administration in subjects who consume moderate amounts of alcohol. Acetaminophen 102-115 glutamic--pyruvic transaminase Homo sapiens 46-70 17593074-3 2007 AIM: To determine the effect of 10 days of the maximal therapeutic dose of paracetamol on serum alanine aminotransferase (ALT) activity in subjects who consume 1 to 3 alcoholic beverages per day. Acetaminophen 75-86 glutamic--pyruvic transaminase Homo sapiens 96-120 17609236-14 2007 Since acetaminophen is a weak inhibitor of the COX-1 enzyme, patients with aspirin-induced asthma should not take more than 1000 mg of acetaminophen in a single dose. Acetaminophen 6-19 prostaglandin-endoperoxide synthase 1 Homo sapiens 47-52 17392391-1 2007 CYP2E1 is widely accepted as the sole form of cytochrome P450 responsible for alcohol-mediated increases in acetaminophen (APAP) hepatotoxicity. Acetaminophen 108-121 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 0-6 17392391-1 2007 CYP2E1 is widely accepted as the sole form of cytochrome P450 responsible for alcohol-mediated increases in acetaminophen (APAP) hepatotoxicity. Acetaminophen 123-127 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 0-6 17392391-6 2007 At the time of APAP administration, which followed an 11 h withdrawal from the alcohols, alcohol-induced levels of CYP3A were sustained in both mouse lines, whereas CYP2E1 was decreased to constitutive levels in wild-type mice. Acetaminophen 15-19 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 115-120 17392391-6 2007 At the time of APAP administration, which followed an 11 h withdrawal from the alcohols, alcohol-induced levels of CYP3A were sustained in both mouse lines, whereas CYP2E1 was decreased to constitutive levels in wild-type mice. Acetaminophen 15-19 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 165-171 17688378-7 2007 Additionally, expert opinion is presented herein to aid in reducing the frequency and severity of liver injury from acetaminophen. Acetaminophen 116-129 activation induced cytidine deaminase Homo sapiens 52-55 17185352-3 2007 AIM: To examine the role of JNK in paracetamol-induced acute liver failure (ALF). Acetaminophen 35-46 mitogen-activated protein kinase 8 Mus musculus 28-31 17185352-4 2007 METHODS: A previously developed mouse model of paracetamol poisoning was used to examine the role of JNK in paracetamol-induced ALF. Acetaminophen 108-119 mitogen-activated protein kinase 8 Mus musculus 101-104 17185352-5 2007 RESULTS: Paracetamol-induced hepatic JNK activation both in human and murine paracetamol hepatotoxicity and in our murine model preceded the onset of hepatocyte death. Acetaminophen 9-20 mitogen-activated protein kinase 8 Homo sapiens 37-40 17185352-5 2007 RESULTS: Paracetamol-induced hepatic JNK activation both in human and murine paracetamol hepatotoxicity and in our murine model preceded the onset of hepatocyte death. Acetaminophen 77-88 mitogen-activated protein kinase 8 Homo sapiens 37-40 17185352-6 2007 JNK inhibition in vivo (using two JNK inhibitors with different mechanisms of action) markedly reduced mortality in murine paracetamol hepatotoxicity, with a significant reduction in hepatic necrosis and apoptosis. Acetaminophen 123-134 mitogen-activated protein kinase 8 Mus musculus 0-3 17185352-6 2007 JNK inhibition in vivo (using two JNK inhibitors with different mechanisms of action) markedly reduced mortality in murine paracetamol hepatotoxicity, with a significant reduction in hepatic necrosis and apoptosis. Acetaminophen 123-134 mitogen-activated protein kinase 8 Mus musculus 34-37 17185352-7 2007 In addition, delayed administration of the JNK inhibitor was more effective than N-acetylcysteine after paracetamol poisoning in mice. Acetaminophen 104-115 mitogen-activated protein kinase 8 Mus musculus 43-46 17185352-10 2007 Pharmacological JNK inhibition had no effect on paracetamol metabolism, but markedly inhibited hepatic tumour necrosis foctor alpha (TNF alpha) production after paracetamol poisoning. Acetaminophen 161-172 mitogen-activated protein kinase 8 Mus musculus 16-19 17185352-10 2007 Pharmacological JNK inhibition had no effect on paracetamol metabolism, but markedly inhibited hepatic tumour necrosis foctor alpha (TNF alpha) production after paracetamol poisoning. Acetaminophen 161-172 tumor necrosis factor Mus musculus 133-142 17185352-11 2007 CONCLUSIONS: These data demonstrated a central role for JNK in the pathogenesis of paracetamol-induced liver failure, thereby identifying JNK as an important therapeutic target in the treatment of paracetamol hepatotoxicity. Acetaminophen 83-94 mitogen-activated protein kinase 8 Mus musculus 56-59 17185352-11 2007 CONCLUSIONS: These data demonstrated a central role for JNK in the pathogenesis of paracetamol-induced liver failure, thereby identifying JNK as an important therapeutic target in the treatment of paracetamol hepatotoxicity. Acetaminophen 83-94 mitogen-activated protein kinase 8 Mus musculus 138-141 17185352-11 2007 CONCLUSIONS: These data demonstrated a central role for JNK in the pathogenesis of paracetamol-induced liver failure, thereby identifying JNK as an important therapeutic target in the treatment of paracetamol hepatotoxicity. Acetaminophen 197-208 mitogen-activated protein kinase 8 Mus musculus 56-59 17185352-11 2007 CONCLUSIONS: These data demonstrated a central role for JNK in the pathogenesis of paracetamol-induced liver failure, thereby identifying JNK as an important therapeutic target in the treatment of paracetamol hepatotoxicity. Acetaminophen 197-208 mitogen-activated protein kinase 8 Mus musculus 138-141 17530272-0 2007 Chromatin breakdown by deoxyribonuclease1 promotes acetaminophen-induced liver necrosis: an ultrastructural and histochemical study on male CD-1 mice. Acetaminophen 51-64 deoxyribonuclease I Mus musculus 23-41 17482566-2 2007 In this current study, we identified a phage clone (PARA-061) displaying the cyclic 7-mer peptide sequence N" AC-NPNNLSH-CGGGS C" that binds the low molecular weight organic molecule 4-acetamidophenol (4-AAP; paracetamol). Acetaminophen 183-200 serpin family F member 2 Homo sapiens 204-207 17482566-2 2007 In this current study, we identified a phage clone (PARA-061) displaying the cyclic 7-mer peptide sequence N" AC-NPNNLSH-CGGGS C" that binds the low molecular weight organic molecule 4-acetamidophenol (4-AAP; paracetamol). Acetaminophen 209-220 serpin family F member 2 Homo sapiens 204-207 17497828-3 2007 The potential for inhibition of the CYP isoforms was measured by monitoring the level of the metabolites 6beta-hydroxytestosterone (3A4), dextrorphan (2D6), 4"-hydroxydiclofenac (2C9), and acetaminophen (1A2) formed in the presence of drug candidates using an eight-point titration. Acetaminophen 189-202 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 36-39 17567465-6 2007 TUNEL labeling and caspase 3 activation also increased after acetaminophen. Acetaminophen 61-74 caspase 3 Mus musculus 19-28 17567472-5 2007 Ethanol-inducible CYP2E1 is of interest because of its ability to metabolize and activate many toxicologically important substrates including ethanol, CCl(4), acetaminophen, and N-nitrosodimethylamine, to more toxic products. Acetaminophen 159-172 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 18-24 17567472-6 2007 Major interest in CYP2E1 reflects the ability of this enzyme to oxidize ethanol, to generate reactive products from ethanol oxidation (e.g. acetaldehyde and 1-hydroxyethyl radical), to activate various agents including CCl(4) and acetaminophen into reactive products, and to generate reactive oxygen species. Acetaminophen 230-243 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 18-24 18379621-2 2007 Caffeination as well as administration of vitamins A and E caused significant decreases[P < 0.05] in AST and ALP levels in all test groups when co-administered with paracetamol and in ALT level except in the caffeinated paracetamol + Vitamin E group in which ALT and ALP level except in the caffeinated paracetamol + vitamin E group in which ALT and ALP levels significantly increased [P < 0.05]. Acetaminophen 168-179 PDZ and LIM domain 3 Rattus norvegicus 112-115 17175104-0 2007 Acetaminophen selectively suppresses peripheral prostaglandin E2 release and increases COX-2 gene expression in a clinical model of acute inflammation. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 87-92 17175104-1 2007 Acetaminophen is widely used for pain management as an alternative to NSAIDs and selective COX-2 inhibitors, but its action at a molecular level is still unclear. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 91-96 17175104-8 2007 COX-2 gene expression remained elevated at 24 h with continued ketorolac and acetaminophen treatment. Acetaminophen 77-90 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 17175104-9 2007 COX-1 gene expression was significantly down-regulated at 24 h by ketorolac, rofecoxib and acetaminophen. Acetaminophen 91-104 mitochondrially encoded cytochrome c oxidase I Homo sapiens 0-5 17175104-10 2007 Acetaminophen suppression of PGE2 without inhibiting TXB2 release, when COX-2 gene expression is up-regulated, suggests that acetaminophen is a selective COX-2 inhibitor in vivo. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 154-159 17175104-10 2007 Acetaminophen suppression of PGE2 without inhibiting TXB2 release, when COX-2 gene expression is up-regulated, suggests that acetaminophen is a selective COX-2 inhibitor in vivo. Acetaminophen 125-138 mitochondrially encoded cytochrome c oxidase II Homo sapiens 72-77 17175104-10 2007 Acetaminophen suppression of PGE2 without inhibiting TXB2 release, when COX-2 gene expression is up-regulated, suggests that acetaminophen is a selective COX-2 inhibitor in vivo. Acetaminophen 125-138 mitochondrially encoded cytochrome c oxidase II Homo sapiens 154-159 17175104-11 2007 The up-regulation of COX-2 gene and down-regulation of COX-1 gene expression suggests that acetaminophen may result in changes in COX-derived prostanoids with repeated doses. Acetaminophen 91-104 mitochondrially encoded cytochrome c oxidase II Homo sapiens 21-26 17175104-11 2007 The up-regulation of COX-2 gene and down-regulation of COX-1 gene expression suggests that acetaminophen may result in changes in COX-derived prostanoids with repeated doses. Acetaminophen 91-104 mitochondrially encoded cytochrome c oxidase I Homo sapiens 55-60 17562481-6 2007 With regards to the liver and gastrointestinal tract, Nrf2 knockout mice are more susceptible to acetaminophen-induced hepatocellular injury, benzo[a]pyrene-induced tumor formation and Fas- and TNFalpha -mediated hepatocellular apoptosis. Acetaminophen 97-110 nuclear factor, erythroid derived 2, like 2 Mus musculus 54-58 17437157-7 2007 After LPS stimulation, the expression level of TNF-alpha was lower (175.7 +/- 54.6 versus 465.6 +/- 64.2, p = 0.002), and the increment of TNF-alpha expression was also less significant in the CCl(4)/APAP group (1.5-fold versus 6.5-fold, p = 0.014). Acetaminophen 200-204 tumor necrosis factor Mus musculus 47-56 17439248-0 2007 Hepatoprotective role of endogenous interleukin-13 in a murine model of acetaminophen-induced liver disease. Acetaminophen 72-85 interleukin 13 Mus musculus 36-50 17439248-2 2007 In the present study, we investigated the role of interleukin (IL)-13 in acetaminophen (APAP)-induced liver disease (AILD). Acetaminophen 73-86 interleukin 13 Mus musculus 50-69 17439248-2 2007 In the present study, we investigated the role of interleukin (IL)-13 in acetaminophen (APAP)-induced liver disease (AILD). Acetaminophen 88-92 interleukin 13 Mus musculus 50-69 17439248-3 2007 Following APAP (200 mg/kg) administration to male C57BL/6 wild-type (WT) mice, hepatotoxicity developed up to 24 h post-APAP, with a concomitant increase in serum IL-13 concentration. Acetaminophen 10-14 interleukin 13 Mus musculus 163-168 17439248-4 2007 Pretreatment of these mice with an IL-13-neutralizing antibody exacerbated liver injury, as did APAP administration to IL-13 knockout (KO) mice in comparison to WT mice. Acetaminophen 96-100 interleukin 13 Mus musculus 119-124 17439248-6 2007 In this regard, multiplex antibody arrays were used to identify potential IL-13-regulated biomarkers, including various cytokines and chemokines, as well as nitric oxide (NO), associated with AILD that were present at higher concentrations in the sera of APAP-treated IL-13 KO mice than in WT mice. Acetaminophen 255-259 interleukin 13 Mus musculus 74-79 17188523-11 2007 Paracetamol, significantly decreased the synthesis of TNF-alpha and that of the gelatinases. Acetaminophen 0-11 tumor necrosis factor Homo sapiens 54-63 17188523-13 2007 The inhibitory effect of paracetamol upon TNF-alpha and gelatinases is intriguing. Acetaminophen 25-36 tumor necrosis factor Homo sapiens 42-51 17320862-7 2007 Although paracetamol significantly increased exudate TNF-alpha level compared to the control group and NCX 701 group, neither paracetamol, nor NCX701 treatments changed the levels of exudate IL-1beta significantly. Acetaminophen 9-20 tumor necrosis factor Rattus norvegicus 53-62 17320862-13 2007 Unlike paracetamol, which increased exudate TNF-alpha level, NCX 701 had no effect on TNF-alpha level in the exudates. Acetaminophen 7-18 tumor necrosis factor Rattus norvegicus 44-53 17377112-10 2007 Conversely, a prevention of the increase in TNF-alpha levels was observed only in rats treated with nimesulide or tramadol and paracetamol in combination. Acetaminophen 127-138 tumor necrosis factor Rattus norvegicus 44-53 16690336-7 2007 Following dosing of CFA-injected rats with rofecoxib (Vioxx) or paracetamol, there was a significant decrease in the number of ipsilateral CGRP-IR small and medium DRG neurones in rofecoxib- but not paracetamol-treated rats. Acetaminophen 64-75 calcitonin-related polypeptide alpha Rattus norvegicus 139-143 16690336-9 2007 In conclusion, these data show that changes in ipsilateral CGRP expression within small DRG neurones are consistent with behavioural readouts in both time course, rofecoxib and paracetamol studies in this model of chronic inflammatory pain. Acetaminophen 177-188 calcitonin-related polypeptide alpha Rattus norvegicus 59-63 17403848-9 2007 The highest CSF paracetamol concentration was detected at 57 minutes. Acetaminophen 16-27 colony stimulating factor 2 Homo sapiens 12-15 17207453-2 2007 Sublethal dose of AAP resulted in a decrease in microsomal total glutathione and in the reduced-to-total glutathione ratio; redox state of thiols of ER resident oxidoreductases ERp72, PDI was shifted towards the oxidized form; ER stress-responsive transcription factor ATF6 was activated. Acetaminophen 18-21 protein disulfide isomerase associated 4 Mus musculus 177-182 17207453-2 2007 Sublethal dose of AAP resulted in a decrease in microsomal total glutathione and in the reduced-to-total glutathione ratio; redox state of thiols of ER resident oxidoreductases ERp72, PDI was shifted towards the oxidized form; ER stress-responsive transcription factor ATF6 was activated. Acetaminophen 18-21 protein disulfide isomerase associated 3 Mus musculus 184-187 17207453-2 2007 Sublethal dose of AAP resulted in a decrease in microsomal total glutathione and in the reduced-to-total glutathione ratio; redox state of thiols of ER resident oxidoreductases ERp72, PDI was shifted towards the oxidized form; ER stress-responsive transcription factor ATF6 was activated. Acetaminophen 18-21 activating transcription factor 6 Mus musculus 269-273 17339476-0 2007 Overexpression of suppressor of cytokine signaling-3 in T cells exacerbates acetaminophen-induced hepatotoxicity. Acetaminophen 76-89 suppressor of cytokine signaling 3 Mus musculus 18-52 17339476-4 2007 Mice with a cell-specific overexpression of SOCS3 in T cells (SOCS3Tg, in which Tg is transgenic) exhibited exaggerated hepatic injury after APAP challenge, as evidenced by increased serum alanine aminotransferase levels, augmented hepatic necrosis, and decreased survival relative to the wild-type mice. Acetaminophen 141-145 suppressor of cytokine signaling 3 Mus musculus 44-49 17520838-11 2007 The changes in the pharmacokinetics of acetaminophen resulting from the administration of In-Chen-How are related to an increase in metabolic activity of CYP1A2 and CYP2E1. Acetaminophen 39-52 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 154-160 17520838-11 2007 The changes in the pharmacokinetics of acetaminophen resulting from the administration of In-Chen-How are related to an increase in metabolic activity of CYP1A2 and CYP2E1. Acetaminophen 39-52 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 165-171 17188792-0 2007 Role of NAD(P)H:quinone oxidoreductase 1 in clofibrate-mediated hepatoprotection from acetaminophen. Acetaminophen 86-99 NAD(P)H dehydrogenase, quinone 1 Mus musculus 8-40 17188792-9 2007 Cytochrome P450 enzymes present in microsomes bioactivate APAP to NAPQI, which binds the electrophile trapping agent, N-acetyl cysteine (NAC). Acetaminophen 58-62 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 0-15 17188792-10 2007 We analyzed the formation of APAP-NAC metabolite in the presence of human recombinant NQO1. Acetaminophen 29-33 NAD(P)H quinone dehydrogenase 1 Homo sapiens 86-90 17305405-0 2007 Role of IL-6 in an IL-10 and IL-4 double knockout mouse model uniquely susceptible to acetaminophen-induced liver injury. Acetaminophen 86-99 interleukin 6 Mus musculus 8-12 17305405-0 2007 Role of IL-6 in an IL-10 and IL-4 double knockout mouse model uniquely susceptible to acetaminophen-induced liver injury. Acetaminophen 86-99 interleukin 10 Mus musculus 19-24 17305405-0 2007 Role of IL-6 in an IL-10 and IL-4 double knockout mouse model uniquely susceptible to acetaminophen-induced liver injury. Acetaminophen 86-99 interleukin 4 Mus musculus 29-33 17305405-2 2007 In the current work, we discovered a unique interaction that makes mice deficient in both IL-10 and IL-4 (IL-10/4-/-) highly sensitive to the hepatotoxic effects of acetaminophen (APAP). Acetaminophen 165-178 interleukin 10 Mus musculus 90-95 17305405-2 2007 In the current work, we discovered a unique interaction that makes mice deficient in both IL-10 and IL-4 (IL-10/4-/-) highly sensitive to the hepatotoxic effects of acetaminophen (APAP). Acetaminophen 165-178 interleukin 4 Mus musculus 100-104 17305405-2 2007 In the current work, we discovered a unique interaction that makes mice deficient in both IL-10 and IL-4 (IL-10/4-/-) highly sensitive to the hepatotoxic effects of acetaminophen (APAP). Acetaminophen 165-178 interleukin 4 Mus musculus 106-116 17305405-2 2007 In the current work, we discovered a unique interaction that makes mice deficient in both IL-10 and IL-4 (IL-10/4-/-) highly sensitive to the hepatotoxic effects of acetaminophen (APAP). Acetaminophen 180-184 interleukin 10 Mus musculus 90-95 17305405-2 2007 In the current work, we discovered a unique interaction that makes mice deficient in both IL-10 and IL-4 (IL-10/4-/-) highly sensitive to the hepatotoxic effects of acetaminophen (APAP). Acetaminophen 180-184 interleukin 4 Mus musculus 100-104 17305405-2 2007 In the current work, we discovered a unique interaction that makes mice deficient in both IL-10 and IL-4 (IL-10/4-/-) highly sensitive to the hepatotoxic effects of acetaminophen (APAP). Acetaminophen 180-184 interleukin 4 Mus musculus 106-116 17305405-4 2007 Within 24 h after WT, IL-10-/-, IL-4-/-, or IL-10/4-/- mice were administered APAP, 75% of the IL-10/4-/- mice died of massive hepatic injury while all other genotypes were resistant to liver toxicity at this dose of APAP. Acetaminophen 78-82 interleukin 4 Mus musculus 44-54 17305405-4 2007 Within 24 h after WT, IL-10-/-, IL-4-/-, or IL-10/4-/- mice were administered APAP, 75% of the IL-10/4-/- mice died of massive hepatic injury while all other genotypes were resistant to liver toxicity at this dose of APAP. Acetaminophen 78-82 interleukin 4 Mus musculus 95-105 17366662-0 2007 Mitochondrial protection by the JNK inhibitor leflunomide rescues mice from acetaminophen-induced liver injury. Acetaminophen 76-89 mitogen-activated protein kinase 8 Mus musculus 32-35 17366662-7 2007 Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Acetaminophen 31-35 mitogen-activated protein kinase 8 Mus musculus 76-109 17366662-7 2007 Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Acetaminophen 31-35 mitogen-activated protein kinase 8 Mus musculus 111-114 17366662-7 2007 Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Acetaminophen 31-35 B cell leukemia/lymphoma 2 Mus musculus 144-149 17366662-7 2007 Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Acetaminophen 31-35 BCL2-like 1 Mus musculus 154-160 17366662-10 2007 CONCLUSION: Leflunomide afforded protection against APAP-induced hepatotoxicity in mice through inhibition of JNK-mediated activation of mitochondrial permeabilization. Acetaminophen 52-56 mitogen-activated protein kinase 8 Mus musculus 110-113 17088403-0 2007 Acetaminophen recruits spinal p42/p44 MAPKs and GH/IGF-1 receptors to produce analgesia via the serotonergic system. Acetaminophen 0-13 mitogen activated protein kinase 3 Rattus norvegicus 34-37 17088403-0 2007 Acetaminophen recruits spinal p42/p44 MAPKs and GH/IGF-1 receptors to produce analgesia via the serotonergic system. Acetaminophen 0-13 gonadotropin releasing hormone receptor Rattus norvegicus 48-50 17088403-0 2007 Acetaminophen recruits spinal p42/p44 MAPKs and GH/IGF-1 receptors to produce analgesia via the serotonergic system. Acetaminophen 0-13 insulin-like growth factor 1 Rattus norvegicus 51-56 17088403-4 2007 We show that acetaminophen indirectly stimulates spinal 5-hydroxytryptamine (5-HT)1A receptors in the formalin test, thereby increasing transcript and protein levels of low-affinity neurotrophin receptor, insulin-like growth factor-1 (IGF-1) receptor alpha subunit, and growth hormone receptor and reducing the amount of somatostatin 3 receptor (sst3R) mRNA. Acetaminophen 13-26 insulin-like growth factor 1 Rattus norvegicus 235-240 17088403-4 2007 We show that acetaminophen indirectly stimulates spinal 5-hydroxytryptamine (5-HT)1A receptors in the formalin test, thereby increasing transcript and protein levels of low-affinity neurotrophin receptor, insulin-like growth factor-1 (IGF-1) receptor alpha subunit, and growth hormone receptor and reducing the amount of somatostatin 3 receptor (sst3R) mRNA. Acetaminophen 13-26 gonadotropin releasing hormone receptor Rattus norvegicus 270-284 17088403-6 2007 Indeed, down-regulation of sst3R mRNA depends on acetaminophen-elicited, 5-HT1A receptor-dependent increase in neuronal extracellular signal-regulated kinase 1/2 (ERK1/2) activities that mediate antinociception. Acetaminophen 49-62 mitogen activated protein kinase 3 Rattus norvegicus 120-161 17088403-6 2007 Indeed, down-regulation of sst3R mRNA depends on acetaminophen-elicited, 5-HT1A receptor-dependent increase in neuronal extracellular signal-regulated kinase 1/2 (ERK1/2) activities that mediate antinociception. Acetaminophen 49-62 mitogen activated protein kinase 3 Rattus norvegicus 163-169 17235423-5 2007 Since NAC is already in clinical use in high doses for treating other diseases (e.g., acetaminophen intoxication) and only minor side effects have been observed, there is justified hope that adjunctive therapy with NAC could improve the prognosis of patients with bacterial meningitis. Acetaminophen 86-99 X-linked Kx blood group Homo sapiens 6-9 17235423-5 2007 Since NAC is already in clinical use in high doses for treating other diseases (e.g., acetaminophen intoxication) and only minor side effects have been observed, there is justified hope that adjunctive therapy with NAC could improve the prognosis of patients with bacterial meningitis. Acetaminophen 86-99 X-linked Kx blood group Homo sapiens 215-218 17169476-0 2007 Chemoprotective effect of insulin-like growth factor I against acetaminophen-induced cell death in Chang liver cells via ERK1/2 activation. Acetaminophen 63-76 insulin like growth factor 1 Homo sapiens 26-54 17169476-0 2007 Chemoprotective effect of insulin-like growth factor I against acetaminophen-induced cell death in Chang liver cells via ERK1/2 activation. Acetaminophen 63-76 mitogen-activated protein kinase 3 Homo sapiens 121-127 17169476-5 2007 According to Western blot analysis, treatment with AAP increased the level of poly(ADP-ribose) polymerase (PARP) fragments in cells compared with that in control cells; however, caspase-3, a critical signaling molecule in apoptosis, was not activated after AAP overdose. Acetaminophen 51-54 poly(ADP-ribose) polymerase 1 Homo sapiens 78-105 17169476-5 2007 According to Western blot analysis, treatment with AAP increased the level of poly(ADP-ribose) polymerase (PARP) fragments in cells compared with that in control cells; however, caspase-3, a critical signaling molecule in apoptosis, was not activated after AAP overdose. Acetaminophen 51-54 poly(ADP-ribose) polymerase 1 Homo sapiens 107-111 17169476-5 2007 According to Western blot analysis, treatment with AAP increased the level of poly(ADP-ribose) polymerase (PARP) fragments in cells compared with that in control cells; however, caspase-3, a critical signaling molecule in apoptosis, was not activated after AAP overdose. Acetaminophen 51-54 caspase 3 Homo sapiens 178-187 17169476-8 2007 Compared with AAP treatment alone, IGF-I and AAP co-treatment increased ERK1/2 phosphorylation but inhibited PARP cleavage. Acetaminophen 14-17 insulin like growth factor 1 Homo sapiens 35-40 17169476-9 2007 Thus ERK1/2 activation is instrumental in the protective effect of IGF-I against AAP-induced cell death in Chang liver cells. Acetaminophen 81-84 mitogen-activated protein kinase 3 Homo sapiens 5-11 17169476-9 2007 Thus ERK1/2 activation is instrumental in the protective effect of IGF-I against AAP-induced cell death in Chang liver cells. Acetaminophen 81-84 insulin like growth factor 1 Homo sapiens 67-72 17465855-5 2007 Strikingly, knockout of GPX1 rendered mice resistant to toxicities of drugs including acetaminophen and kainic acid, known as RNS inducers. Acetaminophen 86-99 glutathione peroxidase 1 Mus musculus 24-28 17192482-5 2007 Inhibition of COX-1 with 100 mumol/l acetaminophen did not significantly affect glucose-stimulated insulin secretion. Acetaminophen 37-50 mitochondrially encoded cytochrome c oxidase I Homo sapiens 14-19 17020953-4 2007 Subsequent studies revealed that activation of acetaminophen to an active metabolite is primarily carried out by CYP2E1, an ethanol-inducible cytochrome P450 that was first suggested by characterization of the microsomal ethanol oxidation system. Acetaminophen 47-60 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 113-119 17020953-8 2007 The mechanism of regulation CYP2E1 and its role in acetaminophen toxicity will be discussed. Acetaminophen 51-64 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 28-34 17160478-0 2007 Recombinant platelet-activating factor-acetylhydrolase attenuates paracetamol-induced liver oxidative stress, injury, and regeneration. Acetaminophen 66-77 phospholipase A2 group VII Rattus norvegicus 12-54 17160478-1 2007 The aim of this study was to investigate the effects of platelet-activating factor (PAF) inactivator, recombinant PAF-acetylhydrolase (rPAF-AH), on post-paracetamol treatment functional outcome of the liver in the rat. Acetaminophen 153-164 PCNA clamp associated factor Rattus norvegicus 56-82 17160478-1 2007 The aim of this study was to investigate the effects of platelet-activating factor (PAF) inactivator, recombinant PAF-acetylhydrolase (rPAF-AH), on post-paracetamol treatment functional outcome of the liver in the rat. Acetaminophen 153-164 PCNA clamp associated factor Rattus norvegicus 84-87 17160478-1 2007 The aim of this study was to investigate the effects of platelet-activating factor (PAF) inactivator, recombinant PAF-acetylhydrolase (rPAF-AH), on post-paracetamol treatment functional outcome of the liver in the rat. Acetaminophen 153-164 PCNA clamp associated factor Rattus norvegicus 114-117 17160478-8 2007 These results indicate that the use of PAF inactivator enhances the liver"s recovery from paracetamol intoxication and attenuates the severity of experimental liver injury, providing important means of improving liver function following paracetamol intoxication. Acetaminophen 90-101 PCNA clamp associated factor Rattus norvegicus 39-42 17160478-8 2007 These results indicate that the use of PAF inactivator enhances the liver"s recovery from paracetamol intoxication and attenuates the severity of experimental liver injury, providing important means of improving liver function following paracetamol intoxication. Acetaminophen 237-248 PCNA clamp associated factor Rattus norvegicus 39-42 17164591-2 2007 Numerous drugs are metabolized by UDP-glucuronosyltransferases (UGT) including paracetamol (PCM), a widely used analgesic. Acetaminophen 79-90 beta-1,3-glucuronyltransferase 2 Homo sapiens 34-62 17164591-2 2007 Numerous drugs are metabolized by UDP-glucuronosyltransferases (UGT) including paracetamol (PCM), a widely used analgesic. Acetaminophen 79-90 beta-1,3-glucuronyltransferase 2 Homo sapiens 64-67 17627114-2 2007 An explanation for this difference in pharmacologic activity was provided by the recent discovery of a new cyclooxygenase isoform, cyclooxygenase (COX)-3, that is reported to be inhibited by phenacetin, acetaminophen and dipyrone. Acetaminophen 203-216 cytochrome c oxidase III, mitochondrial Rattus norvegicus 131-153 20020954-5 2007 Pretreatment with Hp-P prevented the APAP-induced elevation of ALT and ALP in murine sera. Acetaminophen 37-41 glutamic pyruvic transaminase, soluble Mus musculus 63-66 17479648-9 2007 In this report it can be assumed that patients, even if heterozygous for a mutation of the GS gene, are at risk for acetaminophen toxicity. Acetaminophen 116-129 glutathione synthetase Homo sapiens 91-93 17045584-1 2006 A cyclooxygenase-1 splice variant (cyclooxygenase-1b), cloned from canine brain, was proposed to be an acetaminophen-sensitive enzyme. Acetaminophen 103-116 prostaglandin-endoperoxide synthase 1 Canis lupus familiaris 2-18 17138759-0 2006 Impact of Cu, Zn-superoxide dismutase and Se-dependent glutathione peroxidase-1 knockouts on acetaminophen-induced cell death and related signaling in murine liver. Acetaminophen 93-106 glutathione peroxidase 1 Mus musculus 55-79 17138759-2 2006 The objective of this study was to compare the impacts of knockout of Cu, Zn-superoxide dismutase (SOD1) and Se-dependent glutathione peroxidase-1 (GPX1) on cell death and related signaling mediated by acetaminophen (APAP), a RNS inducer in liver. Acetaminophen 202-215 superoxide dismutase 1, soluble Mus musculus 99-103 17138759-2 2006 The objective of this study was to compare the impacts of knockout of Cu, Zn-superoxide dismutase (SOD1) and Se-dependent glutathione peroxidase-1 (GPX1) on cell death and related signaling mediated by acetaminophen (APAP), a RNS inducer in liver. Acetaminophen 202-215 glutathione peroxidase 1 Mus musculus 122-146 17138759-2 2006 The objective of this study was to compare the impacts of knockout of Cu, Zn-superoxide dismutase (SOD1) and Se-dependent glutathione peroxidase-1 (GPX1) on cell death and related signaling mediated by acetaminophen (APAP), a RNS inducer in liver. Acetaminophen 202-215 glutathione peroxidase 1 Mus musculus 148-152 17138759-2 2006 The objective of this study was to compare the impacts of knockout of Cu, Zn-superoxide dismutase (SOD1) and Se-dependent glutathione peroxidase-1 (GPX1) on cell death and related signaling mediated by acetaminophen (APAP), a RNS inducer in liver. Acetaminophen 217-221 superoxide dismutase 1, soluble Mus musculus 99-103 17138759-2 2006 The objective of this study was to compare the impacts of knockout of Cu, Zn-superoxide dismutase (SOD1) and Se-dependent glutathione peroxidase-1 (GPX1) on cell death and related signaling mediated by acetaminophen (APAP), a RNS inducer in liver. Acetaminophen 217-221 glutathione peroxidase 1 Mus musculus 122-146 17138759-2 2006 The objective of this study was to compare the impacts of knockout of Cu, Zn-superoxide dismutase (SOD1) and Se-dependent glutathione peroxidase-1 (GPX1) on cell death and related signaling mediated by acetaminophen (APAP), a RNS inducer in liver. Acetaminophen 217-221 glutathione peroxidase 1 Mus musculus 148-152 17138759-7 2006 In conclusion, knockout of GPX1 did not potentiate APAP-induced cell death and related signaling, whereas the SOD1 null blocked APAP-induced hepatic JNK phosphorylation and cell death. Acetaminophen 128-132 superoxide dismutase 1, soluble Mus musculus 110-114 17138759-7 2006 In conclusion, knockout of GPX1 did not potentiate APAP-induced cell death and related signaling, whereas the SOD1 null blocked APAP-induced hepatic JNK phosphorylation and cell death. Acetaminophen 128-132 mitogen-activated protein kinase 8 Mus musculus 149-152 17133485-2 2006 HIP/PAP transgenic mice were protected against acetaminophen-induced acute liver failure and were stimulated to regenerate post-hepatectomy. Acetaminophen 47-60 regenerating islet-derived 3 beta Mus musculus 0-7 16988054-0 2006 Evaluation of the role of multidrug resistance-associated protein (Mrp) 3 and Mrp4 in hepatic basolateral excretion of sulfate and glucuronide metabolites of acetaminophen, 4-methylumbelliferone, and harmol in Abcc3-/- and Abcc4-/- mice. Acetaminophen 158-171 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 26-73 16988054-0 2006 Evaluation of the role of multidrug resistance-associated protein (Mrp) 3 and Mrp4 in hepatic basolateral excretion of sulfate and glucuronide metabolites of acetaminophen, 4-methylumbelliferone, and harmol in Abcc3-/- and Abcc4-/- mice. Acetaminophen 158-171 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 78-82 16988054-2 2006 In the present study, the involvement in this process of Mrp3 and Mrp4, two basolateral efflux transporters, was evaluated by analyzing the hepatic basolateral excretion of the glucuronide and sulfate metabolites of acetaminophen, 4-methylumbelliferone, and harmol in Abcc3(-/-) and Abcc4(-/-) mice using a cassette dosing approach. Acetaminophen 216-229 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 57-61 16988054-2 2006 In the present study, the involvement in this process of Mrp3 and Mrp4, two basolateral efflux transporters, was evaluated by analyzing the hepatic basolateral excretion of the glucuronide and sulfate metabolites of acetaminophen, 4-methylumbelliferone, and harmol in Abcc3(-/-) and Abcc4(-/-) mice using a cassette dosing approach. Acetaminophen 216-229 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 66-70 17202762-4 2006 Comparing gene expression in control rats, CYP3A13 was higher and GSTY2c was lower in adults, suggesting that production of the active metabolite of APAP is higher and its detoxification is lower in adults. Acetaminophen 149-153 cytochrome P450, family 3, subfamily a, polypeptide 9 Rattus norvegicus 43-50 17202762-7 2006 These results suggest that the age-related difference in toxicity would be attributed to a higher expression of CYP3A13, producing the active metabolite of APAP as well as the lower expression of the detoxification enzyme, GSTY2c, in adult rats. Acetaminophen 156-160 cytochrome P450, family 3, subfamily a, polypeptide 9 Rattus norvegicus 112-119 16959944-0 2006 The important role of Bcrp (Abcg2) in the biliary excretion of sulfate and glucuronide metabolites of acetaminophen, 4-methylumbelliferone, and harmol in mice. Acetaminophen 102-115 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 22-26 16959944-0 2006 The important role of Bcrp (Abcg2) in the biliary excretion of sulfate and glucuronide metabolites of acetaminophen, 4-methylumbelliferone, and harmol in mice. Acetaminophen 102-115 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 28-33 17097115-9 2006 Because feline CYP1A2 had a higher K(m) for phenacetin O-deethylase activity with acetaminophen, which cannot be conjugated with glucuronic acid due to UDP-glucuronosyltransferase deficiency, it is supposed that the side effects of phenacetin as a result of toxic intermediates are severe and prolonged in cats. Acetaminophen 82-95 cytochrome P450 family 1 subfamily A member 2 Felis catus 15-21 16979204-0 2006 Leflunomide or A77 1726 protect from acetaminophen-induced cell injury through inhibition of JNK-mediated mitochondrial permeability transition in immortalized human hepatocytes. Acetaminophen 37-50 mitogen-activated protein kinase 8 Homo sapiens 93-96 16979204-8 2006 Instead, we demonstrate that leflunomide (20 microM) inhibited the APAP-induced early (3 h) activation (phosphorylation) of JNK1/2, thus inhibiting phosphorylation of the anti-apoptotic protein Bcl-2 and preventing P-Bcl-2-mediated induction of the mPT. Acetaminophen 67-71 mitogen-activated protein kinase 8 Homo sapiens 124-130 16979204-8 2006 Instead, we demonstrate that leflunomide (20 microM) inhibited the APAP-induced early (3 h) activation (phosphorylation) of JNK1/2, thus inhibiting phosphorylation of the anti-apoptotic protein Bcl-2 and preventing P-Bcl-2-mediated induction of the mPT. Acetaminophen 67-71 BCL2 apoptosis regulator Homo sapiens 194-199 16979204-8 2006 Instead, we demonstrate that leflunomide (20 microM) inhibited the APAP-induced early (3 h) activation (phosphorylation) of JNK1/2, thus inhibiting phosphorylation of the anti-apoptotic protein Bcl-2 and preventing P-Bcl-2-mediated induction of the mPT. Acetaminophen 67-71 BCL2 apoptosis regulator Homo sapiens 217-222 16831125-2 2006 Our objective was to determine impacts of knockout of SOD1 (superoxide dismutase; Cu,Zn-SOD) alone or in combination with selenium-dependent GPX1 (glutathione peroxidase-1) on APAP-induced hepatotoxicity. Acetaminophen 176-180 superoxide dismutase 1, soluble Mus musculus 54-58 16831125-2 2006 Our objective was to determine impacts of knockout of SOD1 (superoxide dismutase; Cu,Zn-SOD) alone or in combination with selenium-dependent GPX1 (glutathione peroxidase-1) on APAP-induced hepatotoxicity. Acetaminophen 176-180 superoxide dismutase 1, soluble Mus musculus 82-91 16831125-2 2006 Our objective was to determine impacts of knockout of SOD1 (superoxide dismutase; Cu,Zn-SOD) alone or in combination with selenium-dependent GPX1 (glutathione peroxidase-1) on APAP-induced hepatotoxicity. Acetaminophen 176-180 glutathione peroxidase 1 Mus musculus 141-145 16831125-2 2006 Our objective was to determine impacts of knockout of SOD1 (superoxide dismutase; Cu,Zn-SOD) alone or in combination with selenium-dependent GPX1 (glutathione peroxidase-1) on APAP-induced hepatotoxicity. Acetaminophen 176-180 glutathione peroxidase 1 Mus musculus 147-171 16831125-5 2006 The protection conferred by SOD1 deletion was associated with a block of the APAP-mediated hepatic protein nitration and a 50% reduction (P<0.05) in activity of a key APAP metabolism enzyme CYP2E1 (cytochrome P450 2E1) in liver. Acetaminophen 77-81 superoxide dismutase 1, soluble Mus musculus 28-32 16831125-7 2006 In conclusion, deletion of SOD1 alone or in combination with GPX1 greatly enhanced mouse resistance to APAP overdose. Acetaminophen 103-107 superoxide dismutase 1, soluble Mus musculus 27-31 16831125-7 2006 In conclusion, deletion of SOD1 alone or in combination with GPX1 greatly enhanced mouse resistance to APAP overdose. Acetaminophen 103-107 glutathione peroxidase 1 Mus musculus 61-65 16831125-8 2006 Our results suggest a possible pro-oxidant role for the physiological level of SOD1 activity in APAP-mediated hepatotoxicity. Acetaminophen 96-100 superoxide dismutase 1, soluble Mus musculus 79-83 16940991-8 2006 Nitroparacetamol prevented the increased plasma nitrate/nitrite and expression of COX-2 and iNOS, whereas paracetamol exerted partial inhibition of COX-2 in lung alone. Acetaminophen 5-16 cytochrome c oxidase II, mitochondrial Rattus norvegicus 82-87 16940991-8 2006 Nitroparacetamol prevented the increased plasma nitrate/nitrite and expression of COX-2 and iNOS, whereas paracetamol exerted partial inhibition of COX-2 in lung alone. Acetaminophen 5-16 nitric oxide synthase 2 Rattus norvegicus 92-96 17076974-0 2006 Retrospective analysis of transient elevations in alanine aminotransferase during long-term treatment with acetaminophen in osteoarthritis clinical trials. Acetaminophen 107-120 glutamic--pyruvic transaminase Homo sapiens 50-74 17076974-1 2006 BACKGROUND: In two recent osteoarthritis trials, alanine aminotransferase (ALT) elevations were observed more frequently in patients receiving acetaminophen 3.9 g daily than in patients receiving placebo, and the rates were higher than aminotransferase values observed in some previous osteoarthritis studies with acetaminophen. Acetaminophen 143-156 glutamic--pyruvic transaminase Homo sapiens 49-73 17076974-1 2006 BACKGROUND: In two recent osteoarthritis trials, alanine aminotransferase (ALT) elevations were observed more frequently in patients receiving acetaminophen 3.9 g daily than in patients receiving placebo, and the rates were higher than aminotransferase values observed in some previous osteoarthritis studies with acetaminophen. Acetaminophen 314-327 glutamic--pyruvic transaminase Homo sapiens 49-73 17218763-14 2006 A cyclooxygenase enzyme induced in cultured cells by some non-steroid anti-inflammatory drugs is also more sensitive to inhibition by paracetamol than cyclooxygenase-2 induced by bacterial lipopolysaccharide. Acetaminophen 134-145 prostaglandin-endoperoxide synthase 2 Homo sapiens 151-167 16941609-3 2006 However, extract-pretreated rats attenuated in a dose-dependent manner, CCl(4) and acetaminophen-induced increases in the activities of ALT, AST, ALP, LDH and SDH in the blood serum. Acetaminophen 83-96 PDZ and LIM domain 3 Rattus norvegicus 146-149 16941609-3 2006 However, extract-pretreated rats attenuated in a dose-dependent manner, CCl(4) and acetaminophen-induced increases in the activities of ALT, AST, ALP, LDH and SDH in the blood serum. Acetaminophen 83-96 serine dehydratase Rattus norvegicus 159-162 16896059-0 2006 Nuclear translocation of endonuclease G and apoptosis-inducing factor during acetaminophen-induced liver cell injury. Acetaminophen 77-90 endonuclease G Mus musculus 25-39 16896059-0 2006 Nuclear translocation of endonuclease G and apoptosis-inducing factor during acetaminophen-induced liver cell injury. Acetaminophen 77-90 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 44-69 16896059-6 2006 Using immunofluorescence microscopy, it was shown that in primary cultured mouse hepatocytes, endonuclease G and AIF translocated to the nucleus between 3 and 6 h after exposure to 5 mM AAP. Acetaminophen 186-189 endonuclease G Mus musculus 94-108 16896059-6 2006 Using immunofluorescence microscopy, it was shown that in primary cultured mouse hepatocytes, endonuclease G and AIF translocated to the nucleus between 3 and 6 h after exposure to 5 mM AAP. Acetaminophen 186-189 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 113-116 16896059-10 2006 The data support the conclusion that endonuclease G and AIF translocate to the nucleus in response to AAP-induced mitochondrial dysfunction and may be responsible, at least in part, for the initial DNA fragmentation during AAP hepatotoxicity. Acetaminophen 102-105 endonuclease G Mus musculus 37-51 16896059-10 2006 The data support the conclusion that endonuclease G and AIF translocate to the nucleus in response to AAP-induced mitochondrial dysfunction and may be responsible, at least in part, for the initial DNA fragmentation during AAP hepatotoxicity. Acetaminophen 102-105 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 56-59 16991207-2 2006 Effects of four nonsteroidal anti-inflammatory drugs including aspirin, paracetamol, sodium salicylate and phenacetin on prolidase (PLD) activity in erythrocytes were investigated. Acetaminophen 72-83 peptidase D Homo sapiens 132-135 16991207-5 2006 Kinetic study of paracetamol on PLD showed that the value of Michaelis constant K(m) for PLD was 1.23 mM. Acetaminophen 17-28 peptidase D Homo sapiens 32-35 16991207-5 2006 Kinetic study of paracetamol on PLD showed that the value of Michaelis constant K(m) for PLD was 1.23 mM. Acetaminophen 17-28 peptidase D Homo sapiens 89-92 16991207-6 2006 The mechanism of PLD inhibition by paracetamol is noncompetitive inhibition, and the inhibitor constant K(i) value obtained in our research was 9.73 x 10(3) microg/L. Acetaminophen 35-46 peptidase D Homo sapiens 17-20 16948781-9 2006 These results indicate that exogenously administered melatonin exhibits a potent hepatoprotective effect against APAP-induced hepatic damage probably downstream of the activity of cytochrome P450 2E1, which works upstream of GSH conjugation in the pathway of APAP metabolism, via its anti-nitrosative and anti-inflammatory activities in addition to its antioxidant activity. Acetaminophen 113-117 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 180-199 16948781-9 2006 These results indicate that exogenously administered melatonin exhibits a potent hepatoprotective effect against APAP-induced hepatic damage probably downstream of the activity of cytochrome P450 2E1, which works upstream of GSH conjugation in the pathway of APAP metabolism, via its anti-nitrosative and anti-inflammatory activities in addition to its antioxidant activity. Acetaminophen 259-263 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 180-199 16930294-0 2006 Involvement of the multidrug resistance P-glycoprotein in acetaminophen-induced toxicity in hepatoma-derived HepG2 and Hep3B cells. Acetaminophen 58-71 ATP binding cassette subfamily B member 1 Homo sapiens 40-54 16930294-2 2006 Although the mechanisms of acetaminophen hepatotoxicity have been well investigated, little is known about the involvement of the P-glycoprotein in acetaminophen transport and toxicity. Acetaminophen 148-161 ATP binding cassette subfamily B member 1 Homo sapiens 130-144 16930294-9 2006 High acetaminophen concentrations increased P-glycoprotein activity and content in both HepG2 and Hep3B cells. Acetaminophen 5-18 ATP binding cassette subfamily B member 1 Homo sapiens 44-58 16930294-10 2006 These observations suggest the involvement of P-glycoprotein in acetaminophen transport. Acetaminophen 64-77 ATP binding cassette subfamily B member 1 Homo sapiens 46-60 16930294-12 2006 We conclude that acetaminophen is a P-glycoprotein substrate and P-glycoprotein is involved in acetaminophen transport and toxicity in HepG2 and Hep3B cells. Acetaminophen 17-30 ATP binding cassette subfamily B member 1 Homo sapiens 36-50 16930294-12 2006 We conclude that acetaminophen is a P-glycoprotein substrate and P-glycoprotein is involved in acetaminophen transport and toxicity in HepG2 and Hep3B cells. Acetaminophen 95-108 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 16930294-13 2006 This study establishes the fact that acetaminophen can modulate P-glycoprotein in tumour cells, suggesting that its routine use in cancer patients in combination with anticancer drugs, may influence the result of chemotherapy. Acetaminophen 37-50 ATP binding cassette subfamily B member 1 Homo sapiens 64-78 16828057-7 2006 CAR translocation into the nucleus of PRIP null livers resulted in the induction of CAR target genes such as CYP2B10, necessary for the conversion of acetaminophen to its hepatotoxic intermediate metabolite, N-acetyl-p-benzoquinone imine. Acetaminophen 150-163 nuclear receptor subfamily 1, group I, member 3 Mus musculus 0-3 16828057-7 2006 CAR translocation into the nucleus of PRIP null livers resulted in the induction of CAR target genes such as CYP2B10, necessary for the conversion of acetaminophen to its hepatotoxic intermediate metabolite, N-acetyl-p-benzoquinone imine. Acetaminophen 150-163 nuclear receptor coactivator 6 Mus musculus 38-42 16828057-7 2006 CAR translocation into the nucleus of PRIP null livers resulted in the induction of CAR target genes such as CYP2B10, necessary for the conversion of acetaminophen to its hepatotoxic intermediate metabolite, N-acetyl-p-benzoquinone imine. Acetaminophen 150-163 nuclear receptor subfamily 1, group I, member 3 Mus musculus 84-87 16828057-7 2006 CAR translocation into the nucleus of PRIP null livers resulted in the induction of CAR target genes such as CYP2B10, necessary for the conversion of acetaminophen to its hepatotoxic intermediate metabolite, N-acetyl-p-benzoquinone imine. Acetaminophen 150-163 cytochrome P450, family 2, subfamily b, polypeptide 10 Mus musculus 109-116 16822497-8 2006 Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. Acetaminophen 85-98 glutamic pyruvic transaminase, soluble Mus musculus 17-20 16822497-8 2006 Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. Acetaminophen 85-98 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 22-25 16822497-8 2006 Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. Acetaminophen 85-98 tumor necrosis factor Mus musculus 53-62 16698862-16 2006 In combination they cause a mild degree of COX-1 inhibition corresponding to that of acetaminophen alone. Acetaminophen 85-98 mitochondrially encoded cytochrome c oxidase I Homo sapiens 43-48 16679384-6 2006 Human myeloperoxidase catalyzed this reaction in the presence of H2O2, and activation of the reaction was observed when incubations were conducted in the presence of acetaminophen at concentrations relevant to those measured in humans. Acetaminophen 166-179 myeloperoxidase Homo sapiens 6-21 16911100-2 2006 The objective of this study was to evaluate if the combination of paracetamol and rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, improves analgesic effects following third molar surgery compared with rofecoxib alone. Acetaminophen 66-77 prostaglandin-endoperoxide synthase 2 Homo sapiens 105-121 16911100-2 2006 The objective of this study was to evaluate if the combination of paracetamol and rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, improves analgesic effects following third molar surgery compared with rofecoxib alone. Acetaminophen 66-77 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-128 16687475-3 2006 Serum alanine aminotransferase/aspartate aminotransferase levels and histopathology revealed the greatest liver damage at 24 and 48 h after high-dose acetaminophen corresponding to the time of greatest serum protein alterations. Acetaminophen 150-163 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 31-57 16679073-6 2006 Acetaminophen hepatotoxicity is less common in neonates than in older children and adults, possibly due to reduced oxidative enzyme activity (e.g. CYP 2E1). Acetaminophen 0-13 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 147-154 16797510-4 2006 CYP 2E1 activities detected by 4-nitrocatechol (4-NC) formation were higher in gel entrapped hepatocytes than in hepatocyte monolayers while the addition of CYP 2E1 inhibitor, diethyl-dithiocarbamate (DDC), more significantly reduced acetaminophen-induced toxicity in gel entrapped hepatocytes. Acetaminophen 234-247 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 0-7 16820551-1 2006 CONTEXT: During a clinical trial of a novel hydrocodone/acetaminophen combination, a high incidence of serum alanine aminotransferase (ALT) elevations was observed. Acetaminophen 56-69 glutamic--pyruvic transaminase Homo sapiens 109-133 16636360-2 2006 The authors further evaluated the effects of APAP poisoning and HBO2 on the expression and function of hypoxia-inducible factor 1-alpha (HIF-1alpha) in an effort to further describe the mechanisms of APAP-induced hepatotoxicity. Acetaminophen 45-49 hypoxia inducible factor 1, alpha subunit Mus musculus 103-135 16636360-2 2006 The authors further evaluated the effects of APAP poisoning and HBO2 on the expression and function of hypoxia-inducible factor 1-alpha (HIF-1alpha) in an effort to further describe the mechanisms of APAP-induced hepatotoxicity. Acetaminophen 45-49 hypoxia inducible factor 1, alpha subunit Mus musculus 137-147 16565415-7 2006 Treatment of mice with APAP and SU5416 (25 mg/kg ip at 3 h) resulted in decreased expression of PCNA, a marker of cellular proliferation. Acetaminophen 23-27 proliferating cell nuclear antigen Mus musculus 96-100 16565415-8 2006 Expression of platelet endothelial cell adhesion molecule, a measure of small vessel density, and endothelial nitric oxide synthase (NOS), a downstream target of VEGFR2, were increased at 48 and 72 h following toxic doses of APAP, and treatment with SU5416 decreased their expression. Acetaminophen 225-229 nitric oxide synthase 3, endothelial cell Mus musculus 98-131 16565415-8 2006 Expression of platelet endothelial cell adhesion molecule, a measure of small vessel density, and endothelial nitric oxide synthase (NOS), a downstream target of VEGFR2, were increased at 48 and 72 h following toxic doses of APAP, and treatment with SU5416 decreased their expression. Acetaminophen 225-229 kinase insert domain protein receptor Mus musculus 162-168 16565415-9 2006 These data indicate that endogenous VEGF is critically important to the process of hepatocyte regeneration in APAP-induced hepatotoxicity in the mouse. Acetaminophen 110-114 vascular endothelial growth factor A Mus musculus 36-40 16831600-0 2006 c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity. Acetaminophen 53-66 jun proto-oncogene Mus musculus 0-5 16831600-5 2006 RESULTS: Sustained activation of JNK was observed in cultured mouse hepatocytes and in vivo in the liver after APAP treatment. Acetaminophen 111-115 mitogen-activated protein kinase 8 Mus musculus 33-36 16611625-7 2006 Lower basal Cyp1a2 mRNA levels and lower expression of Cyp1a2 and Cyp3a11 mRNAs after APAP dosing were also observed in females compared with males. Acetaminophen 86-90 cytochrome P450, family 1, subfamily a, polypeptide 2 Mus musculus 55-61 16611625-7 2006 Lower basal Cyp1a2 mRNA levels and lower expression of Cyp1a2 and Cyp3a11 mRNAs after APAP dosing were also observed in females compared with males. Acetaminophen 86-90 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 66-73 16804966-11 2006 The rats intoxicated with acetaminophen also significantly triggered serum TNF-alpha when compared with the control rats. Acetaminophen 26-39 tumor necrosis factor Rattus norvegicus 75-84 16439473-0 2006 Involvement of Toll-like receptor 4 in acetaminophen hepatotoxicity. Acetaminophen 39-52 toll-like receptor 4 Mus musculus 15-35 16439473-1 2006 The objective of this study was to determine whether Toll-like receptor 4 (TLR4) has a role in alcohol-mediated acetaminophen (APAP) hepatotoxicity. Acetaminophen 112-125 toll-like receptor 4 Mus musculus 53-73 16439473-1 2006 The objective of this study was to determine whether Toll-like receptor 4 (TLR4) has a role in alcohol-mediated acetaminophen (APAP) hepatotoxicity. Acetaminophen 112-125 toll-like receptor 4 Mus musculus 75-79 16439473-1 2006 The objective of this study was to determine whether Toll-like receptor 4 (TLR4) has a role in alcohol-mediated acetaminophen (APAP) hepatotoxicity. Acetaminophen 127-131 toll-like receptor 4 Mus musculus 53-73 16439473-1 2006 The objective of this study was to determine whether Toll-like receptor 4 (TLR4) has a role in alcohol-mediated acetaminophen (APAP) hepatotoxicity. Acetaminophen 127-131 toll-like receptor 4 Mus musculus 75-79 16439473-7 2006 In alcohol-pretreated endotoxin-responsive C3H/HeN mice, subsequent exposure to APAP resulted in further increases in liver damage, including severe steatosis, associated with elevated plasma levels of TNF-alpha. Acetaminophen 80-84 tumor necrosis factor Mus musculus 202-211 16554369-10 2006 Taken together, these results indicate that up-regulation of Mrp3 led to an exacerbated basolateral versus canalicular excretion of conjugated APAP in IPL. Acetaminophen 143-147 ATP binding cassette subfamily C member 3 Rattus norvegicus 61-65 16729303-0 2006 Disruption of NaS1 sulfate transport function in mice leads to enhanced acetaminophen-induced hepatotoxicity. Acetaminophen 72-85 solute carrier family 13 (sodium/sulfate symporters), member 1 Mus musculus 14-18 16729303-4 2006 APAP treatment led to increased liver damage and decreased hepatic glutathione levels in the hyposulfatemic Nas1-null mice compared with that in normosulfatemic wild-type mice. Acetaminophen 0-4 solute carrier family 13 (sodium/sulfate symporters), member 1 Mus musculus 108-112 16729303-5 2006 Analysis of urinary APAP metabolites revealed a significantly lower ratio of APAP-sulfate to APAP-glucuronide in the Nas1-null mice. Acetaminophen 20-24 solute carrier family 13 (sodium/sulfate symporters), member 1 Mus musculus 117-121 16729303-7 2006 In conclusion, the results of this study highlight the importance of plasma sulfate level as a key modulator of acetaminophen metabolism and suggest that individuals with reduced NaS1 sulfate transporter function would be more sensitive to hepatotoxic agents. Acetaminophen 112-125 solute carrier family 13 (sodium/sulfate symporters), member 1 Mus musculus 179-183 16729305-1 2006 We previously reported that liver natural killer (NK) and NKT cells play a critical role in mouse model of acetaminophen (APAP)-induced liver injury by producing interferon gamma (IFN-gamma) and modulating chemokine production and subsequent recruitment of neutrophils into the liver. Acetaminophen 107-120 interferon gamma Mus musculus 162-189 16729305-1 2006 We previously reported that liver natural killer (NK) and NKT cells play a critical role in mouse model of acetaminophen (APAP)-induced liver injury by producing interferon gamma (IFN-gamma) and modulating chemokine production and subsequent recruitment of neutrophils into the liver. Acetaminophen 122-126 interferon gamma Mus musculus 162-189 16729305-3 2006 C57BL/6 mice were given an intraperitoneal toxic dose of APAP (500 mg/kg), which caused severe acute liver injury characterized by significant elevation of serum ALT, centrilobular hepatic necrosis, and increased hepatic inflammatory cell accumulation. Acetaminophen 57-61 glutamic pyruvic transaminase, soluble Mus musculus 162-165 16517757-2 2006 SULT1A1 catalyzes the sulfation of small planar phenols such as neurotransmitters, steroid hormones, acetaminophen, and p-nitrophenol (PNP). Acetaminophen 101-114 sulfotransferase family 1A member 1 Homo sapiens 0-7 16449370-11 2006 Correlated with the pain relief, acetaminophen significantly reduced plasma BEND levels, whereas rofecoxib did not do so. Acetaminophen 33-46 proopiomelanocortin Homo sapiens 76-80 16449370-15 2006 CONCLUSIONS: There is a correlation between reduction in circulating BEND and OA pain relief in patients treated with acetaminophen. Acetaminophen 118-131 proopiomelanocortin Homo sapiens 69-73 16674937-0 2006 The involvement of a cyclooxygenase 1 gene-derived protein in the antinociceptive action of paracetamol in mice. Acetaminophen 92-103 prostaglandin-endoperoxide synthase 1 Mus musculus 21-37 16674937-11 2006 The effects of paracetamol on writhing responses and on brain PGE(2) levels were reduced in COX-1, but not COX-2, knockout mice. Acetaminophen 15-26 cytochrome c oxidase I, mitochondrial Mus musculus 92-97 16674937-13 2006 These results suggest that the antinociceptive action of paracetamol may be mediated by inhibition of COX-3. Acetaminophen 57-68 cytochrome c oxidase III, mitochondrial Mus musculus 102-107 16551773-14 2006 CONCLUSIONS: Deficiency of either iNOS or eNOS results in decreased NO production and is associated with reduced hepatocellular injury following APAP poisoning. Acetaminophen 145-149 nitric oxide synthase 2, inducible Mus musculus 34-38 16696573-2 2006 The importance of uridine 5"-diphosphate-glucuronosyltranferases (UGT) 2B15 and other UGT enzymes (1A1, 1A6, and 1A9) in glucuronidating acetaminophen (APAP) is demonstrated. Acetaminophen 137-150 UDP glucuronosyltransferase family 2 member B15 Homo sapiens 18-75 16696573-2 2006 The importance of uridine 5"-diphosphate-glucuronosyltranferases (UGT) 2B15 and other UGT enzymes (1A1, 1A6, and 1A9) in glucuronidating acetaminophen (APAP) is demonstrated. Acetaminophen 137-150 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 66-69 16696573-2 2006 The importance of uridine 5"-diphosphate-glucuronosyltranferases (UGT) 2B15 and other UGT enzymes (1A1, 1A6, and 1A9) in glucuronidating acetaminophen (APAP) is demonstrated. Acetaminophen 152-156 UDP glucuronosyltransferase family 2 member B15 Homo sapiens 18-75 16696573-2 2006 The importance of uridine 5"-diphosphate-glucuronosyltranferases (UGT) 2B15 and other UGT enzymes (1A1, 1A6, and 1A9) in glucuronidating acetaminophen (APAP) is demonstrated. Acetaminophen 152-156 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 66-69 16696573-5 2006 At 10 mM APAP, UGT 1A9 is a significant enzyme responsible for metabolizing APAP in either one of the buffers. Acetaminophen 9-13 UDP glucuronosyltransferase family 1 member A9 Homo sapiens 15-22 16696573-5 2006 At 10 mM APAP, UGT 1A9 is a significant enzyme responsible for metabolizing APAP in either one of the buffers. Acetaminophen 76-80 UDP glucuronosyltransferase family 1 member A9 Homo sapiens 15-22 16696573-7 2006 The contribution of UGT 1A6 at 10 mM APAP concentration became obscured by similar relative activities exhibited by UGTs 1A7, 1A8, and 2B7. Acetaminophen 37-41 UDP glucuronosyltransferase family 1 member A6 Homo sapiens 20-27 16636302-0 2006 Double null of selenium-glutathione peroxidase-1 and copper, zinc-superoxide dismutase enhances resistance of mouse primary hepatocytes to acetaminophen toxicity. Acetaminophen 139-152 glutathione peroxidase 1 Mus musculus 24-48 16636302-3 2006 Compared with the WT cells, the GPX1-/- and DKO hepatocytes were more resistant (P < 0.05) to the APAP-induced cell death but less resistant to the NAPQI-induced cell death. Acetaminophen 101-105 glutathione peroxidase 1 Mus musculus 32-36 16636302-4 2006 The APAP-mediated glutathione (GSH) depletion was greater (P < 0.05) at 6 hrs in the WT cells than in the GPX1-/- and DKO cells, whereas there was no genotype effect on the NAPQI-mediated GSH depletion. Acetaminophen 4-8 glutathione peroxidase 1 Mus musculus 109-113 16801900-9 2006 Patients who received 7.5 g of acetaminophen or more had a lower prothrombin index 52.4 +/- 30.3% vs 74.2 +/- 17.2% (P=0.039), and a lower factor V 54.7 +/- 33.2% vs 83.3 +/- 19.6% (P=0.033). Acetaminophen 31-44 coagulation factor II, thrombin Homo sapiens 65-76 16801900-10 2006 Prothrombin index and bilirubinemia were negatively correlated with time related plasma acetaminophen concentrations. Acetaminophen 88-101 coagulation factor II, thrombin Homo sapiens 0-11 16530163-0 2006 Induction of the nuclear factor HIF-1alpha in acetaminophen toxicity: evidence for oxidative stress. Acetaminophen 46-59 hypoxia inducible factor 1, alpha subunit Mus musculus 32-42 16530163-3 2006 The induction of HIF-1alpha was examined in the livers of mice treated with a toxic dose of APAP (300 mg/kg i.p.) Acetaminophen 92-96 hypoxia inducible factor 1, alpha subunit Mus musculus 17-27 16530163-10 2006 Thus, HIF-1alpha is induced before APAP toxicity and can occur under non-hypoxic conditions. Acetaminophen 35-39 hypoxia inducible factor 1, alpha subunit Mus musculus 6-16 16530163-11 2006 The data suggest a role for oxidative stress in the induction of HIF-1alpha in APAP toxicity. Acetaminophen 79-83 hypoxia inducible factor 1, alpha subunit Mus musculus 65-75 16618120-6 2006 Beta-catenin phosphorylation/degradation and its regulation by Wnt can occur normally in the absence of Thr41 as long as the Ser-X-X-X-Ser motif/spacing is preserved. Acetaminophen 129-130 catenin beta 1 Homo sapiens 0-12 16434548-1 2006 CYP2E1, the primary ethanol-metabolizing cytochrome P450, metabolizes endogenous substrates (e.g., arachidonic acid) and drugs (e.g., acetaminophen, chlorzoxazone) and bioactivates procarcinogens (e.g., tobacco-specific nitrosamines) and toxins (e.g., carbon tetrachloride). Acetaminophen 134-147 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 0-6 16532517-0 2006 Selenium-binding protein 2, the major hepatic target for acetaminophen, shows sex differences in protein abundance. Acetaminophen 57-70 selenium binding protein 2 Mus musculus 0-26 16532517-6 2006 Since SBP2 has been described as the major target for acetaminophen in mouse liver cytosol, these findings are discussed with respect to their possible relevance for sex differences in acetaminophen-mediated toxicity, which have been described in a variety of mammals including mice and rats. Acetaminophen 54-67 selenium binding protein 2 Mus musculus 6-10 16532517-6 2006 Since SBP2 has been described as the major target for acetaminophen in mouse liver cytosol, these findings are discussed with respect to their possible relevance for sex differences in acetaminophen-mediated toxicity, which have been described in a variety of mammals including mice and rats. Acetaminophen 185-198 selenium binding protein 2 Mus musculus 6-10 16677153-2 2006 It is hypothesized that activation of the receptor for advanced glycation end products (RAGE) might contribute to acetaminophen-induced liver toxicity by virtue of its ability to generate reactive oxygen species, at least in part via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and thereby activate downstream signaling pathways leading to cellular injury. Acetaminophen 114-127 advanced glycosylation end product-specific receptor Mus musculus 88-92 16677153-6 2006 Consistent with an important role for RAGE-triggered oxidant stress in acetaminophen-induced injury, a significant reduction of nitrotyrosine protein adducts was observed in hepatic tissue in sRAGE-treated versus vehicle-treated mice receiving acetaminophen, in parallel with significantly increased levels of glutathione. Acetaminophen 71-84 advanced glycosylation end product-specific receptor Mus musculus 38-42 16677153-6 2006 Consistent with an important role for RAGE-triggered oxidant stress in acetaminophen-induced injury, a significant reduction of nitrotyrosine protein adducts was observed in hepatic tissue in sRAGE-treated versus vehicle-treated mice receiving acetaminophen, in parallel with significantly increased levels of glutathione. Acetaminophen 244-257 advanced glycosylation end product-specific receptor Mus musculus 38-42 16677153-8 2006 CONCLUSION: These findings implicate RAGE-dependent mechanisms in acetaminophen-induced liver damage and suggest that blockade of this pathway may impart beneficial effects in toxin-induced liver injury. Acetaminophen 66-79 advanced glycosylation end product-specific receptor Mus musculus 37-41 16530785-0 2006 Acetaminophen attenuates peroxynitrite-activated matrix metalloproteinase-2-mediated troponin I cleavage in the isolated guinea pig myocardium. Acetaminophen 0-13 72 kDa type IV collagenase Cavia porcellus 49-75 16530785-2 2006 We hypothesized that acetaminophen, an effective antioxidant against peroxynitrite, would attenuate activation of MMP-2 and improve cardiac mechanical function. Acetaminophen 21-34 72 kDa type IV collagenase Cavia porcellus 114-119 16530785-8 2006 Western blotting and gel zymography revealed higher 72 kDa (pro-MMP-2) proteolytic activity in heart homogenates of vehicle-treated versus acetaminophen-treated hearts. Acetaminophen 139-152 72 kDa type IV collagenase Cavia porcellus 64-69 16530785-10 2006 We conclude that acetaminophen is cardioprotective, at least in part, by attenuating peroxynitrite-activated, MMP-2-mediated cleavage of TnI. Acetaminophen 17-30 72 kDa type IV collagenase Cavia porcellus 110-115 16330492-0 2006 Ubiquitin-dependent degradation of p53 protein despite phosphorylation at its N terminus by acetaminophen. Acetaminophen 92-105 tumor protein p53 Sus scrofa 35-38 16610002-1 2006 AIM: To investigate the expression and activity of NAD(P)H quinone oxidoreductase 1 (NQO1) in human liver specimens obtained from patients with liver damage due to acetaminophen (APAP) overdose or primary biliary cirrhosis (PBC). Acetaminophen 164-177 NAD(P)H quinone dehydrogenase 1 Homo sapiens 51-83 16610002-1 2006 AIM: To investigate the expression and activity of NAD(P)H quinone oxidoreductase 1 (NQO1) in human liver specimens obtained from patients with liver damage due to acetaminophen (APAP) overdose or primary biliary cirrhosis (PBC). Acetaminophen 164-177 NAD(P)H quinone dehydrogenase 1 Homo sapiens 85-89 16610002-1 2006 AIM: To investigate the expression and activity of NAD(P)H quinone oxidoreductase 1 (NQO1) in human liver specimens obtained from patients with liver damage due to acetaminophen (APAP) overdose or primary biliary cirrhosis (PBC). Acetaminophen 179-183 NAD(P)H quinone dehydrogenase 1 Homo sapiens 51-83 16610002-1 2006 AIM: To investigate the expression and activity of NAD(P)H quinone oxidoreductase 1 (NQO1) in human liver specimens obtained from patients with liver damage due to acetaminophen (APAP) overdose or primary biliary cirrhosis (PBC). Acetaminophen 179-183 NAD(P)H quinone dehydrogenase 1 Homo sapiens 85-89 16610002-5 2006 In both APAP and PBC livers, there was strong induction of NQO1 protein levels on Western blot. Acetaminophen 8-12 NAD(P)H quinone dehydrogenase 1 Homo sapiens 59-63 16610002-8 2006 CONCLUSION: These data demonstrate that NQO1 protein and activity are markedly induced in human livers during both APAP overdose and PBC. Acetaminophen 115-119 NAD(P)H quinone dehydrogenase 1 Homo sapiens 40-44 16181716-3 2006 Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Acetaminophen 0-13 glutamic pyruvic transaminase, soluble Mus musculus 108-132 16181716-3 2006 Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Acetaminophen 0-13 glutamic pyruvic transaminase, soluble Mus musculus 134-137 16181716-3 2006 Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Acetaminophen 0-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 143-169 16181716-3 2006 Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Acetaminophen 0-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 171-174 16181716-3 2006 Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Acetaminophen 0-13 glutamic pyruvic transaminase, soluble Mus musculus 304-307 16181716-3 2006 Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Acetaminophen 0-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 312-315 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 C-reactive protein, pentraxin-related Mus musculus 17-35 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 C-reactive protein, pentraxin-related Mus musculus 37-40 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 Von Willebrand factor Mus musculus 43-64 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 Von Willebrand factor Mus musculus 66-69 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 interleukin 6 Mus musculus 72-76 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 interleukin 10 Mus musculus 78-83 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 tumor necrosis factor Mus musculus 88-97 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 C-reactive protein, pentraxin-related Mus musculus 251-254 16181716-4 2006 Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen 130-143 Von Willebrand factor Mus musculus 256-259 16181716-5 2006 Acetaminophen treatment also significantly increased plasminogen activator inhibitor-1 (PAI-1) activity and plasma fibrinogen level, and decreased antithrombin III (AT-III) and protein C activities (P < 0.05). Acetaminophen 0-13 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 53-86 16181716-5 2006 Acetaminophen treatment also significantly increased plasminogen activator inhibitor-1 (PAI-1) activity and plasma fibrinogen level, and decreased antithrombin III (AT-III) and protein C activities (P < 0.05). Acetaminophen 0-13 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 88-93 16181716-5 2006 Acetaminophen treatment also significantly increased plasminogen activator inhibitor-1 (PAI-1) activity and plasma fibrinogen level, and decreased antithrombin III (AT-III) and protein C activities (P < 0.05). Acetaminophen 0-13 serine (or cysteine) peptidase inhibitor, clade C (antithrombin), member 1 Mus musculus 147-163 16181716-5 2006 Acetaminophen treatment also significantly increased plasminogen activator inhibitor-1 (PAI-1) activity and plasma fibrinogen level, and decreased antithrombin III (AT-III) and protein C activities (P < 0.05). Acetaminophen 0-13 serine (or cysteine) peptidase inhibitor, clade C (antithrombin), member 1 Mus musculus 165-171 16081117-0 2006 Distinct roles of NF-kappaB p50 in the regulation of acetaminophen-induced inflammatory mediator production and hepatotoxicity. Acetaminophen 53-66 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 18-31 16081117-8 2006 Pretreatment of mice with the antioxidant, N-acetylcysteine (NAC) prevented APAP-induced depletion of glutathione and CuZnSOD, as well as hepatotoxicity. Acetaminophen 76-80 superoxide dismutase 1, soluble Mus musculus 118-125 16081117-9 2006 NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta). Acetaminophen 19-23 tumor necrosis factor Mus musculus 45-53 16081117-9 2006 NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta). Acetaminophen 19-23 chemokine (C-X-C motif) ligand 1 Mus musculus 55-61 16081117-9 2006 NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta). Acetaminophen 19-23 interleukin 10 Mus musculus 67-72 16081117-9 2006 NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta). Acetaminophen 19-23 transforming growth factor, beta 1 Mus musculus 192-199 16438952-0 2006 The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors. Acetaminophen 26-37 cannabinoid receptor 1 Rattus norvegicus 82-85 16438952-2 2006 Here we show that in rats, using the hot plate test, the analgesic effect of paracetamol is prevented by two antagonists at cannabinoid CB1 receptors (AM281 and SR141716A) at doses that prevent the analgesic activity of the cannabinoid CB1 agonist HU210. Acetaminophen 77-88 cannabinoid receptor 1 Rattus norvegicus 136-139 16438952-2 2006 Here we show that in rats, using the hot plate test, the analgesic effect of paracetamol is prevented by two antagonists at cannabinoid CB1 receptors (AM281 and SR141716A) at doses that prevent the analgesic activity of the cannabinoid CB1 agonist HU210. Acetaminophen 77-88 cannabinoid receptor 1 Rattus norvegicus 236-239 16377054-7 2006 Furthermore, GGA inhibited increases in hepatic lipid peroxide content and hepatic myeloperoxidase activity after APAP administration. Acetaminophen 114-118 myeloperoxidase Mus musculus 83-98 16172162-8 2006 Both paracetamol- and NO-paracetamol-treated groups showed increased activities of catalase and SOD compared with the vehicle group. Acetaminophen 5-16 catalase Rattus norvegicus 83-91 16172162-8 2006 Both paracetamol- and NO-paracetamol-treated groups showed increased activities of catalase and SOD compared with the vehicle group. Acetaminophen 25-36 catalase Rattus norvegicus 83-91 16188911-8 2006 Acetaminophen concentrations, an indirect measurement of gastric emptying rate, were inversely correlated with total ghrelin concentrations (saline r = -0.76; 95% CI = -0.90, -0.49, GLP-1 r = -0.47; 95% CI = -0.76, -0.04). Acetaminophen 0-13 glucagon like peptide 1 receptor Homo sapiens 182-189 16485898-8 2006 There were also protoxicant genes, such as osteopontin (OPN), with elevated mRNA expression levels in the B6 mice as compared to the SJL mice and with intermediate levels in the F1 mice, suggesting that they may play a role in exacerbating liver injury after APAP treatment. Acetaminophen 259-263 secreted phosphoprotein 1 Mus musculus 43-54 16485898-8 2006 There were also protoxicant genes, such as osteopontin (OPN), with elevated mRNA expression levels in the B6 mice as compared to the SJL mice and with intermediate levels in the F1 mice, suggesting that they may play a role in exacerbating liver injury after APAP treatment. Acetaminophen 259-263 secreted phosphoprotein 1 Mus musculus 56-59 16440339-0 2006 Deoxyribonuclease 1 aggravates acetaminophen-induced liver necrosis in male CD-1 mice. Acetaminophen 31-44 deoxyribonuclease I Mus musculus 0-19 16440339-0 2006 Deoxyribonuclease 1 aggravates acetaminophen-induced liver necrosis in male CD-1 mice. Acetaminophen 31-44 CD1 antigen complex Mus musculus 76-80 16440339-3 2006 In this study, we analyzed the participation of the hepatic endonuclease deoxyribonuclease 1 (DNASE1) during APAP-induced hepatotoxicity by employing a Dnase1 knockout (KO) mouse model. Acetaminophen 109-113 deoxyribonuclease I Mus musculus 73-92 16440339-3 2006 In this study, we analyzed the participation of the hepatic endonuclease deoxyribonuclease 1 (DNASE1) during APAP-induced hepatotoxicity by employing a Dnase1 knockout (KO) mouse model. Acetaminophen 109-113 deoxyribonuclease I Mus musculus 94-100 16420515-0 2006 Effect of platelet-activating factor (PAF) receptor antagonist (BN52021) on acetaminophen-induced acute liver injury and regeneration in rats. Acetaminophen 76-89 platelet-activating factor receptor Rattus norvegicus 10-51 16420515-2 2006 In the present study, the possible influence of PAF-R antagonist (BN52021) on the protection of liver injury after 4-hydroxyacetanilide, N-acetyl-p-aminophenol, paracetamol (APAP) intoxication was investigated. Acetaminophen 115-135 platelet-activating factor receptor Rattus norvegicus 48-53 16420515-2 2006 In the present study, the possible influence of PAF-R antagonist (BN52021) on the protection of liver injury after 4-hydroxyacetanilide, N-acetyl-p-aminophenol, paracetamol (APAP) intoxication was investigated. Acetaminophen 137-159 platelet-activating factor receptor Rattus norvegicus 48-53 16420515-2 2006 In the present study, the possible influence of PAF-R antagonist (BN52021) on the protection of liver injury after 4-hydroxyacetanilide, N-acetyl-p-aminophenol, paracetamol (APAP) intoxication was investigated. Acetaminophen 161-172 platelet-activating factor receptor Rattus norvegicus 48-53 16278372-8 2006 Gstz1(-/-) mice given acetaminophen demonstrated increased hepatotoxicity compared with wild-type mice. Acetaminophen 22-35 glutathione transferase zeta 1 (maleylacetoacetate isomerase) Mus musculus 0-5 16177239-4 2006 The present study further characterizes the expression of multidrug resistance-associated proteins 1-4 (Mrp1-4), breast cancer resistance protein (Bcrp) and sodium-taurocholate co-transporting polypeptide (Ntcp) in mouse liver following administration of the hepatotoxicants acetaminophen (APAP) and carbon tetrachloride (CCl4). Acetaminophen 275-288 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 206-210 16177239-4 2006 The present study further characterizes the expression of multidrug resistance-associated proteins 1-4 (Mrp1-4), breast cancer resistance protein (Bcrp) and sodium-taurocholate co-transporting polypeptide (Ntcp) in mouse liver following administration of the hepatotoxicants acetaminophen (APAP) and carbon tetrachloride (CCl4). Acetaminophen 290-294 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 206-210 16177239-8 2006 Ntcp levels were preserved in APAP-exposed livers and reduced to 30-50% of control after CCl4. Acetaminophen 30-34 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 0-4 16177239-11 2006 Administration of APAP enhanced expression of Mrp2 (1.6-fold), Mrp3 (3.5-fold), and Mrp4 (16-fold). Acetaminophen 18-22 ATP-binding cassette, sub-family C (CFTR/MRP), member 2 Mus musculus 46-50 16177239-11 2006 Administration of APAP enhanced expression of Mrp2 (1.6-fold), Mrp3 (3.5-fold), and Mrp4 (16-fold). Acetaminophen 18-22 ATP-binding cassette, sub-family C (CFTR/MRP), member 3 Mus musculus 63-67 16177239-11 2006 Administration of APAP enhanced expression of Mrp2 (1.6-fold), Mrp3 (3.5-fold), and Mrp4 (16-fold). Acetaminophen 18-22 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 84-88 16140478-0 2006 Cholestasis induced by model organic anions protects from acetaminophen hepatotoxicity in male CD-1 mice. Acetaminophen 58-71 CD1 antigen complex Mus musculus 95-99 16468397-6 2006 With a hypochlorite dose of 57 micromol/L (4 ppm as Cl2), 88% of the acetaminophen (10 micromol/L initial) was transformed in 1 h. The two quinoidal oxidation products 1,4-benzoquinone and NAPQI accounted for 25% and 1.5% of the initial acetaminophen concentration, respectively, at a 1 h reaction time. Acetaminophen 69-82 endogenous retrovirus group W member 5 Homo sapiens 52-55 16468397-6 2006 With a hypochlorite dose of 57 micromol/L (4 ppm as Cl2), 88% of the acetaminophen (10 micromol/L initial) was transformed in 1 h. The two quinoidal oxidation products 1,4-benzoquinone and NAPQI accounted for 25% and 1.5% of the initial acetaminophen concentration, respectively, at a 1 h reaction time. Acetaminophen 237-250 endogenous retrovirus group W member 5 Homo sapiens 52-55 23045133-5 2006 Acetaminophen formation in incubations of phenacetin with a CYP1A2 source is readily measured by HPLC with UV detection. Acetaminophen 0-13 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 60-66 16393943-4 2006 RESULTS: Treatment with APAP (300 mg/kg, orally) to mice fed a regular chow increased ALT levels (519-fold) and caused hepatic centrilobular injury at 6 h. APAP increased hepatic cytochrome-P (CYP)-2E1 mRNA levels (17-fold). Acetaminophen 24-28 glutamic pyruvic transaminase, soluble Mus musculus 86-89 16393943-4 2006 RESULTS: Treatment with APAP (300 mg/kg, orally) to mice fed a regular chow increased ALT levels (519-fold) and caused hepatic centrilobular injury at 6 h. APAP increased hepatic cytochrome-P (CYP)-2E1 mRNA levels (17-fold). Acetaminophen 24-28 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 179-201 16393943-9 2006 CONCLUSIONS: These results suggest that hepatic steatosis elicited by the "Western-style" diet attenuated APAP-induced hepatotoxicity by inhibiting CYP2E1 induction and by minimizing sinusoidal endothelial cell injury, leading to protection of liver microcirculation. Acetaminophen 106-110 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 148-154 16271353-1 2005 The biliary excretion of acetaminophen (APAP) is reduced in transport deficient (TR-) hyperbilirubinemic rats lacking the multidrug resistance-associated protein 2 (Mrp2). Acetaminophen 25-38 ATP binding cassette subfamily C member 2 Rattus norvegicus 122-163 16271353-1 2005 The biliary excretion of acetaminophen (APAP) is reduced in transport deficient (TR-) hyperbilirubinemic rats lacking the multidrug resistance-associated protein 2 (Mrp2). Acetaminophen 25-38 ATP binding cassette subfamily C member 2 Rattus norvegicus 165-169 16271353-1 2005 The biliary excretion of acetaminophen (APAP) is reduced in transport deficient (TR-) hyperbilirubinemic rats lacking the multidrug resistance-associated protein 2 (Mrp2). Acetaminophen 40-44 ATP binding cassette subfamily C member 2 Rattus norvegicus 122-163 16271353-1 2005 The biliary excretion of acetaminophen (APAP) is reduced in transport deficient (TR-) hyperbilirubinemic rats lacking the multidrug resistance-associated protein 2 (Mrp2). Acetaminophen 40-44 ATP binding cassette subfamily C member 2 Rattus norvegicus 165-169 16385241-0 2005 Interactions of alcohol dehydrogenase to p-hydroxyacetophenone-sepharose and p-acetamidophenol-sepharose. Acetaminophen 77-94 aldo-keto reductase family 1 member A1 Rattus norvegicus 16-37 16385241-2 2005 In this study, we investigated ligand specificities to alcohol dehydrogenase (ADH) using p-HAP-sepharose and p-acetamidophenol (AAP)-sepharose. Acetaminophen 109-126 aldo-keto reductase family 1 member A1 Rattus norvegicus 78-81 16385241-2 2005 In this study, we investigated ligand specificities to alcohol dehydrogenase (ADH) using p-HAP-sepharose and p-acetamidophenol (AAP)-sepharose. Acetaminophen 128-131 aldo-keto reductase family 1 member A1 Rattus norvegicus 55-76 16385241-2 2005 In this study, we investigated ligand specificities to alcohol dehydrogenase (ADH) using p-HAP-sepharose and p-acetamidophenol (AAP)-sepharose. Acetaminophen 128-131 aldo-keto reductase family 1 member A1 Rattus norvegicus 78-81 16141365-0 2005 Role of the nuclear receptor pregnane X receptor in acetaminophen hepatotoxicity. Acetaminophen 52-65 nuclear receptor subfamily 1, group I, member 2 Mus musculus 29-48 16141365-2 2005 Pretreatment of mice and rats with inducers of CYP3A increases acetaminophen (APAP) hepatotoxicity. Acetaminophen 63-76 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 47-52 16141365-2 2005 Pretreatment of mice and rats with inducers of CYP3A increases acetaminophen (APAP) hepatotoxicity. Acetaminophen 78-82 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 47-52 16109740-8 2005 Western analysis and confocal immunofluorescent microscopy indicated a marked increase in hepatic expression of multidrug resistance-associated protein 3 (Mrp3) in both groups pretreated with APAP, relative to expression of Mrp2. Acetaminophen 192-196 ATP binding cassette subfamily C member 3 Rattus norvegicus 112-153 16109740-8 2005 Western analysis and confocal immunofluorescent microscopy indicated a marked increase in hepatic expression of multidrug resistance-associated protein 3 (Mrp3) in both groups pretreated with APAP, relative to expression of Mrp2. Acetaminophen 192-196 ATP binding cassette subfamily C member 3 Rattus norvegicus 155-159 16109740-8 2005 Western analysis and confocal immunofluorescent microscopy indicated a marked increase in hepatic expression of multidrug resistance-associated protein 3 (Mrp3) in both groups pretreated with APAP, relative to expression of Mrp2. Acetaminophen 192-196 ATP binding cassette subfamily C member 2 Rattus norvegicus 224-228 16109740-9 2005 ATP-dependent transport of [3H]taurocholate, an Mrp3 substrate, was significantly increased in basolateral liver plasma membrane vesicles from rats pretreated with repeated doses of APAP relative to controls. Acetaminophen 182-186 ATP binding cassette subfamily C member 3 Rattus norvegicus 48-52 16109740-11 2005 These data indicate that APAP pretreatment induced a shift from biliary to urinary elimination of APAP glucuronide, consistent with the increased expression of Mrp3 in the basolateral domain of the hepatocyte. Acetaminophen 25-29 ATP binding cassette subfamily C member 3 Rattus norvegicus 160-164 16141368-2 2005 It was called COX-3 and was reported to be differentially sensitive to inhibition by various nonsteroidal anti-inflammatory drugs (NSAIDs) as well as acetaminophen (Chandrasekharan et al., 2002). Acetaminophen 150-163 mitochondrially encoded cytochrome c oxidase III Homo sapiens 14-19 16157696-10 2005 In conclusion, the data presented in this study define an RXRalpha-Gst regulatory network that controls APAP-GSH conjugation. Acetaminophen 104-108 hematopoietic prostaglandin D synthase Mus musculus 67-70 16157696-0 2005 Retinoid X receptor alpha Regulates the expression of glutathione s-transferase genes and modulates acetaminophen-glutathione conjugation in mouse liver. Acetaminophen 100-113 retinoid X receptor alpha Mus musculus 0-25 16157696-3 2005 The aim of the current study was to evaluate the role of RXRalpha in phase II enzyme-mediated detoxification of APAP. Acetaminophen 112-116 retinoid X receptor alpha Mus musculus 57-65 16157696-4 2005 Wild-type and hepatocyte-specific RXRalpha knockout mice were treated with a toxic dose of APAP (500 mg/kg i.p.). Acetaminophen 91-95 retinoid X receptor alpha Mus musculus 34-42 16157696-10 2005 In conclusion, the data presented in this study define an RXRalpha-Gst regulatory network that controls APAP-GSH conjugation. Acetaminophen 104-108 retinoid X receptor alpha Mus musculus 58-66 16273243-7 2005 beta-galactosidase expression was measured by X-Gal staining in 7.0% of HMG, 17.0% of HOSM-1 and 11.5% of HOSM-2 cells. Acetaminophen 46-47 galactosidase beta 1 Homo sapiens 0-18 16054166-0 2005 Protection against paracetamol-induced hepatic injury by prazosin pre-treatment in CD-1 mice. Acetaminophen 19-30 CD1 antigen complex Mus musculus 83-87 16054166-4 2005 Prazosin (15 mg/kg) pre-treatment provided protection against APAP-induced hepatic injury as evidenced by a significant decrease in serum transaminase (ALT) levels after 5h (p<0.05). Acetaminophen 62-66 glutamic pyruvic transaminase, soluble Mus musculus 152-155 16250050-0 2005 Altered disposition of acetaminophen in mice with a disruption of the Mrp3 gene. Acetaminophen 23-36 prolactin family 2, subfamily c, member 4 Mus musculus 70-74 16250050-3 2005 Because Mrp3 preferentially transports glucuronide conjugates, we investigated the in vivo disposition of acetaminophen (APAP) and its metabolites. Acetaminophen 106-119 prolactin family 2, subfamily c, member 4 Mus musculus 8-12 16250050-3 2005 Because Mrp3 preferentially transports glucuronide conjugates, we investigated the in vivo disposition of acetaminophen (APAP) and its metabolites. Acetaminophen 121-125 prolactin family 2, subfamily c, member 4 Mus musculus 8-12 16526442-1 2005 A simple, sensitive, and selective method for determination of acetaminophen based on its oxidation using N-bromosuccinimide (NBS) to produce a highly fluorescent product. Acetaminophen 63-76 nibrin Homo sapiens 126-129 16230465-17 2005 Significant overlap with acetaminophen hypersensitivity, especially among very young patients, for whom the use of a cyclooxygenase-2-specific medication may not be feasible, severely limits options for medical antipyretic treatment. Acetaminophen 25-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 117-133 16162910-0 2005 Acetaminophen may act through beta endorphin. Acetaminophen 0-13 proopiomelanocortin Homo sapiens 30-44 16192763-11 2005 CONCLUSIONS: Acetaminophen, which is a weak inhibitor of platelet cyclooxygenase 1, has a dose-dependent antiaggregatory effect. Acetaminophen 13-26 prostaglandin-endoperoxide synthase 1 Homo sapiens 66-82 16168751-4 2005 The rats intoxicated with acetaminophen showed significant elevation in the levels of lipid peroxides with decreased levels of protein, GSH, SOD, CAT and impaired tricarboxylic acid cycle enzyme activities. Acetaminophen 26-39 catalase Rattus norvegicus 146-149 16172181-8 2005 Monocyte chemoattractant protein 1 elevation in acetaminophen overdose may represent an innate, immunomodulary response of the liver to earlier events in the toxicity. Acetaminophen 48-61 C-C motif chemokine ligand 2 Homo sapiens 0-34 15879007-1 2005 Cyclooxygenase (COX)-3, a novel COX splice variant, was suggested as the key to unlocking the mystery of the mechanism of action of acetaminophen. Acetaminophen 132-145 mitochondrially encoded cytochrome c oxidase III Homo sapiens 0-22 15879007-2 2005 Although COX-3 might have COX activity in canines, and this activity might be inhibited by acetaminophen, its low expression level and the kinetics indicate unlikely clinical relevance. Acetaminophen 91-104 cytochrome c oxidase subunit III Canis lupus familiaris 9-14 16184570-6 2005 Those surviving non-acetaminophen (paracetamol)-induced ALF without transplantation had higher Gc-globulin levels than nonsurvivors (102 [5-301] mg/L vs. 61 [5-232] mg/L, P = 0.002), whereas there was no significant difference in levels between the groups in patients with acetaminophen-induced ALF. Acetaminophen 20-33 GC vitamin D binding protein Homo sapiens 95-106 16184570-6 2005 Those surviving non-acetaminophen (paracetamol)-induced ALF without transplantation had higher Gc-globulin levels than nonsurvivors (102 [5-301] mg/L vs. 61 [5-232] mg/L, P = 0.002), whereas there was no significant difference in levels between the groups in patients with acetaminophen-induced ALF. Acetaminophen 35-46 GC vitamin D binding protein Homo sapiens 95-106 16184570-10 2005 In contrast to previous studies, this study demonstrated that Gc-globulin has prognostic value in patients with non-acetaminophen-induced ALF, in the same range as the King"s College criteria. Acetaminophen 116-129 GC vitamin D binding protein Homo sapiens 62-73 15987694-2 2005 Here we show that acetaminophen, following deacetylation to its primary amine, is conjugated with arachidonic acid in the brain and the spinal cord to form the potent TRPV1 agonist N-arachidonoylphenolamine (AM404). Acetaminophen 18-31 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 167-172 15987694-5 2005 This novel metabolite of acetaminophen also acts on the endogenous cannabinoid system, which, together with TRPV1 and COX, is present in the pain and thermoregulatory pathways. Acetaminophen 25-38 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 108-113 16116631-0 2005 HIP/PAP accelerates liver regeneration and protects against acetaminophen injury in mice. Acetaminophen 60-73 regenerating islet-derived 3 beta Mus musculus 4-7 16116631-7 2005 Second, we showed that 80% of the HIP/PAP-transgenic mice versus 25% of the control mice were protected against lethal acetaminophen-induced fulminate hepatitis. Acetaminophen 119-132 regenerating islet-derived 3 beta Mus musculus 38-41 16116631-9 2005 Comparison of Cu/Zn superoxide dismutase activity and glutathione reductase-like effects in control and transgenic liver mice indicated that HIP/PAP exerts an antioxidant activity and prevents reactive oxygen species-induced mitochondrial damage by acetaminophen overdose. Acetaminophen 249-262 regenerating islet-derived 3 beta Mus musculus 145-148 16162422-0 2005 Voglibose potentiates the hepatotoxicity of carbon tetrachloride and acetaminophen by inducing CYP2E1 in rats. Acetaminophen 69-82 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 95-101 16098663-8 2005 On the other hand, pretreatment with acetaminophen, a tentative COX-3 inhibitor, also abolished both intra-articular and intracisternal administration of IL-1beta-induced hyperalgesic responses. Acetaminophen 37-50 cytochrome c oxidase III, mitochondrial Rattus norvegicus 64-69 16098663-8 2005 On the other hand, pretreatment with acetaminophen, a tentative COX-3 inhibitor, also abolished both intra-articular and intracisternal administration of IL-1beta-induced hyperalgesic responses. Acetaminophen 37-50 interleukin 1 beta Rattus norvegicus 154-162 16109766-3 2005 Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity. Acetaminophen 300-313 mediator complex subunit 1 Mus musculus 42-45 16109766-3 2005 Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity. Acetaminophen 300-313 mediator complex subunit 1 Mus musculus 74-77 15995853-0 2005 Platelet-activating factor (PAF) involvement in acetaminophen-induced liver toxicity and regeneration. Acetaminophen 48-61 PCNA clamp associated factor Rattus norvegicus 0-26 15995853-0 2005 Platelet-activating factor (PAF) involvement in acetaminophen-induced liver toxicity and regeneration. Acetaminophen 48-61 PCNA clamp associated factor Rattus norvegicus 28-31 15995853-5 2005 The administration of a toxic dose of acetaminophen (3.5 g/kg) in rats caused acute hepatic injury, as evident by alterations of biochemical (serum enzymes: ALT, AST and ALP) and liver histopathological (degree of inflammation and apoptosis) indices between 20 and 40 h post-treatment. Acetaminophen 38-51 PDZ and LIM domain 3 Rattus norvegicus 170-173 15995853-8 2005 The enzyme activity was relatively low at all time points examined before the rise in PAF activity, peaking later, at 72, 84 and 96 h. Our data demonstrate that PAF is involved in the pathogenesis of acute liver failure and in augmented compensatory liver tissue repair post-acetaminophen treatment. Acetaminophen 275-288 PCNA clamp associated factor Rattus norvegicus 161-164 16083531-8 2005 In transfected insect cells, canine COX-3 protein is expressed and was selectively inhibited by acetaminophen. Acetaminophen 96-109 cytochrome c oxidase subunit III Canis lupus familiaris 36-41 16083531-9 2005 However, in humans and rodents an acetaminophen sensitive COX-3 protein is not expressed because the retention of intron-1 adds 94 and 98 nucleotides to the COX-3 mRNA structure respectively. Acetaminophen 34-47 mitochondrially encoded cytochrome c oxidase III Homo sapiens 58-63 16083531-9 2005 However, in humans and rodents an acetaminophen sensitive COX-3 protein is not expressed because the retention of intron-1 adds 94 and 98 nucleotides to the COX-3 mRNA structure respectively. Acetaminophen 34-47 mitochondrially encoded cytochrome c oxidase III Homo sapiens 157-162 16083531-10 2005 Since the genetic code is a triplicate code (3 nucleotides to form one amino acid), the retention of the intron in both species results in a frame shift in the RNA message and the production of a truncated protein with a completely different amino acid sequence than COX-1 or COX-2 lacking acetaminophen sensitivity. Acetaminophen 290-303 mitochondrially encoded cytochrome c oxidase I Homo sapiens 267-272 15878691-6 2005 Diethyldithiocarbamic acid, potassium ethyl xanthate, and indomethacin decreased significantly acetaminophen-induced GSH depletion in the two cell types tested, suggesting the involvement of cytochrome P450 (mainly CYP2E1) and/or prostaglandin H synthetase. Acetaminophen 95-108 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 215-221 15878691-7 2005 In macrophages, acetaminophen decreased the secretion of TNF-alpha (at 4 and 24 h, concentration-related) and IL-6 (at 24 h, at 0.1 mM), and did not affect significantly IL-8 production. Acetaminophen 16-29 tumor necrosis factor Homo sapiens 57-66 15878691-7 2005 In macrophages, acetaminophen decreased the secretion of TNF-alpha (at 4 and 24 h, concentration-related) and IL-6 (at 24 h, at 0.1 mM), and did not affect significantly IL-8 production. Acetaminophen 16-29 interleukin 6 Homo sapiens 110-114 15878691-8 2005 These in vitro observations demonstrate that clinically relevant concentrations of acetaminophen decreased: (i) intracellular GSH in human pulmonary macrophages and type II pneumocytes and (ii) the secretion of TNF-alpha and possibly IL-6 by human pulmonary macrophages. Acetaminophen 83-96 tumor necrosis factor Homo sapiens 211-220 15878691-8 2005 These in vitro observations demonstrate that clinically relevant concentrations of acetaminophen decreased: (i) intracellular GSH in human pulmonary macrophages and type II pneumocytes and (ii) the secretion of TNF-alpha and possibly IL-6 by human pulmonary macrophages. Acetaminophen 83-96 interleukin 6 Homo sapiens 234-238 15997088-7 2005 Furthermore, the expression of lysyl hydroxylase 2 was shown to be increased in the livers of APAP-treated mice compared to untreated controls. Acetaminophen 94-98 procollagen lysine, 2-oxoglutarate 5-dioxygenase 2 Mus musculus 31-50 15764585-8 2005 Finally, CAR was recently found to play a pivotal role in effecting the severe acetaminophen-induced liver damage. Acetaminophen 79-92 nuclear receptor subfamily 1 group I member 3 Homo sapiens 9-12 15764585-9 2005 Interestingly, transgenic mice expressing DN1 were resistant to the acetaminophen-induced hepatotoxicity and expression of a series of the known CAR target genes was specifically repressed in these transgenic mice. Acetaminophen 68-81 immunoglobulin heavy diversity 6-13 Homo sapiens 42-45 15962927-3 2005 Although it has been shown in mouse studies that the disruption of key regulatory factors, such as cyclooxygenase-2 (COX-2), interleukin (IL)-6, and IL-10, increased susceptibility to DILD caused by acetaminophen (APAP), no single factor seems to be absolute. Acetaminophen 199-212 prostaglandin-endoperoxide synthase 2 Mus musculus 99-115 15907624-4 2005 Correlation coefficients for calibration curves in the range 0.2-200 microg ml-1 for acetaminophen and 0.3-3 microg ml-1 for p-aminophenol were higher than 0.999. Acetaminophen 85-98 interleukin 17F Homo sapiens 76-80 15907624-5 2005 The sensitivity of detection is 4.2 ng ml-1 for acetaminophen and 11.2 ng ml-1 for p-aminophenol. Acetaminophen 48-61 interleukin 17F Homo sapiens 39-43 15775706-6 2005 However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Acetaminophen 47-51 tumor necrosis factor Mus musculus 123-132 15775706-6 2005 However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Acetaminophen 47-51 interleukin 1 beta Mus musculus 134-142 15775706-6 2005 However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Acetaminophen 47-51 interferon gamma Mus musculus 146-155 15775706-7 2005 Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Acetaminophen 53-57 tumor necrosis factor Mus musculus 122-131 15775706-7 2005 Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Acetaminophen 53-57 interleukin 1 beta Mus musculus 133-141 15775706-7 2005 Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Acetaminophen 53-57 interferon gamma Mus musculus 145-154 15897803-11 2005 Antipyretic interventions including acetaminophen and external cooling were associated with lower circulating HSP70 levels. Acetaminophen 36-49 heat shock protein family A (Hsp70) member 4 Homo sapiens 110-115 15772367-6 2005 Western blots of cell lysates showed that hepatocytes maintained CYP1A, 2B, 3A2 but gradually lost CYP2E1, which is the main metabolic enzyme for acetaminophen, carbon tetrachloride, and DMF. Acetaminophen 146-159 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 99-105 15847421-1 2005 Synthesis and structural properties of AgX-bearing bis(4-pyridyl)dimethylsilane (X- = NO2-, NO3-, CF3SO3-, and PF6-). Acetaminophen 41-43 NBL1, DAN family BMP antagonist Homo sapiens 92-95 15847421-1 2005 Synthesis and structural properties of AgX-bearing bis(4-pyridyl)dimethylsilane (X- = NO2-, NO3-, CF3SO3-, and PF6-). Acetaminophen 41-43 sperm associated antigen 17 Homo sapiens 111-114 15650114-1 2005 A splice variant of cyclooxygenase-1 (COX-1), COX-1b (previously termed as COX-3), has been identified in canine tissues as an acetaminophen-sensitive isoform, but the sequence of COX-1b mRNA and the encoded protein are not known in rats. Acetaminophen 127-140 prostaglandin-endoperoxide synthase 1 Canis lupus familiaris 20-36 15650114-1 2005 A splice variant of cyclooxygenase-1 (COX-1), COX-1b (previously termed as COX-3), has been identified in canine tissues as an acetaminophen-sensitive isoform, but the sequence of COX-1b mRNA and the encoded protein are not known in rats. Acetaminophen 127-140 prostaglandin-endoperoxide synthase 1 Canis lupus familiaris 38-43 15650114-1 2005 A splice variant of cyclooxygenase-1 (COX-1), COX-1b (previously termed as COX-3), has been identified in canine tissues as an acetaminophen-sensitive isoform, but the sequence of COX-1b mRNA and the encoded protein are not known in rats. Acetaminophen 127-140 cytochrome c oxidase subunit III Canis lupus familiaris 75-80 15763370-8 2005 at 48, 24, and 2 h before acetaminophen) attenuated the acetaminophen-induced acute increase in serum ALT and AST activities, replenished the depleted hepatic GSH, and considerably reduced the histopathological alterations in a manner similar to N-acetylcysteine, a sulfhydryls donor. Acetaminophen 56-69 glutamic pyruvic transaminase, soluble Mus musculus 102-105 15763370-8 2005 at 48, 24, and 2 h before acetaminophen) attenuated the acetaminophen-induced acute increase in serum ALT and AST activities, replenished the depleted hepatic GSH, and considerably reduced the histopathological alterations in a manner similar to N-acetylcysteine, a sulfhydryls donor. Acetaminophen 56-69 solute carrier family 17 member 5 Homo sapiens 110-113 15618346-1 2005 Acetaminophen is a widely used antipyretic and analgesic drug whose mechanism of action has recently been suggested to involve inhibitory effects on prostaglandin synthesis via a newly discovered cyclooxygenase variant (COX-3). Acetaminophen 0-13 cytochrome c oxidase III, mitochondrial Rattus norvegicus 220-225 15618346-9 2005 Our results show that prostaglandin production in CECs during basal and stimulated conditions is very sensitive to inhibition by acetaminophen and suggest that acetaminophen acts against COX-2 and not COX-1 or COX-3. Acetaminophen 160-173 cytochrome c oxidase II, mitochondrial Rattus norvegicus 187-192 15705740-7 2005 Here, we have used an in vitro model of cyclo-oxygenase-2 activity (A549 cells stimulated with IL-1beta) to show that acetaminophen is an effective inhibitor of cyclo-oxygenase activity in intact cells. Acetaminophen 118-131 prostaglandin-endoperoxide synthase 2 Homo sapiens 40-57 15705740-7 2005 Here, we have used an in vitro model of cyclo-oxygenase-2 activity (A549 cells stimulated with IL-1beta) to show that acetaminophen is an effective inhibitor of cyclo-oxygenase activity in intact cells. Acetaminophen 118-131 interleukin 1 beta Homo sapiens 95-103 15875720-3 2005 Paracetamol administration significantly reduced hepatic glycogen, glutathione (GSH), glutathione-S-transferase (GST), glutathione peroxidase (GPX) and glutathione reductase (GSH-R). Acetaminophen 0-11 hematopoietic prostaglandin D synthase Rattus norvegicus 86-111 15875720-3 2005 Paracetamol administration significantly reduced hepatic glycogen, glutathione (GSH), glutathione-S-transferase (GST), glutathione peroxidase (GPX) and glutathione reductase (GSH-R). Acetaminophen 0-11 hematopoietic prostaglandin D synthase Rattus norvegicus 113-116 15875720-3 2005 Paracetamol administration significantly reduced hepatic glycogen, glutathione (GSH), glutathione-S-transferase (GST), glutathione peroxidase (GPX) and glutathione reductase (GSH-R). Acetaminophen 0-11 glutathione-disulfide reductase Rattus norvegicus 152-173 15763343-10 2005 In human liver osteoactivin was increased in fulminant hepatitis and paracetamol intoxication. Acetaminophen 69-80 glycoprotein nmb Homo sapiens 15-27 15576447-1 2005 The cytochrome P450 (P450) CYP2E1 enzyme metabolizes and activates a wide array of toxicological substrates, including alcohols, the widely used analgesic acetaminophen, acetone, benzene, halothane, and carcinogens such as azoxymethane and dimethylhydrazine. Acetaminophen 155-168 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 27-33 15576447-7 2005 The response to the CYP2E1 substrate acetaminophen was explored in the CYP2E1-humanized mice. Acetaminophen 37-50 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 20-26 15576447-7 2005 The response to the CYP2E1 substrate acetaminophen was explored in the CYP2E1-humanized mice. Acetaminophen 37-50 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 71-77 15576447-8 2005 Hepatotoxicity, resulting from the CYP2E1-mediated activation of acetaminophen, was demonstrated in the livers of CYP2E1-humanized mice by elevated serum alanine aminotransferase levels, increased hepatocyte necrosis, and decreased P450 levels. Acetaminophen 65-78 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 35-41 15576447-8 2005 Hepatotoxicity, resulting from the CYP2E1-mediated activation of acetaminophen, was demonstrated in the livers of CYP2E1-humanized mice by elevated serum alanine aminotransferase levels, increased hepatocyte necrosis, and decreased P450 levels. Acetaminophen 65-78 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 114-120 15576447-9 2005 These data establish that in this humanized mouse model, human CYP2E1 is functional and can metabolize and activate different CYP2E1 substrates such as chlorzoxazone, p-nitrophenol, acetaminophen, and acetone. Acetaminophen 182-195 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 63-69 15576447-9 2005 These data establish that in this humanized mouse model, human CYP2E1 is functional and can metabolize and activate different CYP2E1 substrates such as chlorzoxazone, p-nitrophenol, acetaminophen, and acetone. Acetaminophen 182-195 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 126-132 15550675-0 2005 In vivo mechanisms of tissue-selective drug toxicity: effects of liver-specific knockout of the NADPH-cytochrome P450 reductase gene on acetaminophen toxicity in kidney, lung, and nasal mucosa. Acetaminophen 136-149 cytochrome p450 oxidoreductase Mus musculus 96-127 15550675-3 2005 The aim of this study was to determine whether extrahepatic acetaminophen toxicity is altered in a mouse model that has liver-specific deletion of the NADPH-cytochrome P450 reductase (Cpr) gene. Acetaminophen 60-73 cytochrome p450 oxidoreductase Mus musculus 184-187 15550675-4 2005 Liver-specific Cpr-null (Null) mice were resistant to acetaminophen hepatotoxicity, and they showed faster acetaminophen clearance than did wild-type mice at a toxic acetaminophen dose (400 mg/kg i.p.). Acetaminophen 54-67 cytochrome p450 oxidoreductase Mus musculus 15-18 15550675-4 2005 Liver-specific Cpr-null (Null) mice were resistant to acetaminophen hepatotoxicity, and they showed faster acetaminophen clearance than did wild-type mice at a toxic acetaminophen dose (400 mg/kg i.p.). Acetaminophen 107-120 cytochrome p450 oxidoreductase Mus musculus 15-18 15550675-4 2005 Liver-specific Cpr-null (Null) mice were resistant to acetaminophen hepatotoxicity, and they showed faster acetaminophen clearance than did wild-type mice at a toxic acetaminophen dose (400 mg/kg i.p.). Acetaminophen 107-120 cytochrome p450 oxidoreductase Mus musculus 15-18 15601672-0 2005 Pathophysiological role of poly(ADP-ribose) polymerase (PARP) activation during acetaminophen-induced liver cell necrosis in mice. Acetaminophen 80-93 poly (ADP-ribose) polymerase family, member 1 Mus musculus 27-54 15601672-0 2005 Pathophysiological role of poly(ADP-ribose) polymerase (PARP) activation during acetaminophen-induced liver cell necrosis in mice. Acetaminophen 80-93 poly (ADP-ribose) polymerase family, member 1 Mus musculus 56-60 15707775-5 2005 Activity of the antioxidant enzymes in the liver inhibited by APAP was increased in the majority of groups after administration of the substances tested: catalase (CAT) by 55%, glutathione peroxidase (GPx) by 50%, glutathione reductase (GR) by 35% and glutathione S-transferase (GST) by 60%. Acetaminophen 62-66 catalase Rattus norvegicus 154-162 15707775-5 2005 Activity of the antioxidant enzymes in the liver inhibited by APAP was increased in the majority of groups after administration of the substances tested: catalase (CAT) by 55%, glutathione peroxidase (GPx) by 50%, glutathione reductase (GR) by 35% and glutathione S-transferase (GST) by 60%. Acetaminophen 62-66 catalase Rattus norvegicus 164-167 15707775-5 2005 Activity of the antioxidant enzymes in the liver inhibited by APAP was increased in the majority of groups after administration of the substances tested: catalase (CAT) by 55%, glutathione peroxidase (GPx) by 50%, glutathione reductase (GR) by 35% and glutathione S-transferase (GST) by 60%. Acetaminophen 62-66 glutathione-disulfide reductase Rattus norvegicus 214-235 15707775-5 2005 Activity of the antioxidant enzymes in the liver inhibited by APAP was increased in the majority of groups after administration of the substances tested: catalase (CAT) by 55%, glutathione peroxidase (GPx) by 50%, glutathione reductase (GR) by 35% and glutathione S-transferase (GST) by 60%. Acetaminophen 62-66 glutathione-disulfide reductase Rattus norvegicus 237-239 15707775-5 2005 Activity of the antioxidant enzymes in the liver inhibited by APAP was increased in the majority of groups after administration of the substances tested: catalase (CAT) by 55%, glutathione peroxidase (GPx) by 50%, glutathione reductase (GR) by 35% and glutathione S-transferase (GST) by 60%. Acetaminophen 62-66 hematopoietic prostaglandin D synthase Rattus norvegicus 252-277 15707775-5 2005 Activity of the antioxidant enzymes in the liver inhibited by APAP was increased in the majority of groups after administration of the substances tested: catalase (CAT) by 55%, glutathione peroxidase (GPx) by 50%, glutathione reductase (GR) by 35% and glutathione S-transferase (GST) by 60%. Acetaminophen 62-66 hematopoietic prostaglandin D synthase Rattus norvegicus 279-282 21783484-3 2005 In the present study, we examined whether acute treatment with paracetamol changes delta-ALA-D activity. Acetaminophen 63-74 aminolevulinate dehydratase Homo sapiens 83-94 21783484-5 2005 Paracetamol (1200mg/kg for three days 4h after the injection of DMSO, diphenyl diselenide (100mumol/kg) or ebselen (100mumol/kg) caused an inhibition of about 40% (P < 0.01) in hepatic delta-ALA-D. Acetaminophen 0-11 aminolevulinate dehydratase Homo sapiens 188-199 15673306-0 2005 Role of Bcl-xL in paracetamol-induced tubular epithelial cell death. Acetaminophen 18-29 BCL2 like 1 Homo sapiens 8-14 15673306-5 2005 RESULTS: While paracetamol did not change the mRNA expression of the antiapoptotic gene bcl-xL, it decreased Bcl-xL protein levels. Acetaminophen 15-26 BCL2 like 1 Homo sapiens 109-115 15673306-8 2005 Overexpression of a human bcl-xL transgene decreased apoptosis induced by paracetamol by 60% at 24 hours and increased long-term cell survival. Acetaminophen 74-85 BCL2 like 1 Homo sapiens 26-32 15626590-4 2005 This hypothermic effect of paracetamol was reduced in COX-1 but not in COX-2 gene-deleted mice. Acetaminophen 27-38 cytochrome c oxidase I, mitochondrial Mus musculus 54-59 15626590-5 2005 These results support the view that analgesia and hypothermia due to paracetamol are mediated by inhibition of a third COX isoenzyme (designated COX-3). Acetaminophen 69-80 cytochrome c oxidase III, mitochondrial Mus musculus 145-150 15626590-7 2005 Diclofenac-induced COX-2 is inhibited with low concentrations of paracetamol, whereas LPS-induced COX-2 is insensitive to paracetamol inhibition. Acetaminophen 65-76 cytochrome c oxidase II, mitochondrial Mus musculus 19-24 15852486-3 2005 A single dose of acetaminophen significantly elevated the levels of lipid peroxides (LPO) with decreased levels of free radical scavenger enzymes (SOD, CAT, GSH, GPx, GST) in liver homogenate. Acetaminophen 17-30 catalase Rattus norvegicus 152-155 15659293-0 2005 Nociceptin/orphanin FQ prevents the antinociceptive action of paracetamol on the rat hot plate test. Acetaminophen 62-73 prepronociceptin Rattus norvegicus 0-10 15659293-0 2005 Nociceptin/orphanin FQ prevents the antinociceptive action of paracetamol on the rat hot plate test. Acetaminophen 62-73 prepronociceptin Rattus norvegicus 11-22 15659293-5 2005 In this study, we examined the antianalgesic effect of nociceptin/orphanin FQ and its analogue R-K on paracetamol-induced analgesia and evaluated by means of the hot plate test in rats. Acetaminophen 102-113 prepronociceptin Rattus norvegicus 55-65 15659293-5 2005 In this study, we examined the antianalgesic effect of nociceptin/orphanin FQ and its analogue R-K on paracetamol-induced analgesia and evaluated by means of the hot plate test in rats. Acetaminophen 102-113 prepronociceptin Rattus norvegicus 66-77 15659293-7 2005 Nociceptin/orphanin FQ and R-K showed a dose-dependent antagonism on the antinociceptive effect of paracetamol, and the activity of both drugs was significantly reduced by the antagonist [Nphe1] Arg14, Lys15-N/OFQ-NH2 (UFP-101). Acetaminophen 99-110 prepronociceptin Rattus norvegicus 0-10 15659293-7 2005 Nociceptin/orphanin FQ and R-K showed a dose-dependent antagonism on the antinociceptive effect of paracetamol, and the activity of both drugs was significantly reduced by the antagonist [Nphe1] Arg14, Lys15-N/OFQ-NH2 (UFP-101). Acetaminophen 99-110 prepronociceptin Rattus norvegicus 11-22 15659293-8 2005 These data indicate that nociceptin/orphanin FQ and R-K have an antianalgesic effect on the analgesia produced by a nonopioid analgesic drug, like paracetamol, that seems to develop within the brain. Acetaminophen 147-158 prepronociceptin Rattus norvegicus 25-35 15659293-8 2005 These data indicate that nociceptin/orphanin FQ and R-K have an antianalgesic effect on the analgesia produced by a nonopioid analgesic drug, like paracetamol, that seems to develop within the brain. Acetaminophen 147-158 prepronociceptin Rattus norvegicus 36-47 15603755-5 2005 CYP2E1 is the rate-limiting enzyme that initiates the cascade of events leading to acetaminophen hepatotoxicity; in the absence of this P450, toxicity will only be apparent at high concentrations. Acetaminophen 83-96 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 0-6 15662292-5 2005 Paracetamol is a weak inhibitor of PG synthesis of COX-1 and COX-2 in broken cell systems, but, by contrast, therapeutic concentrations of paracetamol inhibit PG synthesis in intact cells in vitro when the levels of the substrate arachidonic acid are low (less than about 5 mumol/L). Acetaminophen 0-11 mitochondrially encoded cytochrome c oxidase I Homo sapiens 51-56 15662292-5 2005 Paracetamol is a weak inhibitor of PG synthesis of COX-1 and COX-2 in broken cell systems, but, by contrast, therapeutic concentrations of paracetamol inhibit PG synthesis in intact cells in vitro when the levels of the substrate arachidonic acid are low (less than about 5 mumol/L). Acetaminophen 0-11 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-66 15662292-7 2005 Thus, the apparent selectivity of paracetamol may be due to inhibition of COX-2-dependent pathways that are proceeding at low rates. Acetaminophen 34-45 prostaglandin-endoperoxide synthase 2 Homo sapiens 74-79 15662292-9 2005 COX-3, a splice variant of COX-1, has been suggested to be the site of action of paracetamol, but genomic and kinetic analysis indicates that this selective interaction is unlikely to be clinically relevant. Acetaminophen 81-92 mitochondrially encoded cytochrome c oxidase III Homo sapiens 0-5 15662292-9 2005 COX-3, a splice variant of COX-1, has been suggested to be the site of action of paracetamol, but genomic and kinetic analysis indicates that this selective interaction is unlikely to be clinically relevant. Acetaminophen 81-92 mitochondrially encoded cytochrome c oxidase I Homo sapiens 27-32 15662292-11 2005 The action of paracetamol at a molecular level is unclear but could be related to the production of reactive metabolites by the peroxidase function of COX-2, which could deplete glutathione, a cofactor of enzymes such as PGE synthase. Acetaminophen 14-25 prostaglandin-endoperoxide synthase 2 Homo sapiens 151-156 15635226-12 2005 The 70% release time, T70, of acetaminophen from the matrix particles (Act : Cht=1 : 5) increased in pH 1.2 fluid by about 9-fold and in pH 6.8 fluid by about 5-fold compared to crystalline acetaminophen. Acetaminophen 30-43 solute carrier family 5 member 7 Homo sapiens 77-82 15647642-0 2005 The administration of N-acetylcysteine causes a decrease in prothrombin time in patients with paracetamol overdose but without evidence of liver impairment. Acetaminophen 94-105 coagulation factor II, thrombin Homo sapiens 60-71 15647642-1 2005 OBJECTIVE: To explore the effect of intravenous N-acetylcysteine (NAC) on the prothrombin time (PT) in patients with paracetamol overdose and persistent normal liver profile. Acetaminophen 117-128 coagulation factor II, thrombin Homo sapiens 78-89 15619225-0 2005 Lipopolysaccharide-binding protein modulates acetaminophen-induced liver injury in mice. Acetaminophen 45-58 lipopolysaccharide binding protein Mus musculus 0-34 15619225-4 2005 We found that LBP KO mice were protected from acetaminophen-induced hepatotoxicity. Acetaminophen 46-59 lipopolysaccharide binding protein Mus musculus 14-17 15619225-5 2005 At 350 mg/kg of acetaminophen, LBP KO mice had significantly less liver injury and necrosis than wild-type mice. Acetaminophen 16-29 lipopolysaccharide binding protein Mus musculus 31-34 15619225-6 2005 Repletion studies in LBP KO mice using an LBP-adenoviral construct resulted in significantly more hepatic injury and necrosis after acetaminophen exposure compared with mice receiving the control adenoviral construct. Acetaminophen 132-145 lipopolysaccharide binding protein Mus musculus 21-24 15619225-6 2005 Repletion studies in LBP KO mice using an LBP-adenoviral construct resulted in significantly more hepatic injury and necrosis after acetaminophen exposure compared with mice receiving the control adenoviral construct. Acetaminophen 132-145 lipopolysaccharide binding protein Mus musculus 42-45 15619225-7 2005 In conclusion, LBP KO mice are protected from toxicity with a decrease in hepatic necrosis following acetaminophen challenge. Acetaminophen 101-114 lipopolysaccharide binding protein Mus musculus 15-18 15619225-8 2005 This suggests a novel role for LBP in modulating acetaminophen-induced liver injury. Acetaminophen 49-62 lipopolysaccharide binding protein Mus musculus 31-34 15690478-0 2005 Alpha-fetoprotein is a predictor of outcome in acetaminophen-induced liver injury. Acetaminophen 47-60 alpha fetoprotein Homo sapiens 0-17 15690478-2 2005 This study evaluated the prognostic value of serial AFP measurements in patients with severe acetaminophen-induced liver injury. Acetaminophen 93-106 alpha fetoprotein Homo sapiens 52-55 15690478-3 2005 Prospectively, serial measurements of AFP were performed in 239 patients with acetaminophen intoxication and a peak alanine aminotransferase (ALT) level above 1000 U/L. Acetaminophen 78-91 alpha fetoprotein Homo sapiens 38-41 15690478-10 2005 In conclusion, an increase in AFP was strongly associated with a favorable outcome in patients with acetaminophen-induced liver injury. Acetaminophen 100-113 alpha fetoprotein Homo sapiens 30-33 15669031-11 2005 The ALT and AST levels were also increased significantly (P < 0.001) after acetaminophen treatment but were not reduced with MESNA. Acetaminophen 78-91 glutamic pyruvic transaminase, soluble Mus musculus 4-7 15669031-11 2005 The ALT and AST levels were also increased significantly (P < 0.001) after acetaminophen treatment but were not reduced with MESNA. Acetaminophen 78-91 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 12-15 15629515-5 2005 RESULTS: Acetaminophen-induced ALT leakage was attenuated by co-administration of cyclosporin A. Acetaminophen 9-22 glutamic pyruvic transaminase, soluble Mus musculus 31-34 16047719-5 2005 We report a very infrequent case of a patient with NSAID, paracetamol and COX-2 selective inhibitors sensitivity in whom we induced tolerance to paracetamol and celecoxib using the leukotriene receptor antagonist montelukast prior to oral challenges. Acetaminophen 145-156 prostaglandin-endoperoxide synthase 2 Homo sapiens 74-79 15328377-7 2005 In addition, despite apparently compensatory increases in total microsomal cytochrome P450 content in the liver and kidney, the decreases in CPR expression were accompanied by reductions in systemic clearance of pentobarbital, as well as in hepatic microsomal metabolism of acetaminophen and testosterone. Acetaminophen 274-287 cytochrome p450 oxidoreductase Mus musculus 141-144 16399343-5 2005 UGT1A6 is also involved in conjugation of the drug paracetamol (acetaminophen) and of phenolic metabolites of benzo[a]pyrene (together with rat UGT1A7 and human UGT1A9). Acetaminophen 51-62 UDP glucuronosyltransferase family 1 member A6 Rattus norvegicus 0-6 16399343-5 2005 UGT1A6 is also involved in conjugation of the drug paracetamol (acetaminophen) and of phenolic metabolites of benzo[a]pyrene (together with rat UGT1A7 and human UGT1A9). Acetaminophen 64-77 UDP glucuronosyltransferase family 1 member A6 Rattus norvegicus 0-6 16399343-5 2005 UGT1A6 is also involved in conjugation of the drug paracetamol (acetaminophen) and of phenolic metabolites of benzo[a]pyrene (together with rat UGT1A7 and human UGT1A9). Acetaminophen 64-77 UDP glucuronosyltransferase family 1 member A6 Rattus norvegicus 144-150 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 160-173 ATP-binding cassette glutathione S-conjugate transporter YCF1 Saccharomyces cerevisiae S288C 102-107 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 160-173 DNA-binding transcription factor YAP1 Saccharomyces cerevisiae S288C 121-126 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 160-173 ATP-binding cassette bilirubin transporter BPT1 Saccharomyces cerevisiae S288C 132-137 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 160-173 ATP-binding cassette transporter SNQ2 Saccharomyces cerevisiae S288C 241-246 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 160-173 Flr1p Saccharomyces cerevisiae S288C 251-256 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 160-173 DNA-binding transcription factor YAP1 Saccharomyces cerevisiae S288C 274-279 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 288-301 ATP-binding cassette glutathione S-conjugate transporter YCF1 Saccharomyces cerevisiae S288C 102-107 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 288-301 DNA-binding transcription factor YAP1 Saccharomyces cerevisiae S288C 121-126 15632430-8 2005 Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. Acetaminophen 288-301 ATP-binding cassette bilirubin transporter BPT1 Saccharomyces cerevisiae S288C 132-137 15632430-9 2005 The Yap1p-dependent resistance to acetaminophen required a functional Pdr1p or Pdr3p protein, but not a functional Yrr1p. Acetaminophen 34-47 DNA-binding transcription factor YAP1 Saccharomyces cerevisiae S288C 4-9 15632430-9 2005 The Yap1p-dependent resistance to acetaminophen required a functional Pdr1p or Pdr3p protein, but not a functional Yrr1p. Acetaminophen 34-47 drug-responsive transcription factor PDR1 Saccharomyces cerevisiae S288C 70-75 15632430-9 2005 The Yap1p-dependent resistance to acetaminophen required a functional Pdr1p or Pdr3p protein, but not a functional Yrr1p. Acetaminophen 34-47 drug-responsive transcription factor PDR3 Saccharomyces cerevisiae S288C 79-84 15632430-10 2005 In contrast, resistance mediated by Pdr1p/Pdr3p did not require a functional Yap1p, and revealed a distinct hierarchy in the resistance to acetaminophen. Acetaminophen 139-152 drug-responsive transcription factor PDR1 Saccharomyces cerevisiae S288C 36-41 15632430-10 2005 In contrast, resistance mediated by Pdr1p/Pdr3p did not require a functional Yap1p, and revealed a distinct hierarchy in the resistance to acetaminophen. Acetaminophen 139-152 drug-responsive transcription factor PDR3 Saccharomyces cerevisiae S288C 42-47 16060123-5 2005 Those with higher AST levels tended to be younger and to have lower APAP levels on admission. Acetaminophen 68-72 solute carrier family 17 member 5 Homo sapiens 18-21 16156951-6 2005 Acetaminophen significantly increased the levels of TBARS, the DNA damage and SOD, AST and ALT activities. Acetaminophen 0-13 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 83-86 16689128-3 2005 According ACR and EULAR guidelines paracetamol had to be the first pharmacological choice based on efficacy, tolerability and cost. Acetaminophen 35-46 acrosin Homo sapiens 10-13 15456921-2 2005 The purpose of this study was to examine the involvement of matrix metalloproteinases (MMPs) in the hepatic microvascular injury elicied by APAP. Acetaminophen 140-144 matrix metallopeptidase 2 Mus musculus 87-91 15456921-5 2005 The levels of mRNAs and activities of MMP-2 and MMP-9 in the liver were increased from 1 h through 6 h after APAP gavage. Acetaminophen 109-113 matrix metallopeptidase 2 Mus musculus 38-43 15456921-5 2005 The levels of mRNAs and activities of MMP-2 and MMP-9 in the liver were increased from 1 h through 6 h after APAP gavage. Acetaminophen 109-113 matrix metallopeptidase 9 Mus musculus 48-53 15456921-9 2005 The present study showed that increased MMPs during APAP intoxication are associated with hepatocellular damage and with hepatic microcirculatory dysfunction including impaired sinusoidal perfusion and infiltration of erythrocytes in Disse space. Acetaminophen 52-56 matrix metallopeptidase 2 Mus musculus 40-44 15496496-6 2005 Hepatotoxic doses of APAP and CCl4 increased Ho-1 and Nqo1 mRNA levels by 22- and 2.5-fold, respectively, and reduced Oatp1a1, 1a4, and Ntcp mRNA levels in liver. Acetaminophen 21-25 NAD(P)H dehydrogenase, quinone 1 Mus musculus 54-58 15496496-6 2005 Hepatotoxic doses of APAP and CCl4 increased Ho-1 and Nqo1 mRNA levels by 22- and 2.5-fold, respectively, and reduced Oatp1a1, 1a4, and Ntcp mRNA levels in liver. Acetaminophen 21-25 solute carrier organic anion transporter family, member 1a1 Mus musculus 118-125 15496496-6 2005 Hepatotoxic doses of APAP and CCl4 increased Ho-1 and Nqo1 mRNA levels by 22- and 2.5-fold, respectively, and reduced Oatp1a1, 1a4, and Ntcp mRNA levels in liver. Acetaminophen 21-25 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 136-140 15496496-7 2005 By contrast, expression of Mrps 1-4 was increased after treatment with APAP and CCl4. Acetaminophen 71-75 mitochondrial ribosomal protein S14 Mus musculus 27-35 15496496-8 2005 Notably, a marked elevation of Mrp4 mRNA expression was observed 24 h after APAP 400 mg/kg (5-fold) and CCl4 25 microl/kg (37-fold). Acetaminophen 76-80 prolactin family 2, subfamily c, member 5 Mus musculus 31-35 15501608-8 2004 Plasma alanine aminotransferase (ALT) levels were increased 2 and 4 h after APAP administration when compared to vehicle (VEH) controls. Acetaminophen 76-80 glutamic pyruvic transaminase, soluble Mus musculus 7-31 15501608-8 2004 Plasma alanine aminotransferase (ALT) levels were increased 2 and 4 h after APAP administration when compared to vehicle (VEH) controls. Acetaminophen 76-80 glutamic pyruvic transaminase, soluble Mus musculus 33-36 15501608-11 2004 In contrast, when APAP was administered to SAMe pretreated mice, ALT and liver weights were comparable to the VEH and SAMe groups. Acetaminophen 18-22 glutamic pyruvic transaminase, soluble Mus musculus 65-68 15610734-1 2004 The nuclear receptor CAR is a xenobiotic responsive transcription factor that plays a central role in the clearance of drugs and bilirubin while promoting cocaine and acetaminophen toxicity. Acetaminophen 167-180 nuclear receptor subfamily 1, group I, member 3 Mus musculus 21-24 15606129-0 2004 Time course toxicogenomic profiles in CD-1 mice after nontoxic and nonlethal hepatotoxic paracetamol administration. Acetaminophen 89-100 CD1 antigen complex Mus musculus 38-42 15579005-10 2004 If COX-3 really represents the target for acetaminophen must be called into question. Acetaminophen 42-55 mitochondrially encoded cytochrome c oxidase III Homo sapiens 3-8 15456926-0 2004 Enhanced acetaminophen toxicity by activation of the pregnane X receptor. Acetaminophen 9-22 nuclear receptor subfamily 1, group I, member 2 Mus musculus 53-72 15456926-2 2004 Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 125-138 nuclear receptor subfamily 1, group I, member 2 Mus musculus 14-17 15456926-2 2004 Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 125-138 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 73-91 15456926-2 2004 Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 125-138 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 93-98 15456926-2 2004 Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 140-144 nuclear receptor subfamily 1, group I, member 2 Mus musculus 14-17 15456926-2 2004 Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 140-144 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 73-91 15456926-2 2004 Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 140-144 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 93-98 15456926-3 2004 Therefore, it was hypothesized that activation of PXR plays a major role in APAP-induced hepatotoxicity. Acetaminophen 76-80 nuclear receptor subfamily 1, group I, member 2 Mus musculus 50-53 15353245-3 2004 However, the constant S/P ratio during acetaminophen disposition and the finding that P-glycoprotein (P-gp), a protein recognized to pump substrates out of the cell, is expressed in duct cells of the submandibular glands questions the mechanisms involved in acetaminophen salivary secretion. Acetaminophen 258-271 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 86-100 15353245-3 2004 However, the constant S/P ratio during acetaminophen disposition and the finding that P-glycoprotein (P-gp), a protein recognized to pump substrates out of the cell, is expressed in duct cells of the submandibular glands questions the mechanisms involved in acetaminophen salivary secretion. Acetaminophen 258-271 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 102-106 15353245-4 2004 Thus, we intended to evaluate the existence of a P-glycoprotein-mediated transport of acetaminophen in rat submandibular glands. Acetaminophen 86-99 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 49-63 15469856-0 2004 Increased plasma biotinidase activity in rats with paracetamol-induced acute liver injury. Acetaminophen 51-62 biotinidase Rattus norvegicus 17-28 15469856-4 2004 METHODS: After 4-, 24-, and 40-h treatment of rats with either subtoxic (350 mg/kg body wt) or toxic dose (1000 mg per kg) of paracetamol intraperitoneally, biotinidase activity was assayed in the liver and plasma along with the albumin concentration and ALT activity. Acetaminophen 126-137 biotinidase Rattus norvegicus 157-168 15469856-6 2004 However, 24 and 40 h after the toxic dose of paracetamol, biotinidase activity was decreased in the liver and increased in the plasma as compared with the control, when plasma ALT was increased. Acetaminophen 45-56 biotinidase Rattus norvegicus 58-69 15469856-7 2004 CONCLUSION: The increase in plasma biotinidase activity may serve as an indicator of paracetamol-induced acute liver injury in the rat. Acetaminophen 85-96 biotinidase Rattus norvegicus 35-46 15486922-8 2004 Apoptosis indicated by nuclear changes, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and caspase-3 activation also increased after acetaminophen administration. Acetaminophen 157-170 caspase 3 Mus musculus 115-124 15501530-6 2004 Besides, the iNOS mRNA level was up-regulated, the total NOS activity, largely calcium-independent, was significantly induced, and the NO(x) production was significantly stimulated by U-II. Acetaminophen 138-140 urotensin 2 Rattus norvegicus 184-188 15363587-4 2004 Plasma SDH at 12 h after APAP alone was 1630 U/l and BUN was 19 mg/dl versus 20 U/l and 10 mg/dl, respectively, in controls. Acetaminophen 25-29 serine dehydratase Mus musculus 7-10 15363587-5 2004 Either simultaneous or 2 h delayed treatment with 5beta-S significantly decreased the APAP-induced SDH increase while only the simultaneous pretreatment prevented the BUN elevation. Acetaminophen 86-90 serine dehydratase Mus musculus 99-102 15554233-7 2004 CYP2E1 also activates some commonly used drugs (such as acetaminophen) to their toxic metabolites, and promotes carcinogenesis. Acetaminophen 56-69 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 0-6 15554248-2 2004 It has been previously shown that acetaminophen is metabolically activated by CYP enzymes to N-acetyl-p-benzoquinone imine. Acetaminophen 34-47 peptidylprolyl isomerase G Homo sapiens 78-81 15754502-3 2004 At that time, serum aspartate aminotransferase activity in only AAP-treated group was higher than in both control and AAP plus adzuki extract (AAPA)-treated groups, while hepatic glutathione content and hepatic glutathione reductase and catalase activities in the AAP-treated group were lower than in the control group in contrast to the reverse in the AAPA-treated group. Acetaminophen 64-67 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 20-46 15272053-8 2004 The inhibitory effect of meclizine also suppresses acetaminophen-induced liver toxicity in humanized CAR mice. Acetaminophen 51-64 nuclear receptor subfamily 1, group I, member 3 Mus musculus 101-104 15513872-6 2004 RESULTS: Ethanol binging enhanced APAP-induced liver injury as indicated by ALT levels. Acetaminophen 34-38 glutamic pyruvic transaminase, soluble Mus musculus 76-79 15513872-8 2004 ALT levels after APAP were exacerbated in ethanol-binged mice treated with GdCl3, but APAP-induced hepatic microcirculatory dysfunction was not changed significantly. Acetaminophen 17-21 glutamic pyruvic transaminase, soluble Mus musculus 0-3 15467911-4 2004 We investigated the effects of paracetamol and its toxic metabolite N-acetyl-para-benzoquinoneimine (NAPQI) on in vitro vitamin K-dependent gamma-carboxylase (VKD-carb) and vitamin K epoxide reductase (VKOR) activities. Acetaminophen 31-42 gamma-glutamyl carboxylase Homo sapiens 120-157 15467911-9 2004 Unexpectedly, N-acetylcysteine was found to inhibit VKOR activity at concentrations that are obtained during rescue therapy of paracetamol intoxication. Acetaminophen 127-138 vitamin K epoxide reductase complex subunit 1 Homo sapiens 52-56 15467911-10 2004 We conclude that, the potentiation of the oral anticoagulant effect by paracetamol is likely to result from NAPQI-induced inhibition of enzymes of the vitamin K cycle, particularly VKD-carb. Acetaminophen 71-82 gamma-glutamyl carboxylase Homo sapiens 181-189 15518006-0 2004 [Effect of N-acetylcysteine on prothrombin index in patients with uncomplicated paracetamol poisoning]. Acetaminophen 80-91 coagulation factor II, thrombin Homo sapiens 31-42 15345658-4 2004 Here, we demonstrated that administering mice with 40 micromol kg(-1) NCX-1000, but not UDCA, improves liver histopathology and reduces mortality caused by 330 micromol kg(-1) APAP from 60 to 25% (P<0.01). Acetaminophen 176-180 T cell leukemia, homeobox 2 Mus musculus 70-73 15345658-5 2004 Administration of NCX-1000, in a therapeutic manner, that is, 2 h after acetaminophen (APAP) intoxication reduced mortality, improved liver histopathology and prevented liver IFN-gamma, TNF-alpha, Fas/Fas ligand and inducible nitric oxide synthase (iNOS) mRNA accumulation caused by APAP. Acetaminophen 72-85 T cell leukemia, homeobox 2 Mus musculus 18-21 15345658-5 2004 Administration of NCX-1000, in a therapeutic manner, that is, 2 h after acetaminophen (APAP) intoxication reduced mortality, improved liver histopathology and prevented liver IFN-gamma, TNF-alpha, Fas/Fas ligand and inducible nitric oxide synthase (iNOS) mRNA accumulation caused by APAP. Acetaminophen 87-91 T cell leukemia, homeobox 2 Mus musculus 18-21 15345658-13 2004 NCX-1000, but not UDCA, concentration-dependently (ED(50)=16 microm) protected against Deltapsi(m) depolarization and reduced transition from apoptosis to necrosis caused by 6.6 mm APAP. Acetaminophen 181-185 T cell leukemia, homeobox 2 Mus musculus 0-3 15345658-17 2004 In conclusion, NCX-1000 is effective in protecting against APAP-induced hepatotoxicity when administered in a therapeutic manner. Acetaminophen 59-63 T cell leukemia, homeobox 2 Mus musculus 15-18 15322266-0 2004 Acetaminophen: a central analgesic drug that involves a spinal tropisetron-sensitive, non-5-HT(3) receptor-mediated effect. Acetaminophen 0-13 5-hydroxytryptamine receptor 3A Rattus norvegicus 90-106 15322266-1 2004 The reversal of the antinociceptive effect of systemically administered acetaminophen (paracetamol) by intrathecal administration of the potent 5-HT(3) receptor antagonist tropisetron has been reported in rats subjected to the paw pressure test, suggesting that acetaminophen action is mediated through spinal 5-HT(3) receptors. Acetaminophen 72-85 5-hydroxytryptamine receptor 3A Rattus norvegicus 144-160 15322266-1 2004 The reversal of the antinociceptive effect of systemically administered acetaminophen (paracetamol) by intrathecal administration of the potent 5-HT(3) receptor antagonist tropisetron has been reported in rats subjected to the paw pressure test, suggesting that acetaminophen action is mediated through spinal 5-HT(3) receptors. Acetaminophen 87-98 5-hydroxytryptamine receptor 3A Rattus norvegicus 144-160 15322266-1 2004 The reversal of the antinociceptive effect of systemically administered acetaminophen (paracetamol) by intrathecal administration of the potent 5-HT(3) receptor antagonist tropisetron has been reported in rats subjected to the paw pressure test, suggesting that acetaminophen action is mediated through spinal 5-HT(3) receptors. Acetaminophen 262-275 5-hydroxytryptamine receptor 3A Rattus norvegicus 144-160 15276087-0 2004 Effect of acetaminophen on expression and activity of rat liver multidrug resistance-associated protein 2 and P-glycoprotein. Acetaminophen 10-23 ATP binding cassette subfamily C member 2 Rattus norvegicus 64-105 15276087-0 2004 Effect of acetaminophen on expression and activity of rat liver multidrug resistance-associated protein 2 and P-glycoprotein. Acetaminophen 10-23 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 110-124 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 27-40 ATP binding cassette subfamily C member 2 Rattus norvegicus 132-173 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 27-40 ATP binding cassette subfamily C member 2 Rattus norvegicus 175-179 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 27-40 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 185-199 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 27-40 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 201-205 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 42-46 ATP binding cassette subfamily C member 2 Rattus norvegicus 132-173 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 42-46 ATP binding cassette subfamily C member 2 Rattus norvegicus 175-179 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 42-46 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 185-199 15276087-1 2004 We evaluated the effect of acetaminophen (APAP), given as a single, 1g/kg body weight dose, on expression and activity of rat liver multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein (P-gp), two major canalicular drug transporters. Acetaminophen 42-46 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 201-205 15276087-3 2004 APAP induced an increase in plasma membrane content of Mrp2 detected by western blotting, consistent with increased detection of the protein at the canalicular level by immunoflourescence microscopy. Acetaminophen 0-4 ATP binding cassette subfamily C member 2 Rattus norvegicus 55-59 15276087-4 2004 In vivo biliary excretion of dinitrophenyl-S-glutathione, a well known Mrp2 substrate, was slightly but significantly increased by APAP, agreeing well with upregulation of the transporter. Acetaminophen 131-135 ATP binding cassette subfamily C member 2 Rattus norvegicus 71-75 15276087-5 2004 Basal biliary excretion of oxidized glutathione, an endogenous Mrp2 substrate, was also increased by APAP, likely indicating increased hepatic synthesis as a result of APAP-induced oxidative stress followed by accelerated canalicular secretion mediated by Mrp2. Acetaminophen 101-105 ATP binding cassette subfamily C member 2 Rattus norvegicus 63-67 15276087-5 2004 Basal biliary excretion of oxidized glutathione, an endogenous Mrp2 substrate, was also increased by APAP, likely indicating increased hepatic synthesis as a result of APAP-induced oxidative stress followed by accelerated canalicular secretion mediated by Mrp2. Acetaminophen 101-105 ATP binding cassette subfamily C member 2 Rattus norvegicus 256-260 15276087-7 2004 Because specific APAP-conjugated metabolites are Mrp2 substrates, we postulate that induction of Mrp2 by APAP may represent an adaptive mechanism to accelerate liver disposition of the drug. Acetaminophen 17-21 ATP binding cassette subfamily C member 2 Rattus norvegicus 49-53 15276087-7 2004 Because specific APAP-conjugated metabolites are Mrp2 substrates, we postulate that induction of Mrp2 by APAP may represent an adaptive mechanism to accelerate liver disposition of the drug. Acetaminophen 17-21 ATP binding cassette subfamily C member 2 Rattus norvegicus 97-101 15276087-7 2004 Because specific APAP-conjugated metabolites are Mrp2 substrates, we postulate that induction of Mrp2 by APAP may represent an adaptive mechanism to accelerate liver disposition of the drug. Acetaminophen 105-109 ATP binding cassette subfamily C member 2 Rattus norvegicus 49-53 15276087-7 2004 Because specific APAP-conjugated metabolites are Mrp2 substrates, we postulate that induction of Mrp2 by APAP may represent an adaptive mechanism to accelerate liver disposition of the drug. Acetaminophen 105-109 ATP binding cassette subfamily C member 2 Rattus norvegicus 97-101 15276087-8 2004 In addition, increased Mrp2-mediated elimination of oxidized glutathione may be essential in maintaining the redox equilibrium in the hepatocyte under conditions of APAP-induced oxidative stress. Acetaminophen 165-169 ATP binding cassette subfamily C member 2 Rattus norvegicus 23-27 15291509-5 2004 The protective effects were evidenced by a complete blockage of the NAPAP-induced elevation of plasma alanine aminotransferase (ALT) activity, decreased concentration of thiobarbituric acid reactive substances (TBARS) to the control level, and a partial prevention of reduced glutathione (GSH) depletion in the liver tissue. Acetaminophen 68-73 glutamic pyruvic transaminase, soluble Mus musculus 102-126 15291509-5 2004 The protective effects were evidenced by a complete blockage of the NAPAP-induced elevation of plasma alanine aminotransferase (ALT) activity, decreased concentration of thiobarbituric acid reactive substances (TBARS) to the control level, and a partial prevention of reduced glutathione (GSH) depletion in the liver tissue. Acetaminophen 68-73 glutamic pyruvic transaminase, soluble Mus musculus 128-131 15242817-0 2004 Acetaminophen alters microsomal ryanodine Ca2+ channel in HepG2 cells overexpressing CYP2E1. Acetaminophen 0-13 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 85-91 15242817-3 2004 The aim of the current work was to find out if the metabolism of acetaminophen by CYP2E1 affects ryanodine-sensitive Ca2+ stores in the endoplasmic reticulum of transduced HepG2 cells. Acetaminophen 65-78 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 82-88 15242817-4 2004 Five millimoles acetaminophen decreased proliferation of CYP2E1-overexpressing HepG2 cells, increased cytosolic Ca2+ levels and produced significant cytotoxicity, while only little, mostly anti-proliferative effects were found in HepG2 cells lacking CYP2E1. Acetaminophen 16-29 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 57-63 15242817-4 2004 Five millimoles acetaminophen decreased proliferation of CYP2E1-overexpressing HepG2 cells, increased cytosolic Ca2+ levels and produced significant cytotoxicity, while only little, mostly anti-proliferative effects were found in HepG2 cells lacking CYP2E1. Acetaminophen 16-29 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 250-256 15242817-6 2004 Acetaminophen cytotoxicity was significantly higher in CYP2E1 expressing cells with depleted glutathione. Acetaminophen 0-13 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 55-61 15242817-11 2004 Our results confirm significant role of CYP2E1 in metabolic activation of acetaminophen and indicate that ryanodine receptors located in the liver endoplasmic reticulum are sensitive targets for acetaminophen metabolites. Acetaminophen 74-87 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 40-46 15242817-11 2004 Our results confirm significant role of CYP2E1 in metabolic activation of acetaminophen and indicate that ryanodine receptors located in the liver endoplasmic reticulum are sensitive targets for acetaminophen metabolites. Acetaminophen 195-208 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 40-46 15148345-1 2004 It has been suggested recently that cyclooxygenase-3, formed as a splice variant of cyclooxygenase-1, is the enzymatic target for acetaminophen. Acetaminophen 130-143 prostaglandin-endoperoxide synthase 1 Rattus norvegicus 36-52 15148345-1 2004 It has been suggested recently that cyclooxygenase-3, formed as a splice variant of cyclooxygenase-1, is the enzymatic target for acetaminophen. Acetaminophen 130-143 prostaglandin-endoperoxide synthase 1 Rattus norvegicus 84-100 15240996-8 2004 Our results showed that APAP administration induced changes typical of confluent centrilobular necrosis by histological examination and a marked elevation in serum alanine aminotransferase (ALT) activity. Acetaminophen 24-28 glutamic pyruvic transaminase, soluble Mus musculus 164-188 15240996-8 2004 Our results showed that APAP administration induced changes typical of confluent centrilobular necrosis by histological examination and a marked elevation in serum alanine aminotransferase (ALT) activity. Acetaminophen 24-28 glutamic pyruvic transaminase, soluble Mus musculus 190-193 15284531-2 2004 The UGT1A6 protein is expressed predominantly in liver and metabolizes small phenolic drugs including acetaminophen, salicylates and many beta-blockers. Acetaminophen 102-115 UDP glucuronosyltransferase family 1 member A6 Homo sapiens 4-10 15263079-0 2004 Acetaminophen-induced hypothermia in mice is mediated by a prostaglandin endoperoxide synthase 1 gene-derived protein. Acetaminophen 0-13 prostaglandin-endoperoxide synthase 1 Mus musculus 59-96 15263079-8 2004 We propose that acetaminophen is a selective inhibitor of a COX-1 variant and this enzyme is involved in the continual synthesis of PGE(2) that maintains a normal body temperature. Acetaminophen 16-29 cytochrome c oxidase I, mitochondrial Mus musculus 60-65 15263079-9 2004 Thus, acetaminophen reduces basal body temperature below normal in mice most likely by inhibiting COX-3. Acetaminophen 6-19 cytochrome c oxidase III, mitochondrial Mus musculus 98-103 15367379-6 2004 There have been some recently well-publicized investigations of COX-1 and -2 enzyme variants that may assist in our eventual conceptual understanding of the mechanisms of action of acetaminophen. Acetaminophen 181-194 mitochondrially encoded cytochrome c oxidase I Homo sapiens 64-76 15487710-10 2004 Clinical applications of the method are illustrated by data for (a) PAP concentrations in 255 urine samples from workers at a rubber plant, and (b) PAP elimination in serial urine samples from 5 volunteers after an oral dose (500 mg) of acetaminophen. Acetaminophen 237-250 poly(A) polymerase alpha Homo sapiens 148-151 15178484-2 2004 Here, the effect of acetaminophen on the metabolism of daunorubicin and doxorubicin by isolated enzymes lactoperoxidase and myeloperoxidase, and by myeloperoxidase-containing human leukemia HL-60 cells was investigated using spectrophotometric and EPR techniques. Acetaminophen 20-33 myeloperoxidase Homo sapiens 124-139 15178484-2 2004 Here, the effect of acetaminophen on the metabolism of daunorubicin and doxorubicin by isolated enzymes lactoperoxidase and myeloperoxidase, and by myeloperoxidase-containing human leukemia HL-60 cells was investigated using spectrophotometric and EPR techniques. Acetaminophen 20-33 myeloperoxidase Homo sapiens 148-163 15178484-3 2004 We report that at pharmacological concentrations acetaminophen strongly stimulates oxidation of the anthracyclines by lactoperoxidase and myeloperoxidase systems, which results in irreversibly altered (colorless) products. Acetaminophen 49-62 myeloperoxidase Homo sapiens 138-153 15298073-2 2004 NicOx is developing NCX-701, a nitric oxide-releasing derivative of paracetamol (acetaminophen), for the potential treatment of inflammation and pain. Acetaminophen 68-79 T cell leukemia homeobox 2 Homo sapiens 20-23 15298073-2 2004 NicOx is developing NCX-701, a nitric oxide-releasing derivative of paracetamol (acetaminophen), for the potential treatment of inflammation and pain. Acetaminophen 81-94 T cell leukemia homeobox 2 Homo sapiens 20-23 15532721-0 2004 Adenovirus mediated overexpression of CYP2E1 increases sensitivity of HepG2 cells to acetaminophen induced cytotoxicity. Acetaminophen 85-98 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 38-44 15532721-2 2004 Acetaminophen (APAP) toxicity to HepG2 cells infected with Ad-CYP2E1 was characterized as a preliminary proof of principle experiment to validate the functionality of the CYP2E1 adenovirus. Acetaminophen 0-13 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 62-68 15532721-2 2004 Acetaminophen (APAP) toxicity to HepG2 cells infected with Ad-CYP2E1 was characterized as a preliminary proof of principle experiment to validate the functionality of the CYP2E1 adenovirus. Acetaminophen 0-13 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 171-177 15532721-2 2004 Acetaminophen (APAP) toxicity to HepG2 cells infected with Ad-CYP2E1 was characterized as a preliminary proof of principle experiment to validate the functionality of the CYP2E1 adenovirus. Acetaminophen 15-19 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 62-68 15532721-2 2004 Acetaminophen (APAP) toxicity to HepG2 cells infected with Ad-CYP2E1 was characterized as a preliminary proof of principle experiment to validate the functionality of the CYP2E1 adenovirus. Acetaminophen 15-19 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 171-177 15532721-4 2004 The APAP cytotoxicity was dependent on both the concentration of APAP and the multiplicity of infection of the Ad-CYP2E1 virus. Acetaminophen 4-8 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 114-120 15532721-6 2004 After treatment with APAP, mitochondrial membrane potential was dramatically decreased in the CYP2E1-expressing cells. Acetaminophen 21-25 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 94-100 15532721-8 2004 These results demonstrate that adenovirus-mediated overexpression of human CYP2E1 activates APAP to reactive metabolites which damage mitochondria, form protein adducts, and result in toxicity to HepG2 cells. Acetaminophen 92-96 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 75-81 15359896-5 2004 MT-I/II null mice were found to be much more sensitive than wild-type mice to the toxicity caused by free radical-inducing factors, which include paraquat, acetaminophen, ethanol, X-ray, ultraviolet B, carbon tetrachloride, cisplatin, doxorubicin, cerulein and streptozotocin. Acetaminophen 156-169 metallothionein 1 Mus musculus 0-7 15200281-0 2004 Correlation of MCP1 with toxicity in acetaminophen overdose. Acetaminophen 37-50 C-C motif chemokine ligand 2 Homo sapiens 15-19 15214507-1 2004 We previously showed that acetaminophen administration to rats increases forebrain serotonin levels as a result of the inhibition of liver tryptophan-2,3-dioxygenase (TDO). Acetaminophen 26-39 tryptophan 2,3-dioxygenase Rattus norvegicus 139-165 15214507-1 2004 We previously showed that acetaminophen administration to rats increases forebrain serotonin levels as a result of the inhibition of liver tryptophan-2,3-dioxygenase (TDO). Acetaminophen 26-39 tryptophan 2,3-dioxygenase Rattus norvegicus 167-170 15214507-3 2004 The results show that acetaminophen alone increases brain serotonin as well as norepinephrine levels with a concomitant inhibition of liver TDO activity. Acetaminophen 22-35 tryptophan 2,3-dioxygenase Rattus norvegicus 140-143 15175798-6 2004 The CYP2C9 polymorphisms independently predicted low warfarin requirements after adjusting for Body Mass Index, age, acetaminophen use, and race (OR 24.80; 95% CI 3.83-160.78). Acetaminophen 117-130 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 4-10 15175798-10 2004 In conclusion, CYP2C9*2 or *3 compound heterozygotes and homozygotes have low warfarin requirements even after excluding liver disease, excessive alcohol or acetaminophen consumption, low body weight, advancing age, and drug interactions. Acetaminophen 157-170 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 15-21 15120964-10 2004 ID1 expression was also increased by dimethylnitrosamine, acetylaminofluorene and acetaminophen in both primary hepatocytes and HepG2. Acetaminophen 82-95 inhibitor of DNA binding 1, HLH protein Homo sapiens 0-3 15174783-3 2004 AIM: (1) To correlate serum acetaminophen levels in febrile infants and children with the following parameters: aspartate aminotransferase (AST) levels, fever, vomiting and/or decreased caloric intake; and (2) to assess parental knowledge regarding the medication dosage and hazards of acetaminophen. Acetaminophen 28-41 solute carrier family 17 member 5 Homo sapiens 112-138 15174783-3 2004 AIM: (1) To correlate serum acetaminophen levels in febrile infants and children with the following parameters: aspartate aminotransferase (AST) levels, fever, vomiting and/or decreased caloric intake; and (2) to assess parental knowledge regarding the medication dosage and hazards of acetaminophen. Acetaminophen 28-41 solute carrier family 17 member 5 Homo sapiens 140-143 15125691-10 2004 The apoptogenic effect of acetaminophen was assessed by flow cytometry of annexin V binding, nuclear hypodiploidity, intracellular Ca2+, as well as by ultrastructural examination. Acetaminophen 26-39 annexin A5 Homo sapiens 74-83 15122755-0 2004 Activation of hepatic Nrf2 in vivo by acetaminophen in CD-1 mice. Acetaminophen 38-51 nuclear factor, erythroid derived 2, like 2 Mus musculus 22-26 15122755-2 2004 Enhanced liver damage in Nrf2-deficient mice treated with acetaminophen suggests a critical role for Nrf2; however, direct evidence for Nrf2 activation following acetaminophen exposure was previously lacking. Acetaminophen 58-71 nuclear factor, erythroid derived 2, like 2 Mus musculus 25-29 15122755-2 2004 Enhanced liver damage in Nrf2-deficient mice treated with acetaminophen suggests a critical role for Nrf2; however, direct evidence for Nrf2 activation following acetaminophen exposure was previously lacking. Acetaminophen 58-71 nuclear factor, erythroid derived 2, like 2 Mus musculus 101-105 15122755-3 2004 We show that acetaminophen can initiate nuclear translocation of Nrf2 in vivo, with maximum levels reached after 1 hour, in a dose dependent manner, at doses below those causing overt liver damage. Acetaminophen 13-26 nuclear factor, erythroid derived 2, like 2 Mus musculus 65-69 15122755-7 2004 To investigate acetaminophen-induced Nrf2 activation we compared the actions of 2 other GSH depleters, diethyl maleate (DEM) and buthionine sulphoximine (BSO), only 1 of which (DEM) can function as a Michael acceptor. Acetaminophen 15-28 nuclear factor, erythroid derived 2, like 2 Mus musculus 37-41 15122293-2 2004 For example, recent work suggests that the long-sought-after target of the analgesic acetaminophen is a neural-specific, alternatively spliced isoform of cyclooxygenase 1 (COX-1). Acetaminophen 85-98 prostaglandin-endoperoxide synthase 1 Homo sapiens 154-170 15122293-2 2004 For example, recent work suggests that the long-sought-after target of the analgesic acetaminophen is a neural-specific, alternatively spliced isoform of cyclooxygenase 1 (COX-1). Acetaminophen 85-98 prostaglandin-endoperoxide synthase 1 Homo sapiens 172-177 15010265-0 2004 Potential roles of hepatic heat shock protein 25 and 70i in protection of mice against acetaminophen-induced liver injury. Acetaminophen 87-100 heat shock protein 1 Mus musculus 27-48 15010265-1 2004 The aim of the present study was to assess the contribution of the level of expression of heat shock protein 25 (HSP25), 60 (HSP60), 70 (HSC70) and 70i (HSP70i) in mouse livers after a lethal dose of acetaminophen (APAP) to their survival. Acetaminophen 200-213 heat shock protein 1 Mus musculus 90-111 15010265-1 2004 The aim of the present study was to assess the contribution of the level of expression of heat shock protein 25 (HSP25), 60 (HSP60), 70 (HSC70) and 70i (HSP70i) in mouse livers after a lethal dose of acetaminophen (APAP) to their survival. Acetaminophen 200-213 heat shock protein 1 Mus musculus 113-118 15010265-1 2004 The aim of the present study was to assess the contribution of the level of expression of heat shock protein 25 (HSP25), 60 (HSP60), 70 (HSC70) and 70i (HSP70i) in mouse livers after a lethal dose of acetaminophen (APAP) to their survival. Acetaminophen 200-213 heat shock protein 1 (chaperonin) Mus musculus 125-130 15010265-7 2004 We found a remarkable difference in the patterns of hepatic HSP25 and HSP70i induction in mice that survived after APAP treatment. Acetaminophen 115-119 heat shock protein 1 Mus musculus 60-65 15078344-0 2004 Characterization of the acetaminophen-induced degradation of cytochrome P450-3A4 and the proteolytic pathway. Acetaminophen 24-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 15078344-1 2004 It has been shown that large doses of acetaminophen can result in increased degradation of the hepatic cytochrome P450 (CYP) enzymes in vivo; however, the proteolytic pathways have not been identified. Acetaminophen 38-51 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 103-118 15078344-1 2004 It has been shown that large doses of acetaminophen can result in increased degradation of the hepatic cytochrome P450 (CYP) enzymes in vivo; however, the proteolytic pathways have not been identified. Acetaminophen 38-51 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 120-123 15078344-2 2004 We found that incubating transfected HepG2 cells that express CYP3A4 or a reconstituted microsomal model containing human liver microsomes and cytosol, high concentrations of acetaminophen could induce a dose- and time-dependent degradation of CYP3A4. Acetaminophen 175-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 15078344-2 2004 We found that incubating transfected HepG2 cells that express CYP3A4 or a reconstituted microsomal model containing human liver microsomes and cytosol, high concentrations of acetaminophen could induce a dose- and time-dependent degradation of CYP3A4. Acetaminophen 175-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 244-250 15078344-7 2004 Both pepstatin A and anti-cathepsin D neutralizing antibody decreased acetaminophen-induced degradation of CYP3A4 in microsomal model systems. Acetaminophen 70-83 cathepsin D Homo sapiens 26-37 15078344-7 2004 Both pepstatin A and anti-cathepsin D neutralizing antibody decreased acetaminophen-induced degradation of CYP3A4 in microsomal model systems. Acetaminophen 70-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 15078344-8 2004 Pepstatin A also blocked the acetaminophen-induced degradation of the CYP3A4 in a transfected HepG2 cell line. Acetaminophen 29-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 15078344-9 2004 Incubating the 3A4 cells in the presence of acetaminophen also increased cathepsin D content and activity. Acetaminophen 44-57 cathepsin D Homo sapiens 73-84 15078344-10 2004 The lysosomal pathway, mainly mediated by cathepsin D, appears to be the major proteolytic pathway involved in the degradation of the P450 enzymes induced by toxic doses of acetaminophen. Acetaminophen 173-186 cathepsin D Homo sapiens 42-53 15058617-6 2004 Other dental therapeutic agents are substrates for CYP2C9 (celecoxib, ibuprofen and naproxen), CYP2D6 (codeine and tramadol), CYP3A4 (methylprednisolone) and CYP2E1 (acetaminophen). Acetaminophen 166-179 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 158-164 14978233-7 2004 However, GSH diminished RXRalpha-deficient mice were resistant to acetaminophen (APAP)-induced hepatotoxicity. Acetaminophen 66-79 retinoid X receptor alpha Mus musculus 24-32 14978233-7 2004 However, GSH diminished RXRalpha-deficient mice were resistant to acetaminophen (APAP)-induced hepatotoxicity. Acetaminophen 81-85 retinoid X receptor alpha Mus musculus 24-32 14978233-8 2004 Analysis of phase I detoxification genes revealed that CYP1A2 and CYP3A11 were up-regulated in wild-type mice but down-regulated in RXRalpha-deficient mice after APAP administration. Acetaminophen 162-166 cytochrome P450, family 1, subfamily a, polypeptide 2 Mus musculus 55-61 14978233-8 2004 Analysis of phase I detoxification genes revealed that CYP1A2 and CYP3A11 were up-regulated in wild-type mice but down-regulated in RXRalpha-deficient mice after APAP administration. Acetaminophen 162-166 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 66-73 14978233-8 2004 Analysis of phase I detoxification genes revealed that CYP1A2 and CYP3A11 were up-regulated in wild-type mice but down-regulated in RXRalpha-deficient mice after APAP administration. Acetaminophen 162-166 retinoid X receptor alpha Mus musculus 132-140 14978233-10 2004 Regulation of hepatic GSH levels by RXRalpha is essential to protect hepatocytes from oxidative stress, whereas up-regulation of phase I drug metabolism genes by RXRalpha may render the liver more sensitive to APAP-induced toxicity. Acetaminophen 210-214 retinoid X receptor alpha Mus musculus 162-170 15031674-5 2004 APAP significantly reduced the 8- oxodG incision activity in the nucleus by decreasing the activity and content of a DNA repair enzyme, Ogg1. Acetaminophen 0-4 8-oxoguanine DNA glycosylase Homo sapiens 136-140 14767996-4 2004 Similarly, Fah(-/-) animals with liver injury were also resistant to apoptosis induced by the Fas ligand Jo-2 and to necrosis-like cell death induced by acetaminophen (APAP). Acetaminophen 153-166 fumarylacetoacetate hydrolase Mus musculus 11-14 14767996-4 2004 Similarly, Fah(-/-) animals with liver injury were also resistant to apoptosis induced by the Fas ligand Jo-2 and to necrosis-like cell death induced by acetaminophen (APAP). Acetaminophen 168-172 fumarylacetoacetate hydrolase Mus musculus 11-14 15180166-2 2004 The underlying cause of GS is a polymorphism in the promotor region of the uridine diphosphate glucuronosyltransferase isoform 1A1 gene (UGT1A1*28), its encoded enzyme being responsible for the glucuronidation of bilirubin and presumably acetaminophen. Acetaminophen 238-251 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 137-143 15180166-4 2004 Patients with GS might be more susceptible to unexpected side effects while taking acetaminophen and other drugs which are substrates of UGT1A1. Acetaminophen 83-96 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 137-143 15180166-9 2004 The metabolic ratios unchanged acetaminophen/acetaminophen glucuronide in UGT1A1-wildtypes, heterozygotes and mutants showed no statistically significant differences. Acetaminophen 31-44 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 74-80 14747384-6 2004 However, paracetamol-induced apoptosis is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome c or Smac/DIABLO. Acetaminophen 9-20 caspase 9 Mus musculus 98-107 14747384-6 2004 However, paracetamol-induced apoptosis is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome c or Smac/DIABLO. Acetaminophen 9-20 caspase 3 Mus musculus 112-121 14747384-6 2004 However, paracetamol-induced apoptosis is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome c or Smac/DIABLO. Acetaminophen 9-20 diablo, IAP-binding mitochondrial protein Mus musculus 171-177 14747384-8 2004 Interestingly, after treatment of murine tubular cells with paracetamol and calpain inhibitors, the caspase-12 cleavage product was still detectable, and calpain inhibitors were unable to protect tubular cells from paracetamol-induced apoptosis. Acetaminophen 60-71 caspase 12 Mus musculus 100-110 15202496-0 2004 Kinetic and structural analysis of the inhibition of adenosine deaminase by acetaminophen. Acetaminophen 76-89 adenosine deaminase Homo sapiens 53-72 15202496-1 2004 Kinetic and thermodynamic studies have been made on the effect of acetaminophen on the activity and structure of adenosine deaminase in 50 mM sodium phosphate buffer pH 7.5, at two temperatures of 27 and 37 degrees C using UV spectrophotometry, circular dichroism (CD) and fluorescence spectroscopy. Acetaminophen 66-79 adenosine deaminase Homo sapiens 113-132 14610229-0 2004 Targeted disruption of the olfactory mucosa-specific Cyp2g1 gene: impact on acetaminophen toxicity in the lateral nasal gland, and tissue-selective effects on Cyp2a5 expression. Acetaminophen 76-89 cytochrome P450, family 2, subfamily g, polypeptide 1 Mus musculus 53-59 14729123-2 2004 Preincubation with nitroparacetamol or nitroflurbiprofen (but not paracetamol or flurbiprofen) caused dose-related inhibition of the formation of interleukin 1 beta (IC(50)s, 44.5 and 362 microM, n=12) and tumour necrosis factor-alpha (IC(50)s, 9.0 and 0.0009 microM, n=12). Acetaminophen 24-35 interleukin 1 beta Homo sapiens 146-164 12969830-15 2004 These results suggest that NO derived from iNOS contributes to APAP-induced parenchymal cell injury and hepatic microcirculatory disturbances. Acetaminophen 63-67 nitric oxide synthase 2, inducible Mus musculus 43-47 14725611-0 2004 Mechanism of acetaminophen-induced apoptosis in cultured cells: roles of caspase-3, DNA fragmentation factor, and the Ca2+ and Mg2+ endonuclease DNAS1L3. Acetaminophen 13-26 caspase 3 Homo sapiens 73-82 14725611-0 2004 Mechanism of acetaminophen-induced apoptosis in cultured cells: roles of caspase-3, DNA fragmentation factor, and the Ca2+ and Mg2+ endonuclease DNAS1L3. Acetaminophen 13-26 deoxyribonuclease 1 like 3 Homo sapiens 145-152 14725611-6 2004 Ectopic expression of human caspase-3 significantly potentiated the cytotoxic effect of acetaminophen and promoted the release of cytochrome c into the cytosol of treated cells suggesting a direct role for caspase-3 in acetaminophen-induced apoptosis. Acetaminophen 88-101 caspase 3 Homo sapiens 28-37 14725611-6 2004 Ectopic expression of human caspase-3 significantly potentiated the cytotoxic effect of acetaminophen and promoted the release of cytochrome c into the cytosol of treated cells suggesting a direct role for caspase-3 in acetaminophen-induced apoptosis. Acetaminophen 219-232 caspase 3 Homo sapiens 28-37 14725611-6 2004 Ectopic expression of human caspase-3 significantly potentiated the cytotoxic effect of acetaminophen and promoted the release of cytochrome c into the cytosol of treated cells suggesting a direct role for caspase-3 in acetaminophen-induced apoptosis. Acetaminophen 219-232 cytochrome c, somatic Homo sapiens 130-142 14725611-6 2004 Ectopic expression of human caspase-3 significantly potentiated the cytotoxic effect of acetaminophen and promoted the release of cytochrome c into the cytosol of treated cells suggesting a direct role for caspase-3 in acetaminophen-induced apoptosis. Acetaminophen 219-232 caspase 3 Homo sapiens 206-215 14725611-8 2004 DFF45 gene knockout rendered thymocytes resistant against acetaminophen-induced generation of both large and internucleosomal DNA fragments. Acetaminophen 58-71 DNA fragmentation factor subunit alpha Homo sapiens 0-5 14725611-9 2004 The treatment of HeLa cells with acetaminophen resulted in internuclesomal DNA fragmentation only after transfection of these cells with a plasmid encoding the DNAS1L3 gene suggesting that this endonuclease is required for acetaminophen-induced internucleosomal DNA fragmentation. Acetaminophen 33-46 deoxyribonuclease 1 like 3 Homo sapiens 160-167 14725611-9 2004 The treatment of HeLa cells with acetaminophen resulted in internuclesomal DNA fragmentation only after transfection of these cells with a plasmid encoding the DNAS1L3 gene suggesting that this endonuclease is required for acetaminophen-induced internucleosomal DNA fragmentation. Acetaminophen 223-236 deoxyribonuclease 1 like 3 Homo sapiens 160-167 14725611-10 2004 DNAS1L3 expression potentiated the cytotoxic effect of acetaminophen in HeLa cells suggesting an active role in the death process induced by this drug. Acetaminophen 55-68 deoxyribonuclease 1 like 3 Homo sapiens 0-7 14725611-11 2004 Altogether, these results demonstrate the specific roles of caspase-3, DNA fragmentation factor, and DNAS1L3 in the process of acetaminophen-induced apoptosis in cultured cells. Acetaminophen 127-140 caspase 3 Homo sapiens 60-69 14725611-11 2004 Altogether, these results demonstrate the specific roles of caspase-3, DNA fragmentation factor, and DNAS1L3 in the process of acetaminophen-induced apoptosis in cultured cells. Acetaminophen 127-140 deoxyribonuclease 1 like 3 Homo sapiens 101-108 15500197-2 2004 A further aim was to demonstrate the efficacy of 500 mg ASA + 30 mg PSE and of 1000 mg paracetamol (CAS 103-90-2) + 60 mg PSE (active control) in the symptomatic treatment of nasal congestion. Acetaminophen 87-98 BCAR1 scaffold protein, Cas family member Homo sapiens 100-103 14677070-3 2004 In the present study, antibodies against the vesicular glutamate transporter 2 (VGLUT2), a transmembrane protein responsible for loading glutamate into synaptic vesicles, were used to investigate whether some of the nerve terminals contacting NEBs in rat lungs might use glutamate as a neurotransmitter. Acetaminophen 243-247 solute carrier family 17 member 6 Rattus norvegicus 45-78 14677070-3 2004 In the present study, antibodies against the vesicular glutamate transporter 2 (VGLUT2), a transmembrane protein responsible for loading glutamate into synaptic vesicles, were used to investigate whether some of the nerve terminals contacting NEBs in rat lungs might use glutamate as a neurotransmitter. Acetaminophen 243-247 solute carrier family 17 member 6 Rattus norvegicus 80-86 15027815-0 2004 The role of cytochrome-P450 inhibitors in the prevention of hepatotoxicity after paracetamol overdose in rats. Acetaminophen 81-92 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 12-27 15674847-7 2004 APAP also caused severe centrilobular necrosis and marked increase in serum enzyme ALT activity (38-fold). Acetaminophen 0-4 glutamic pyruvic transaminase, soluble Mus musculus 83-86 15674847-9 2004 There were profound increases in serum TNF-alpha levels at 4 h following APAP administration in nonsupplemented compared to antioxidant-treated animals, but no significant differences noted after 24 h. Serum amyloid A increased in APAP-challenged mice irrespective of antioxidant treatment. Acetaminophen 73-77 tumor necrosis factor Mus musculus 39-48 15674847-9 2004 There were profound increases in serum TNF-alpha levels at 4 h following APAP administration in nonsupplemented compared to antioxidant-treated animals, but no significant differences noted after 24 h. Serum amyloid A increased in APAP-challenged mice irrespective of antioxidant treatment. Acetaminophen 231-235 tumor necrosis factor Mus musculus 39-48 14557383-0 2004 The pathogenic roles of tumor necrosis factor receptor p55 in acetaminophen-induced liver injury in mice. Acetaminophen 62-75 tumor necrosis factor receptor superfamily, member 1a Mus musculus 55-58 14557383-1 2004 Acetaminophen (APAP) causes a massive production of intrahepatic tumor necrosis factor alpha (TNF-alpha). Acetaminophen 0-13 tumor necrosis factor Mus musculus 65-92 14557383-1 2004 Acetaminophen (APAP) causes a massive production of intrahepatic tumor necrosis factor alpha (TNF-alpha). Acetaminophen 0-13 tumor necrosis factor Mus musculus 94-103 14557383-1 2004 Acetaminophen (APAP) causes a massive production of intrahepatic tumor necrosis factor alpha (TNF-alpha). Acetaminophen 15-19 tumor necrosis factor Mus musculus 65-92 14557383-1 2004 Acetaminophen (APAP) causes a massive production of intrahepatic tumor necrosis factor alpha (TNF-alpha). Acetaminophen 15-19 tumor necrosis factor Mus musculus 94-103 14557383-3 2004 Hence, we examined pathogenic roles of the TNF-alpha-TNF receptor with a molecular weight of 55 kDa (TNF-Rp55) axis in APAP-induced hepatotoxicity using TNF-Rp55-deficient [TNF-Rp55-knockout (KO)] mice. Acetaminophen 119-123 tumor necrosis factor Mus musculus 43-52 14557383-3 2004 Hence, we examined pathogenic roles of the TNF-alpha-TNF receptor with a molecular weight of 55 kDa (TNF-Rp55) axis in APAP-induced hepatotoxicity using TNF-Rp55-deficient [TNF-Rp55-knockout (KO)] mice. Acetaminophen 119-123 tumor necrosis factor receptor superfamily, member 1a Mus musculus 101-109 14557383-4 2004 When wild-type (WT) BALB/c and TNF-Rp55-KO mice were intraperitoneally injected with a lethal dose of APAP (750 mg/kg), the mortality of TNF-Rp55-KO mice was marginally but significantly reduced compared with WT mice. Acetaminophen 102-106 tumor necrosis factor receptor superfamily, member 1a Mus musculus 31-39 14557383-4 2004 When wild-type (WT) BALB/c and TNF-Rp55-KO mice were intraperitoneally injected with a lethal dose of APAP (750 mg/kg), the mortality of TNF-Rp55-KO mice was marginally but significantly reduced compared with WT mice. Acetaminophen 102-106 tumor necrosis factor receptor superfamily, member 1a Mus musculus 137-145 14557383-8 2004 On the contrary, serum transaminase elevation and histopathological changes were attenuated in TNF-Rp55-KO mice injected with APAP (600 mg/kg). Acetaminophen 126-130 tumor necrosis factor receptor superfamily, member 1a Mus musculus 95-103 15671697-4 2004 The acetaminophen-induced rats showed significant elevation in levels of the serum marker enzymes aspartate transaminase and alanine transaminase and of lipid peroxides in liver tissue with decreased levels of antioxidant enzymes such as superoxide dismutase and catalase. Acetaminophen 4-17 catalase Rattus norvegicus 263-271 14654171-0 2003 Effect of a potent iNOS inhibitor (ONO-1714) on acetaminophen-induced hepatotoxicity in the rat. Acetaminophen 48-61 nitric oxide synthase 2 Rattus norvegicus 19-23 14654171-2 2003 The present study was undertaken to evaluate the effect of ONO-1714, a potent and specific inhibitor of inducible NO synthase (iNOS), on acetaminophen-induced hepatotoxicity in the rats. Acetaminophen 137-150 nitric oxide synthase 2 Rattus norvegicus 104-125 14654171-2 2003 The present study was undertaken to evaluate the effect of ONO-1714, a potent and specific inhibitor of inducible NO synthase (iNOS), on acetaminophen-induced hepatotoxicity in the rats. Acetaminophen 137-150 nitric oxide synthase 2 Rattus norvegicus 127-131 14654171-6 2003 These findings demonstrate that oral ONO-1714, an iNOS inhibitor, protects against acetaminophen-evoked hepatic inflammation/injury, strongly suggesting that NO produced by iNOS plays a key role in the pathogenesis of this drug-induced hepatotoxicity. Acetaminophen 83-96 nitric oxide synthase 2 Rattus norvegicus 50-54 14654171-6 2003 These findings demonstrate that oral ONO-1714, an iNOS inhibitor, protects against acetaminophen-evoked hepatic inflammation/injury, strongly suggesting that NO produced by iNOS plays a key role in the pathogenesis of this drug-induced hepatotoxicity. Acetaminophen 83-96 nitric oxide synthase 2 Rattus norvegicus 173-177 14664905-0 2003 Acetaminophen down-regulates interleukin-1beta-induced nuclear factor-kappaB nuclear translocation in a human astrocytic cell line. Acetaminophen 0-13 interleukin 1 beta Homo sapiens 29-46 14664905-1 2003 In previous studies performed to elucidate acetaminophen mechanism of action, we demonstrated that acetaminophen inhibits prostaglandin E2 production by interleukin (IL)-1beta-stimulated T98G human astrocytic cells, without affecting cyclooxygenase-2 enzymatic activity. Acetaminophen 99-112 interleukin 1 beta Homo sapiens 153-175 14664905-1 2003 In previous studies performed to elucidate acetaminophen mechanism of action, we demonstrated that acetaminophen inhibits prostaglandin E2 production by interleukin (IL)-1beta-stimulated T98G human astrocytic cells, without affecting cyclooxygenase-2 enzymatic activity. Acetaminophen 99-112 prostaglandin-endoperoxide synthase 2 Homo sapiens 234-250 14664905-3 2003 Western blot analysis of IkappaBalpha protein in the cytoplasm of IL-1beta-stimulated T98G cells and electrophoretic mobility shift assay (EMSA) on corresponding nuclear extracts indicate that acetaminophen (10-1000 microM) dose-dependently inhibits both IkappaBalpha degradation and NF-kappaB nuclear translocation. Acetaminophen 193-206 NFKB inhibitor alpha Homo sapiens 25-37 14664905-3 2003 Western blot analysis of IkappaBalpha protein in the cytoplasm of IL-1beta-stimulated T98G cells and electrophoretic mobility shift assay (EMSA) on corresponding nuclear extracts indicate that acetaminophen (10-1000 microM) dose-dependently inhibits both IkappaBalpha degradation and NF-kappaB nuclear translocation. Acetaminophen 193-206 interleukin 1 beta Homo sapiens 66-74 14664905-3 2003 Western blot analysis of IkappaBalpha protein in the cytoplasm of IL-1beta-stimulated T98G cells and electrophoretic mobility shift assay (EMSA) on corresponding nuclear extracts indicate that acetaminophen (10-1000 microM) dose-dependently inhibits both IkappaBalpha degradation and NF-kappaB nuclear translocation. Acetaminophen 193-206 NFKB inhibitor alpha Homo sapiens 255-267 14664905-5 2003 These data indicate that therapeutic concentrations of acetaminophen induce an inhibition of IL-1beta-dependent NF-kappaB nuclear translocation. Acetaminophen 55-68 interleukin 1 beta Homo sapiens 93-101 14666925-7 2003 Using the system, we determined the ability of mVEGF:DF-1 cells to enhance acetaminophen sensor function in vivo, by inducing neovascularization at sites of sensor implantation in the ex ova CAM model. Acetaminophen 75-88 vascular endothelial growth factor A Mus musculus 47-52 14666925-11 2003 Alternatively, the sensors implanted with mVEGF:DF-1 cells displayed massive neovascularization and equally massive sensor response to intravenous injection of acetaminophen (VEGF:DF-1, 1387.50 +/- 276.42 nA). Acetaminophen 160-173 vascular endothelial growth factor A Mus musculus 42-47 14666925-11 2003 Alternatively, the sensors implanted with mVEGF:DF-1 cells displayed massive neovascularization and equally massive sensor response to intravenous injection of acetaminophen (VEGF:DF-1, 1387.50 +/- 276.42 nA). Acetaminophen 160-173 vascular endothelial growth factor A Gallus gallus 43-47 14625346-13 2003 Acetaminophen did not cause hepatic lipid peroxidation in wild-type mice but did cause lipid peroxidation in iNOS knockout mice. Acetaminophen 0-13 nitric oxide synthase 2, inducible Mus musculus 109-113 14625346-18 2003 IL-1beta is increased early in acetaminophen toxicity and may be important in iNOS induction. Acetaminophen 31-44 interleukin 1 beta Mus musculus 0-8 14611809-9 2003 However, lung levels of the chemokine, eotaxin, and the cytokine, IL-12, were significantly elevated in the acetaminophen challenged animals that were fed, but not in the fasted group. Acetaminophen 108-121 chemokine (C-C motif) ligand 11 Mus musculus 39-46 14611809-10 2003 The immunoneutralization of eotaxin, but not IL-12 or TNF-alpha, improved the histological appearance of the lung in fed mice challenged with acetaminophen. Acetaminophen 142-155 chemokine (C-C motif) ligand 11 Mus musculus 28-35 14527829-4 2003 Arabic gum administration dramatically reduced acetaminophen-induced hepatotoxicity as evidenced by reduced serum alanine (ALT) and aspartate aminotransferase (AST) activities. Acetaminophen 47-60 glutamic pyruvic transaminase, soluble Mus musculus 123-126 14527829-4 2003 Arabic gum administration dramatically reduced acetaminophen-induced hepatotoxicity as evidenced by reduced serum alanine (ALT) and aspartate aminotransferase (AST) activities. Acetaminophen 47-60 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 132-158 14527829-4 2003 Arabic gum administration dramatically reduced acetaminophen-induced hepatotoxicity as evidenced by reduced serum alanine (ALT) and aspartate aminotransferase (AST) activities. Acetaminophen 47-60 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 160-163 14644624-0 2003 Role of tumor necrosis factor receptor 1 (p55) in hepatocyte proliferation during acetaminophen-induced toxicity in mice. Acetaminophen 82-95 tumor necrosis factor receptor superfamily, member 1a Mus musculus 8-40 14644624-0 2003 Role of tumor necrosis factor receptor 1 (p55) in hepatocyte proliferation during acetaminophen-induced toxicity in mice. Acetaminophen 82-95 tumor necrosis factor receptor superfamily, member 1a Mus musculus 42-45 14644624-2 2003 In these studies, TNF receptor 1 (TNFR1) knockout mice were used to analyze the role of TNF-alpha in hepatocyte proliferation during acetaminophen-induced hepatotoxicity. Acetaminophen 133-146 tumor necrosis factor Mus musculus 88-97 14644624-5 2003 In contrast, in TNFR1-/- mice, which exhibit exaggerated acetaminophen hepatotoxicity, hepatocyte proliferation, and expression of cyclin D1 and cyclin A, as well as the cyclin dependent kinases, Cdk4 and Cdk2, were reduced. Acetaminophen 57-70 tumor necrosis factor receptor superfamily, member 1a Mus musculus 16-21 14644624-6 2003 The cyclin-dependent kinase inhibitor p21 was also induced in the liver following acetaminophen administration. Acetaminophen 82-95 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 38-41 14644624-9 2003 In both WT and TNFR1-/- mice, acetaminophen caused a rapid increase in total PI-3K within 3 h. Acetaminophen also increased phosphorylated PI-3K, but this was delayed 6-12 h in TNFR1-/- mice. Acetaminophen 30-43 tumor necrosis factor receptor superfamily, member 1a Mus musculus 15-20 14644624-9 2003 In both WT and TNFR1-/- mice, acetaminophen caused a rapid increase in total PI-3K within 3 h. Acetaminophen also increased phosphorylated PI-3K, but this was delayed 6-12 h in TNFR1-/- mice. Acetaminophen 30-43 tumor necrosis factor receptor superfamily, member 1a Mus musculus 177-182 14644624-9 2003 In both WT and TNFR1-/- mice, acetaminophen caused a rapid increase in total PI-3K within 3 h. Acetaminophen also increased phosphorylated PI-3K, but this was delayed 6-12 h in TNFR1-/- mice. Acetaminophen 95-108 tumor necrosis factor receptor superfamily, member 1a Mus musculus 15-20 14644624-9 2003 In both WT and TNFR1-/- mice, acetaminophen caused a rapid increase in total PI-3K within 3 h. Acetaminophen also increased phosphorylated PI-3K, but this was delayed 6-12 h in TNFR1-/- mice. Acetaminophen 95-108 tumor necrosis factor receptor superfamily, member 1a Mus musculus 177-182 14644624-10 2003 Expression of Akt, a downstream target of PI-3K, was increased in both WT and TNFR1-/- mice in response to acetaminophen. Acetaminophen 107-120 thymoma viral proto-oncogene 1 Mus musculus 14-17 14644624-10 2003 Expression of Akt, a downstream target of PI-3K, was increased in both WT and TNFR1-/- mice in response to acetaminophen. Acetaminophen 107-120 tumor necrosis factor receptor superfamily, member 1a Mus musculus 78-83 14644624-12 2003 Acetaminophen-induced expression of phosphorylated STAT3, a key regulator of cytokine-induced hepatocyte proliferation, was also delayed in TNFR1-/- mice relative to WT. Acetaminophen 0-13 signal transducer and activator of transcription 3 Mus musculus 51-56 14644624-12 2003 Acetaminophen-induced expression of phosphorylated STAT3, a key regulator of cytokine-induced hepatocyte proliferation, was also delayed in TNFR1-/- mice relative to WT. Acetaminophen 0-13 tumor necrosis factor receptor superfamily, member 1a Mus musculus 140-145 14644624-13 2003 These data suggest that TNF-alpha signaling through TNFR1 is important in regulating hepatocyte proliferation following acetaminophen-induced tissue injury. Acetaminophen 120-133 tumor necrosis factor Mus musculus 24-33 14644624-13 2003 These data suggest that TNF-alpha signaling through TNFR1 is important in regulating hepatocyte proliferation following acetaminophen-induced tissue injury. Acetaminophen 120-133 tumor necrosis factor receptor superfamily, member 1a Mus musculus 52-57 14644624-14 2003 Delayed cytokine signaling may account for reduced hepatocyte proliferation and contribute to exaggerated acetaminophen-induced hepatotoxicity in TNFR1-/- mice. Acetaminophen 106-119 tumor necrosis factor receptor superfamily, member 1a Mus musculus 146-151 12842828-7 2003 In WT mice, acetaminophen caused a time-dependent increase in activator protein-1 nuclear binding activity and in c-Jun expression. Acetaminophen 12-25 jun proto-oncogene Mus musculus 62-81 12842828-7 2003 In WT mice, acetaminophen caused a time-dependent increase in activator protein-1 nuclear binding activity and in c-Jun expression. Acetaminophen 12-25 jun proto-oncogene Mus musculus 114-119 12842828-10 2003 A transient decrease in this activity was observed 3 h after acetaminophen in WT mice, followed by an increase that was maximal after 6-12 h. In contrast, in TNFR1-/- mice, acetaminophen-induced decreases in NF-kappaB activity were prolonged and did not return to control levels for 24 h. These data indicate that TNF-alpha signaling through TNFR1 plays an important role in regulating the expression of antioxidants in this model. Acetaminophen 173-186 tumor necrosis factor receptor superfamily, member 1a Mus musculus 158-163 12842828-10 2003 A transient decrease in this activity was observed 3 h after acetaminophen in WT mice, followed by an increase that was maximal after 6-12 h. In contrast, in TNFR1-/- mice, acetaminophen-induced decreases in NF-kappaB activity were prolonged and did not return to control levels for 24 h. These data indicate that TNF-alpha signaling through TNFR1 plays an important role in regulating the expression of antioxidants in this model. Acetaminophen 173-186 tumor necrosis factor Mus musculus 314-323 12842828-10 2003 A transient decrease in this activity was observed 3 h after acetaminophen in WT mice, followed by an increase that was maximal after 6-12 h. In contrast, in TNFR1-/- mice, acetaminophen-induced decreases in NF-kappaB activity were prolonged and did not return to control levels for 24 h. These data indicate that TNF-alpha signaling through TNFR1 plays an important role in regulating the expression of antioxidants in this model. Acetaminophen 173-186 tumor necrosis factor receptor superfamily, member 1a Mus musculus 342-347 12842828-11 2003 Reduced generation of antioxidants may contribute to the increased sensitivity of TNFR1-/- mice to acetaminophen. Acetaminophen 99-112 tumor necrosis factor receptor superfamily, member 1a Mus musculus 82-87 14586387-8 2003 Induction of CYP2E1 activity by cigarette smoking could contribute to tobacco-induced cancer, alcohol-induced liver disease, and the risk of acetaminophen hepatotoxicity. Acetaminophen 141-154 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 13-19 14686484-0 2003 Prothrombin time prolongation in paracetamol poisoning: a relevant marker of hepatic failure? Acetaminophen 33-44 coagulation factor II, thrombin Homo sapiens 0-11 14686484-1 2003 The association between paracetamol overdose and prolonged prothrombin time due to hepatic failure is well recognized. Acetaminophen 24-35 coagulation factor II, thrombin Homo sapiens 59-70 14686484-2 2003 However, little is known of the possibility that paracetamol overdose can prolong the prothrombin time without overt hepatic failure. Acetaminophen 49-60 coagulation factor II, thrombin Homo sapiens 86-97 14686484-4 2003 The three reported cases provide further evidence that paracetamol overdose can be associated with a prolongation in the prothrombin time without overt hepatic failure. Acetaminophen 55-66 coagulation factor II, thrombin Homo sapiens 121-132 14600435-1 2003 Cyclooxygenase-3 (COX-3), a new acetaminophen-sensitive isoform of the COX family, has recently been cloned from canine tissues. Acetaminophen 32-45 prostaglandin-endoperoxide synthase 1 Rattus norvegicus 0-16 14730095-4 2003 Indomethacin (IND), an inhibitor preferentially acting on COX-1, as well as nimesulide (NIM) and celecoxib (CECOX), i.e. preferential and selective inhibitor of COX-2, respectively, administered icv almost completely blocked the antinociceptive effect of ACETA in Randall-Selitto method. Acetaminophen 255-260 mitochondrially encoded cytochrome c oxidase II Homo sapiens 161-166 14580368-3 2003 A novel COX-1 splice variant termed COX-3, sensitive to acetaminophen, was recently discovered by Simmons et al., and is considered to play a key role in the biosynthesis of prostanoids known to be important mediators in pain and fever. Acetaminophen 56-69 mitochondrially encoded cytochrome c oxidase I Homo sapiens 8-13 14580368-3 2003 A novel COX-1 splice variant termed COX-3, sensitive to acetaminophen, was recently discovered by Simmons et al., and is considered to play a key role in the biosynthesis of prostanoids known to be important mediators in pain and fever. Acetaminophen 56-69 mitochondrially encoded cytochrome c oxidase III Homo sapiens 36-41 12944590-1 2003 Mitochondrial oxidant stress and peroxynitrite formation have been implicated in the pathophysiology of acetaminophen-induced (AAP-induced) liver injury. Acetaminophen 104-117 active avoidance performance Mus musculus 127-130 14693272-4 2003 X-gal staining of cells exposed to Ad5-lacZ showed that the adenoviral vector was capable of transducing each of the cell lines. Acetaminophen 0-1 Alzheimer disease, familial, type 5 Homo sapiens 35-38 14550746-0 2003 Exaggerated hepatotoxicity of acetaminophen in mice lacking tumor necrosis factor receptor-1. Acetaminophen 30-43 tumor necrosis factor receptor superfamily, member 1a Mus musculus 60-92 14550746-6 2003 TNFR1(-/-) mice were found to be significantly more sensitive to the hepatotoxic effects of acetaminophen than wild-type mice. Acetaminophen 92-105 tumor necrosis factor receptor superfamily, member 1a Mus musculus 0-5 14550746-8 2003 Acetaminophen-induced expression of MCP-1, IL-1beta, CTGF, and MMP-9 mRNA was also delayed or reduced in TNFR1(-/-) mice relative to wild-type mice. Acetaminophen 0-13 chemokine (C-C motif) ligand 2 Mus musculus 36-41 14550746-8 2003 Acetaminophen-induced expression of MCP-1, IL-1beta, CTGF, and MMP-9 mRNA was also delayed or reduced in TNFR1(-/-) mice relative to wild-type mice. Acetaminophen 0-13 interleukin 1 beta Mus musculus 43-51 14550746-8 2003 Acetaminophen-induced expression of MCP-1, IL-1beta, CTGF, and MMP-9 mRNA was also delayed or reduced in TNFR1(-/-) mice relative to wild-type mice. Acetaminophen 0-13 cellular communication network factor 2 Mus musculus 53-57 14550746-8 2003 Acetaminophen-induced expression of MCP-1, IL-1beta, CTGF, and MMP-9 mRNA was also delayed or reduced in TNFR1(-/-) mice relative to wild-type mice. Acetaminophen 0-13 matrix metallopeptidase 9 Mus musculus 63-68 14550746-8 2003 Acetaminophen-induced expression of MCP-1, IL-1beta, CTGF, and MMP-9 mRNA was also delayed or reduced in TNFR1(-/-) mice relative to wild-type mice. Acetaminophen 0-13 tumor necrosis factor receptor superfamily, member 1a Mus musculus 105-110 14550746-10 2003 These data demonstrate that signaling through TNFR1 is important in inflammatory mediator production and toxicity induced by acetaminophen. Acetaminophen 125-138 tumor necrosis factor receptor superfamily, member 1a Mus musculus 46-51 13679052-0 2003 Interleukin 6 and hepatocyte regeneration in acetaminophen toxicity in the mouse. Acetaminophen 45-58 interleukin 6 Mus musculus 0-13 15266956-5 2003 significantly (P < 0.001) reduced CCl4 or PC-induced elevations of the levels of SGOT, SGPT, ALP and TBARS, while the reduced concentration of SOD due to CCl4 or PC was reversed. Acetaminophen 45-47 C-C motif chemokine ligand 4 Rattus norvegicus 37-41 15266956-5 2003 significantly (P < 0.001) reduced CCl4 or PC-induced elevations of the levels of SGOT, SGPT, ALP and TBARS, while the reduced concentration of SOD due to CCl4 or PC was reversed. Acetaminophen 45-47 C-C motif chemokine ligand 4 Rattus norvegicus 157-161 15266956-5 2003 significantly (P < 0.001) reduced CCl4 or PC-induced elevations of the levels of SGOT, SGPT, ALP and TBARS, while the reduced concentration of SOD due to CCl4 or PC was reversed. Acetaminophen 165-167 C-C motif chemokine ligand 4 Rattus norvegicus 37-41 14601627-1 2003 Acetaminophen (APAP) is biotransformed by hepatic cytochrome P450 (CYP) enzymes to the cataractogenic metabolite N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 0-13 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 50-65 14601627-1 2003 Acetaminophen (APAP) is biotransformed by hepatic cytochrome P450 (CYP) enzymes to the cataractogenic metabolite N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 0-13 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 67-70 14601627-1 2003 Acetaminophen (APAP) is biotransformed by hepatic cytochrome P450 (CYP) enzymes to the cataractogenic metabolite N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 15-19 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 50-65 14601627-1 2003 Acetaminophen (APAP) is biotransformed by hepatic cytochrome P450 (CYP) enzymes to the cataractogenic metabolite N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 15-19 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 67-70 12954812-3 2003 AAP (300 mg/kg) induced severe centrilobular necrosis and increased plasma alanine aminotransferase (ALT) activities (24 h: 3680 +/- 320 U/liter) in fasted C3Heb/FeJ mice. Acetaminophen 0-3 glutamic pyruvic transaminase, soluble Mus musculus 75-99 12954812-3 2003 AAP (300 mg/kg) induced severe centrilobular necrosis and increased plasma alanine aminotransferase (ALT) activities (24 h: 3680 +/- 320 U/liter) in fasted C3Heb/FeJ mice. Acetaminophen 0-3 glutamic pyruvic transaminase, soluble Mus musculus 101-104 12883092-2 2003 Mice were dosed with 300 mg/kg of APAP and sacrificed at 1, 2, 4, 8, and 12 h. Serum aspartate aminotransferase (AST) was elevated by 4 h. The relative amount of NT correlated with toxicity and was localized in the necrotic cells. Acetaminophen 34-38 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 85-111 12730105-0 2003 Decreased factor VIII levels during acetaminophen-induced murine fulminant hepatic failure. Acetaminophen 36-49 coagulation factor VIII Mus musculus 10-21 12730105-4 2003 We have attempted to identify nonhepatocytic sites of fVIII biosynthesis by inducing FHF in mice using acetaminophen overdose, a common cause of human FHF. Acetaminophen 103-116 coagulation factor VIII Mus musculus 54-59 12730105-6 2003 However, acetaminophen-treated mice demonstrated markedly reduced fVIII activity, contrary to the observation in human FHF. Acetaminophen 9-22 coagulation factor VIII Mus musculus 66-71 12925481-6 2003 The NT is a modification of the PT7+ to continuously monitor PO(2), PCO(2), pH and temperature in newborns. Acetaminophen 4-6 zinc finger protein 79 Homo sapiens 32-35 12920174-0 2003 Induction of multidrug resistance protein 3 in rat liver is associated with altered vectorial excretion of acetaminophen metabolites. Acetaminophen 107-120 ATP binding cassette subfamily C member 3 Rattus norvegicus 13-43 12958197-0 2003 Activation of PPAR-alpha in streptozotocin-induced diabetes is essential for resistance against acetaminophen toxicity. Acetaminophen 96-109 peroxisome proliferator activated receptor alpha Mus musculus 14-24 12958197-9 2003 These findings suggest PPAR-alpha activation as a hepatoprotective adaptive response mediating protection against APAP in diabetes. Acetaminophen 114-118 peroxisome proliferator activated receptor alpha Mus musculus 23-33 14567971-2 2003 The activity of hCAR is regulated by a variety of xenobiotics including clotrimazole and acetaminophen metabolites. Acetaminophen 89-102 CXADR Ig-like cell adhesion molecule Homo sapiens 16-20 12871658-2 2003 NCX-701 (nitroparacetamol), in contrast to paracetamol, is an effective antinociceptive drug in normal animals but their effectiveness in monoarthritis has not been compared. Acetaminophen 14-25 solute carrier family 8 member A1 Rattus norvegicus 0-3 12969438-5 2003 Pretreatment and growth factors protect against acetaminophen toxicity by suppressing the expression of Cyp1A2, thereby reducing the production of the intermediate N-acetyl-p-benzoquinone imine (NAPQI). Acetaminophen 48-61 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 104-110 12969438-6 2003 Suppression of Cyp1A2 expression by pretreatment is assumed to be due to a growth-stimulating effect of low concentrations of acetaminophen. Acetaminophen 126-139 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 15-21 12893300-0 2003 Catalytic oxidation of acetaminophen by tyrosinase in the presence of L-proline: a kinetic study. Acetaminophen 23-36 tyrosinase Homo sapiens 40-50 12893300-1 2003 A kinetic study of acetaminophen oxidation by tyrosinase in the presence of a physiological nucleophilic agent such as the amino acid L-proline is performed in the present paper. Acetaminophen 19-32 tyrosinase Homo sapiens 46-56 12875976-2 2003 Additional studies demonstrate that exogenous macrophage inflammatory protein (MIP)-2, another CXC chemokine, is therapeutic in a murine acetaminophen toxicity model when other therapies fail. Acetaminophen 137-150 chemokine (C-X-C motif) ligand 2 Mus musculus 46-85 14504673-0 2003 Differential involvement of central 5-HT1B and 5-HT3 receptor subtypes in the antinociceptive effect of paracetamol. Acetaminophen 104-115 5-hydroxytryptamine receptor 1B Rattus norvegicus 36-42 14504673-0 2003 Differential involvement of central 5-HT1B and 5-HT3 receptor subtypes in the antinociceptive effect of paracetamol. Acetaminophen 104-115 5-hydroxytryptamine receptor 3A Rattus norvegicus 47-61 14504673-10 2003 CONCLUSIONS: Our data indicate that 5-HT1B but not 5-HT3 receptors are involved in the antinociceptive effect of paracetamol in our experimental conditions. Acetaminophen 113-124 5-hydroxytryptamine receptor 1B Rattus norvegicus 36-42 12712236-2 2003 We describe here a case of a re-used liver allograft, originating from an insulin-intoxicated donor and transplanted at first into a recipient presenting with hyperacute liver failure due to paracetamol intoxication. Acetaminophen 191-202 insulin Homo sapiens 74-81 12814621-0 2003 Quantification of acetaminophen by oxidation with tyrosinase in the presence of Besthorn"s hydrazone. Acetaminophen 18-31 tyrosinase Homo sapiens 50-60 12814621-1 2003 A method for the quantitative determination of acetaminophen by measuring the kinetics of its oxidation by the enzyme tyrosinase in the presence of the nucleophilic agent 3-methyl-2-benzothiazolone hydrazone (Besthorn"s hydrazone) is described. Acetaminophen 47-60 tyrosinase Homo sapiens 118-128 14592545-3 2003 Yet purified COX enzymes are poorly inhibited by acetaminophen, particularly under conditions of high oxidant tone and elevated substrate levels. Acetaminophen 49-62 cytochrome c oxidase subunit 8A Homo sapiens 13-16 14592545-5 2003 COX-3, a variant of COX-1, has been found in canine brain and is inhibited by acetaminophen and dipyrone at physiological concentrations. Acetaminophen 78-91 cytochrome c oxidase subunit III Canis lupus familiaris 0-5 14592545-5 2003 COX-3, a variant of COX-1, has been found in canine brain and is inhibited by acetaminophen and dipyrone at physiological concentrations. Acetaminophen 78-91 cytochrome c oxidase subunit I Canis lupus familiaris 20-25 14592556-4 2003 Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses <1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it. Acetaminophen 95-108 cytochrome c oxidase I, mitochondrial Rattus norvegicus 18-23 14592556-4 2003 Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses <1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it. Acetaminophen 95-108 cytochrome c oxidase III, mitochondrial Rattus norvegicus 28-33 14592556-4 2003 Pretreatment with COX-1 and COX-3 inhibitors (aspirin at a low dose of 1 mg kg(-1), SC 560 and acetaminophen, 0.3-3 mg kg(-1)) slightly augmented thrombolysis by ACE-I, while COX-2 inhibitors (nimesulide and coxibs at doses <1 mg kg(-1) and aspirin at a high dose of 50 mg kg(-1)) or a kinin B2 receptor antagonist (icatibant) abolished it. Acetaminophen 95-108 cytochrome c oxidase II, mitochondrial Rattus norvegicus 175-180 14567536-6 2003 Interleukin-6 and tumour necrosis factor-alpha levels increased in both patient groups, but were higher in paracetamol overdose. Acetaminophen 107-118 interleukin 6 Homo sapiens 0-46 14567536-9 2003 It is hypothesized that in acute paracetamol-induced liver injury, immune activation leads to tissue factor-initiated consumption of factors II, V, VII and X, but that levels of factors IX and XI are better preserved because of inhibition of the thrombin-induced amplification phase of coagulation. Acetaminophen 33-44 coagulation factor II, thrombin Homo sapiens 246-254 12811364-1 2003 BACKGROUND AND OBJECTIVES: Acetaminophen (INN, paracetamol) is metabolized to N-acetyl-p-benzoquinone imine (NAPQI), a hepatotoxic metabolite, predominantly by cytochrome P450 (CYP) 2E1. Acetaminophen 27-40 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 160-185 12811364-1 2003 BACKGROUND AND OBJECTIVES: Acetaminophen (INN, paracetamol) is metabolized to N-acetyl-p-benzoquinone imine (NAPQI), a hepatotoxic metabolite, predominantly by cytochrome P450 (CYP) 2E1. Acetaminophen 47-58 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 160-185 12756215-1 2003 The involvement of the canalicular multidrug resistance protein 2 (Mrp2) in the hepatobiliary excretion of acetaminophen (APAP)-glutathione (GSH) conjugate and its derivatives was investigated using transport-deficient (TR- rats. Acetaminophen 107-120 ATP binding cassette subfamily C member 2 Rattus norvegicus 67-71 12756215-1 2003 The involvement of the canalicular multidrug resistance protein 2 (Mrp2) in the hepatobiliary excretion of acetaminophen (APAP)-glutathione (GSH) conjugate and its derivatives was investigated using transport-deficient (TR- rats. Acetaminophen 122-126 ATP binding cassette subfamily C member 2 Rattus norvegicus 67-71 12756215-8 2003 Our results support the direct involvement of Mrp2 in the hepatobiliary excretion of several conjugated metabolites of APAP, including APAP-GSH and APAP-NAC, and provide relevant information on processes that may be involved with both their hepatic basolateral transport and renal elimination. Acetaminophen 119-123 ATP binding cassette subfamily C member 2 Rattus norvegicus 46-50 12756215-8 2003 Our results support the direct involvement of Mrp2 in the hepatobiliary excretion of several conjugated metabolites of APAP, including APAP-GSH and APAP-NAC, and provide relevant information on processes that may be involved with both their hepatic basolateral transport and renal elimination. Acetaminophen 135-139 ATP binding cassette subfamily C member 2 Rattus norvegicus 46-50 12756215-8 2003 Our results support the direct involvement of Mrp2 in the hepatobiliary excretion of several conjugated metabolites of APAP, including APAP-GSH and APAP-NAC, and provide relevant information on processes that may be involved with both their hepatic basolateral transport and renal elimination. Acetaminophen 135-139 ATP binding cassette subfamily C member 2 Rattus norvegicus 46-50 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 102-115 tumor necrosis factor Mus musculus 186-207 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 102-115 tumor necrosis factor Mus musculus 209-212 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 102-115 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 341-347 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 102-115 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 349-358 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 117-121 tumor necrosis factor Mus musculus 186-207 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 117-121 tumor necrosis factor Mus musculus 209-212 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 117-121 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 341-347 12774022-1 2003 We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. Acetaminophen 117-121 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 349-358 12774022-5 2003 Glutathione depletion by DEM or APAP was associated with inhibition of TNF-induced NF-kappaB transactivation of anti-apoptotic genes, including inducible nitric oxide synthase (i-NOS). Acetaminophen 32-36 tumor necrosis factor Mus musculus 71-74 12774022-5 2003 Glutathione depletion by DEM or APAP was associated with inhibition of TNF-induced NF-kappaB transactivation of anti-apoptotic genes, including inducible nitric oxide synthase (i-NOS). Acetaminophen 32-36 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 83-92 12774022-5 2003 Glutathione depletion by DEM or APAP was associated with inhibition of TNF-induced NF-kappaB transactivation of anti-apoptotic genes, including inducible nitric oxide synthase (i-NOS). Acetaminophen 32-36 nitric oxide synthase 2, inducible Mus musculus 144-175 12774022-5 2003 Glutathione depletion by DEM or APAP was associated with inhibition of TNF-induced NF-kappaB transactivation of anti-apoptotic genes, including inducible nitric oxide synthase (i-NOS). Acetaminophen 32-36 nitric oxide synthase 2, inducible Mus musculus 177-182 12700423-4 2003 HPLC analysis of plasma and urine revealed lower plasma t1/2, increased volume of distribution (Vd), and increased plasma clearance (CLp) of APAP in the DB mice and no difference in APAP-glucuronide, a major metabolite in mice. Acetaminophen 141-145 hyaluronan and proteoglycan link protein 1 Mus musculus 133-136 12700423-6 2003 Compensatory cell division measured via 3H-thymidine pulse labeling and immunohistochemical staining for proliferating cell nuclear antigen (PCNA) indicated earlier onset of S-phase in the DB mice after exposure to APAP. Acetaminophen 215-219 proliferating cell nuclear antigen Mus musculus 105-139 12700423-6 2003 Compensatory cell division measured via 3H-thymidine pulse labeling and immunohistochemical staining for proliferating cell nuclear antigen (PCNA) indicated earlier onset of S-phase in the DB mice after exposure to APAP. Acetaminophen 215-219 proliferating cell nuclear antigen Mus musculus 141-145 12752891-14 2003 CONCLUSIONS: Drug utilization data indicate that COX-2 inhibitors are frequently used first line for degenerative osteoarthritis in the absence of overt inflammation, without prior adequate trial of paracetamol and with disregard for the cautions and contraindications of these agents. Acetaminophen 199-210 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-54 12699383-4 2003 Autodock was used to dock chlorzoxazone, p-nitrophenol, N-nitrosodimethylamine, acetominophen, caffeine, theophylline, and methoxyflurane into the model CYP2E1 employing a model oxyferryl heme with charges based on density functional theoretical parametrization. Acetaminophen 80-93 cytochrome P450 2E1 Oryctolagus cuniculus 153-159 12705907-0 2003 Role of interleukin-6 in hepatic heat shock protein expression and protection against acetaminophen-induced liver disease. Acetaminophen 86-99 interleukin 6 Mus musculus 8-21 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 45-58 interleukin 6 Mus musculus 121-125 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 45-58 interleukin 11 Mus musculus 149-154 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 45-58 leukemia inhibitory factor Mus musculus 156-182 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 45-58 oncostatin M Mus musculus 188-200 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 60-64 interleukin 6 Mus musculus 121-125 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 60-64 interleukin 11 Mus musculus 149-154 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 60-64 leukemia inhibitory factor Mus musculus 156-182 12705907-3 2003 Following the induction of liver injury with acetaminophen (APAP), a time-dependent increase in liver mRNA expression of IL-6 and its family members IL-11, leukemia inhibitory factor, and oncostatin M was observed in wild type (WT) mice, suggesting a possible hepatoprotective role played by this cytokine family. Acetaminophen 60-64 oncostatin M Mus musculus 188-200 12705907-4 2003 Indeed, mice lacking IL-6 (IL-6-/-) were more susceptible than were WT mice to APAP-induced liver injury. Acetaminophen 79-83 interleukin 6 Mus musculus 21-25 12705907-4 2003 Indeed, mice lacking IL-6 (IL-6-/-) were more susceptible than were WT mice to APAP-induced liver injury. Acetaminophen 79-83 interleukin 6 Mus musculus 27-31 12705907-5 2003 The increased susceptibility of the IL-6-/- mice was associated with a deficiency in the expression of hepatic heat shock protein (HSP)25, 32, and 40 as well as inducible HSP70 following APAP treatment. Acetaminophen 187-191 interleukin 6 Mus musculus 36-40 12692475-0 2003 Acetaminophen modifies hippocampal synaptic plasticity via a presynaptic 5-HT2 receptor. Acetaminophen 0-13 5-hydroxytryptamine receptor 2A Homo sapiens 73-87 12692475-1 2003 Acetaminophen (APAP) has recently been found to target COX-3, a newly identified COX isozyme. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase III Homo sapiens 55-60 12692475-1 2003 Acetaminophen (APAP) has recently been found to target COX-3, a newly identified COX isozyme. Acetaminophen 15-19 mitochondrially encoded cytochrome c oxidase III Homo sapiens 55-60 12692475-6 2003 The results suggest that APAP-induced modification of synaptic plasticity at hippocampal lateral perforant path-dentate granule cell synapses may be mediated by a presynaptic 5-HT(2) receptor. Acetaminophen 25-29 5-hydroxytryptamine receptor 2A Homo sapiens 175-191 12649360-8 2003 Chloroquine administration in paracetamol treated rats induced a significant reduction (p < 0.05) in urine flow rate and a significant increase in plasma vasopressin (p < 0.001). Acetaminophen 30-41 arginine vasopressin Rattus norvegicus 157-168 12871412-5 2003 FVIII was raised in paracetamol overdose patients but normal in those with cirrhosis (mean levels 1.95 and 1.01 IU mL(-1), respectively). Acetaminophen 20-31 coagulation factor VIII Homo sapiens 0-5 12776852-3 2003 In a two-bottle paradigm, 10 rats with a history of brain damage following status epilepticus from a single systemic injection of lithium and pilocarpine were given options to consume freely either tap water or 1 mg/cc of acetaminophen in tap water. Acetaminophen 222-235 nuclear RNA export factor 1 Rattus norvegicus 239-242 12660052-0 2003 COX-3: just another COX or the solitary elusive target of paracetamol? Acetaminophen 58-69 mitochondrially encoded cytochrome c oxidase III Homo sapiens 0-5 12606921-0 2003 The role of 5-HT1A/B autoreceptors in the antinociceptive effect of systemic administration of acetaminophen. Acetaminophen 95-108 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 12-18 12606921-7 2003 WAY 100635 (0.2-0.8 mg/kg; 5-HT1A antagonist) induced an increase in the antinociceptive effect of 600 mg/kg acetaminophen, but this increase was not dose related. Acetaminophen 109-122 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 27-33 12606921-8 2003 Conversely, 8-OH-DPAT (0.25-1 mg/kg; 5-HT1A agonist) decreased the antinociceptive effect of acetaminophen. Acetaminophen 93-106 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 37-43 12606921-9 2003 SB 216641 (0.2-0.8 mg/kg; 5-HT1B antagonist) induced a dose-related increase in the antinociceptive effect of acetaminophen, and CP 93129 (0.25 mg/kg; 5-HT1B agonist) significantly decreased the antinociceptive effect of acetaminophen. Acetaminophen 110-123 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 26-32 12606921-9 2003 SB 216641 (0.2-0.8 mg/kg; 5-HT1B antagonist) induced a dose-related increase in the antinociceptive effect of acetaminophen, and CP 93129 (0.25 mg/kg; 5-HT1B agonist) significantly decreased the antinociceptive effect of acetaminophen. Acetaminophen 221-234 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 26-32 12606921-10 2003 CONCLUSIONS: These results suggest that the combination of acetaminophen with compounds having 5-HT1A and 5-HT1B antagonist properties could be a new strategy to improve the analgesia of acetaminophen, thanks to its mild serotonergic properties. Acetaminophen 59-72 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 95-112 12606921-10 2003 CONCLUSIONS: These results suggest that the combination of acetaminophen with compounds having 5-HT1A and 5-HT1B antagonist properties could be a new strategy to improve the analgesia of acetaminophen, thanks to its mild serotonergic properties. Acetaminophen 187-200 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 95-112 12601353-7 2003 We analyzed daily TPO levels for the first week of hospitalization in 12 patients with acetaminophen-induced ALF and observed a gradual increase from a median admission level of 50 (5 to 339) pg/mL to a median peak level of 406 (125 to 1,081) pg/mL occurring on day 5 (3 to 6). Acetaminophen 87-100 thrombopoietin Homo sapiens 18-21 12601353-11 2003 Despite severe hepatic dysfunction, serum TPO levels were initially normal and increased during hospitalization in acetaminophen-induced ALF, but did not prevent the development of thrombocytopenia. Acetaminophen 115-128 thrombopoietin Homo sapiens 42-45 12604834-1 2003 The purpose of this study was to test the hypothesis that acetaminophen would alter an estrogen-regulated process in human cells that express endogenous estrogen receptor alpha and beta (ERalpha and ERbeta). Acetaminophen 58-71 estrogen receptor 1 Homo sapiens 153-176 12604834-1 2003 The purpose of this study was to test the hypothesis that acetaminophen would alter an estrogen-regulated process in human cells that express endogenous estrogen receptor alpha and beta (ERalpha and ERbeta). Acetaminophen 58-71 estrogen receptor 1 Homo sapiens 187-194 12604834-1 2003 The purpose of this study was to test the hypothesis that acetaminophen would alter an estrogen-regulated process in human cells that express endogenous estrogen receptor alpha and beta (ERalpha and ERbeta). Acetaminophen 58-71 estrogen receptor 2 Homo sapiens 199-205 12604834-2 2003 Specifically, the extent to which acetaminophen altered the expression of estrogen-inducible alkaline phosphatase in endometrial adenocarcinoma (Ishikawa) cells and directly interacted with ERbeta and ERalpha was determined. Acetaminophen 34-47 estrogen receptor 2 Homo sapiens 190-196 12604834-2 2003 Specifically, the extent to which acetaminophen altered the expression of estrogen-inducible alkaline phosphatase in endometrial adenocarcinoma (Ishikawa) cells and directly interacted with ERbeta and ERalpha was determined. Acetaminophen 34-47 estrogen receptor 1 Homo sapiens 201-208 12604834-10 2003 Competition binding assays with human ERalpha and ERbeta demonstrated 10(6)-fold molar excess acetaminophen did not directly interact significantly with the ligand-binding domain of either receptor. Acetaminophen 94-107 estrogen receptor 1 Homo sapiens 38-45 12604834-10 2003 Competition binding assays with human ERalpha and ERbeta demonstrated 10(6)-fold molar excess acetaminophen did not directly interact significantly with the ligand-binding domain of either receptor. Acetaminophen 94-107 estrogen receptor 2 Homo sapiens 50-56 12598417-2 2003 Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue-selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX-1 and COX-2) through its reducing activity, that is influenced by the different cellular levels of peroxides. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase I Homo sapiens 189-194 12598417-2 2003 Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue-selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX-1 and COX-2) through its reducing activity, that is influenced by the different cellular levels of peroxides. Acetaminophen 0-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 199-204 12598417-13 2003 6 In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX-1 and monocyte COX-2 but in the presence of plasma, the drug almost completely suppressed inducible PGE(2) biosynthesis through its inhibitory effects on both COX-2 and inducible PGES. Acetaminophen 47-60 mitochondrially encoded cytochrome c oxidase I Homo sapiens 105-110 12598417-13 2003 6 In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX-1 and monocyte COX-2 but in the presence of plasma, the drug almost completely suppressed inducible PGE(2) biosynthesis through its inhibitory effects on both COX-2 and inducible PGES. Acetaminophen 47-60 mitochondrially encoded cytochrome c oxidase II Homo sapiens 124-129 12598417-13 2003 6 In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX-1 and monocyte COX-2 but in the presence of plasma, the drug almost completely suppressed inducible PGE(2) biosynthesis through its inhibitory effects on both COX-2 and inducible PGES. Acetaminophen 47-60 mitochondrially encoded cytochrome c oxidase II Homo sapiens 268-273 12598417-13 2003 6 In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX-1 and monocyte COX-2 but in the presence of plasma, the drug almost completely suppressed inducible PGE(2) biosynthesis through its inhibitory effects on both COX-2 and inducible PGES. Acetaminophen 47-60 prostaglandin E synthase Homo sapiens 288-292 12540782-4 2003 V-PYRRO/NO administration dramatically reduced acetaminophen-induced hepatotoxicity in a dose- and time-dependent manner, as evidenced by reduced serum alanine aminotransferase (ALT) activity, reduced hepatic congestion, apoptosis, and improved hepatocellular pathology. Acetaminophen 47-60 glutamic pyruvic transaminase, soluble Mus musculus 152-176 12540782-4 2003 V-PYRRO/NO administration dramatically reduced acetaminophen-induced hepatotoxicity in a dose- and time-dependent manner, as evidenced by reduced serum alanine aminotransferase (ALT) activity, reduced hepatic congestion, apoptosis, and improved hepatocellular pathology. Acetaminophen 47-60 glutamic pyruvic transaminase, soluble Mus musculus 178-181 12547406-11 2003 also reduced the increased expression and activity of liver iNOS induced by acetaminophen. Acetaminophen 76-89 nitric oxide synthase 2, inducible Mus musculus 60-64 12594235-0 2003 Stem cell factor attenuates liver damage in a murine model of acetaminophen-induced hepatic injury. Acetaminophen 62-75 kit ligand Mus musculus 0-16 12594235-4 2003 Upon administration of acetaminophen, the levels of SCF fell dramatically, correlating to damage within the liver. Acetaminophen 23-36 kit ligand Mus musculus 52-55 12594235-6 2003 We next treated mice with anti-SCF before sublethal doses of acetaminophen and significantly increased lethality in anti-SCF-treated animals. Acetaminophen 61-74 kit ligand Mus musculus 31-34 12594235-7 2003 When exogenous SCF was given to mice, the lethality was significantly reduced compared with the control acetaminophen-treated animals and the damage within the liver tissue was attenuated. Acetaminophen 104-117 kit ligand Mus musculus 15-18 14758785-5 2003 Although various biochemical studies point to inhibition of central COX-2 activity, the existence of a COX activity that is selectively susceptible to paracetamol (COX-3?) Acetaminophen 151-162 mitochondrially encoded cytochrome c oxidase III Homo sapiens 164-169 14758789-3 2003 Less well known is that paracetamol is also metabolized to the same reactive compounds by myeloperoxidase and the peroxidase function of cycloxygenase (COX)-1. Acetaminophen 24-35 myeloperoxidase Homo sapiens 90-105 12749738-4 2003 The addition of one or two tramadol/paracetamol 37.5/32 5mg tablets (up to four times daily) for 5 days to existing NSAID or cyclo-oxygenase-2 inhibitor analgesic therapy provided effective pain relief in patients with osteoarthritis flare pain. Acetaminophen 36-47 prostaglandin-endoperoxide synthase 2 Homo sapiens 125-142 15035793-1 2003 Paracetamol and salicylate are weak inhibitors of both isolated cyclooxygenase-1 (COX-1) and COX-2 but are potent inhibitors of prostaglandin (PG) synthesis in intact cells if low concentrations of arachidonic acid are available. Acetaminophen 0-11 prostaglandin-endoperoxide synthase 1 Homo sapiens 64-80 15035793-1 2003 Paracetamol and salicylate are weak inhibitors of both isolated cyclooxygenase-1 (COX-1) and COX-2 but are potent inhibitors of prostaglandin (PG) synthesis in intact cells if low concentrations of arachidonic acid are available. Acetaminophen 0-11 prostaglandin-endoperoxide synthase 1 Homo sapiens 82-87 15035793-1 2003 Paracetamol and salicylate are weak inhibitors of both isolated cyclooxygenase-1 (COX-1) and COX-2 but are potent inhibitors of prostaglandin (PG) synthesis in intact cells if low concentrations of arachidonic acid are available. Acetaminophen 0-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 93-98 15035793-4 2003 Therefore, paracetamol and salicylate may selectively inhibit PG synthesis involving COX-2 because the lower flux through this pathway produces lesser levels of the hydroperoxide, PGG(2), than the pathway involving COX-1. Acetaminophen 11-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-90 15035793-4 2003 Therefore, paracetamol and salicylate may selectively inhibit PG synthesis involving COX-2 because the lower flux through this pathway produces lesser levels of the hydroperoxide, PGG(2), than the pathway involving COX-1. Acetaminophen 11-22 prostaglandin-endoperoxide synthase 1 Homo sapiens 215-220 14569887-3 2003 Paracetamol is a selective inhibitor of COX-2 thus having an analgesic and antipyretic potential. Acetaminophen 0-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 40-45 15686124-6 2003 Acetaminophen produced striking elevations of serum ALT, high MDA levels and a profound decrease in the liver iNOS. Acetaminophen 0-13 nitric oxide synthase 2 Rattus norvegicus 110-114 15686124-7 2003 Administration of FDP attenuated the ALT and MDA elevations and prevented the liver iNOS depletion caused by acetaminophen. Acetaminophen 109-122 nitric oxide synthase 2 Rattus norvegicus 84-88 12553730-0 2002 Tyrosinase-mediated oxidation of acetaminophen to 4-acetamido-o-benzoquinone. Acetaminophen 33-46 tyrosinase Homo sapiens 0-10 12553730-1 2002 Based on its monophenolic structure and given its pharmacological and toxicological importance, the ability of tyrosinase to oxidize acetaminophen was studied for the first time. Acetaminophen 133-146 tyrosinase Homo sapiens 111-121 12553730-3 2002 The duration of this transient phase strongly increased with the drug concentration, which would partly explain why paracetamol oxidation by tyrosinase has not been studied hitherto. Acetaminophen 116-127 tyrosinase Homo sapiens 141-151 12553730-5 2002 Acetaminophen oxidation was inhibited by tropolone, a selective inhibitor of tyrosinase. Acetaminophen 0-13 tyrosinase Homo sapiens 77-87 12553730-6 2002 The presence of the corresponding o-diphenol as intermediate was demonstrated with ascorbic acid by chemical oxidation using NaIO4 and by HPLC analysis, indicating that acetaminophen is oxidized by the monophenolase activity of tyrosinase to its corresponding o-quinone. Acetaminophen 169-182 tyrosinase Homo sapiens 228-238 12433812-1 2002 Chronic ethanol consumption potentiates acetaminophen (APAP) hepatotoxicity through enhanced NAPQI formation via CYP2E1 induction and selective depletion of mitochondrial glutathione. Acetaminophen 40-53 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 113-119 12433812-1 2002 Chronic ethanol consumption potentiates acetaminophen (APAP) hepatotoxicity through enhanced NAPQI formation via CYP2E1 induction and selective depletion of mitochondrial glutathione. Acetaminophen 55-59 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 113-119 12503027-4 2002 In vitro, paracetamol inhibits cyclooxygenase (COX)-1 and -2 in high concentrations but stimulates in low doses. Acetaminophen 10-21 prostaglandin-endoperoxide synthase 1 Mus musculus 31-60 12503027-12 2002 The order of potency of paracetamol on COX-1 or COX-2 in tissue homogenates was as follows: lungs>spleen>brain>J774.2 cells>stomach mucosa. Acetaminophen 24-35 cytochrome c oxidase I, mitochondrial Mus musculus 39-44 12503027-12 2002 The order of potency of paracetamol on COX-1 or COX-2 in tissue homogenates was as follows: lungs>spleen>brain>J774.2 cells>stomach mucosa. Acetaminophen 24-35 cytochrome c oxidase II, mitochondrial Mus musculus 48-53 12503027-13 2002 Paracetamol, 100 mg/kg, inhibited COX-1 in stomach mucosa ex vivo much less effectively than in other tissues. Acetaminophen 0-11 cytochrome c oxidase I, mitochondrial Mus musculus 34-39 12503027-14 2002 CONCLUSIONS: These data support the hypothesis that paracetamol selectively inhibits a COX enzyme which is different from COX-1 or COX-2 and may be a variant of COX-1. Acetaminophen 52-63 cytochrome c oxidase I, mitochondrial Mus musculus 122-127 12503027-14 2002 CONCLUSIONS: These data support the hypothesis that paracetamol selectively inhibits a COX enzyme which is different from COX-1 or COX-2 and may be a variant of COX-1. Acetaminophen 52-63 cytochrome c oxidase I, mitochondrial Mus musculus 161-166 12423644-0 2002 Acetaminophen-glutathione conjugate formation in a coupled cytochrome P-450-glutathione S-transferase assay system mediated by subcellular preparations from adult and weanling rat tissues. Acetaminophen 0-13 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 59-75 12490133-5 2002 These findings suggest that even small increases in CYP3A are sufficient to support caffeine-enhanced APAP toxicity. Acetaminophen 102-106 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 52-57 12434250-8 2002 The reaction between paracetamol (AAP) and bromine is not so fast and more complicated calibration methods are required. Acetaminophen 21-32 serpin family F member 2 Homo sapiens 34-37 12458710-0 2002 Simultaneous determination of paracetamol and caffeine by flow injection-solid phase spectrometry using C18 silica gel as a sensing support. Acetaminophen 30-41 Bardet-Biedl syndrome 9 Homo sapiens 104-107 12242329-0 2002 COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: cloning, structure, and expression. Acetaminophen 47-60 mitochondrially encoded cytochrome c oxidase III Homo sapiens 0-5 12242329-0 2002 COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: cloning, structure, and expression. Acetaminophen 47-60 prostaglandin-endoperoxide synthase 1 Homo sapiens 9-25 12242329-12 2002 Comparison of canine COX-3 activity with murine COX-1 and -2 demonstrates that this enzyme is selectively inhibited by analgesic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine, and dipyrone, and is potently inhibited by some nonsteroidal antiinflammatory drugs. Acetaminophen 155-168 cytochrome c oxidase subunit III Canis lupus familiaris 21-26 12242329-12 2002 Comparison of canine COX-3 activity with murine COX-1 and -2 demonstrates that this enzyme is selectively inhibited by analgesic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine, and dipyrone, and is potently inhibited by some nonsteroidal antiinflammatory drugs. Acetaminophen 155-168 cytochrome c oxidase I, mitochondrial Mus musculus 48-60 12387954-0 2002 N-acetylcysteine for paracetamol poisoning: effect on prothrombin. Acetaminophen 21-32 coagulation factor II, thrombin Homo sapiens 54-65 12387966-0 2002 Effect of acetylcysteine on prothrombin index in paracetamol poisoning without hepatocellular injury. Acetaminophen 49-60 coagulation factor II, thrombin Homo sapiens 28-39 12387966-2 2002 We aimed to assess retrospectively the effect of intravenous acetylcysteine on the prothrombin index in patients with paracetamol poisoning without signs of hepatocellular injury. Acetaminophen 118-129 coagulation factor II, thrombin Homo sapiens 83-94 12376703-0 2002 Modulation of acetaminophen-induced hepatotoxicity by the xenobiotic receptor CAR. Acetaminophen 14-27 nuclear receptor subfamily 1, group I, member 3 Mus musculus 78-81 12376703-1 2002 We have identified the xenobiotic receptor CAR (constitutive androstane receptor) as a key regulator of acetaminophen metabolism and hepatotoxicity. Acetaminophen 104-117 nuclear receptor subfamily 1, group I, member 3 Mus musculus 43-46 12376703-1 2002 We have identified the xenobiotic receptor CAR (constitutive androstane receptor) as a key regulator of acetaminophen metabolism and hepatotoxicity. Acetaminophen 104-117 nuclear receptor subfamily 1, group I, member 3 Mus musculus 48-80 12376703-2 2002 Known CAR activators as well as high doses of acetaminophen induced expression of three acetaminophen-metabolizing enzymes in wild-type but not in CAR null mice, and the CAR null mice were resistant to acetaminophen toxicity. Acetaminophen 88-101 nuclear receptor subfamily 1, group I, member 3 Mus musculus 6-9 12376703-2 2002 Known CAR activators as well as high doses of acetaminophen induced expression of three acetaminophen-metabolizing enzymes in wild-type but not in CAR null mice, and the CAR null mice were resistant to acetaminophen toxicity. Acetaminophen 88-101 nuclear receptor subfamily 1, group I, member 3 Mus musculus 6-9 12376703-3 2002 Inhibition of CAR activity by administration of the inverse agonist ligand androstanol 1 hour after acetaminophen treatment blocked hepatotoxicity in wild type but not in CAR null mice. Acetaminophen 100-113 nuclear receptor subfamily 1, group I, member 3 Mus musculus 14-17 12368192-7 2002 In human liver diseases, DMBT1 was expressed in ductular reactions after infection with hepatitis B and acetaminophen intoxication, but not in primary biliary cirrhosis, primary sclerosing cholangitis, and obstruction of the large bile duct. Acetaminophen 104-117 deleted in malignant brain tumors 1 Homo sapiens 25-30 12392966-0 2002 Reduced hepatotoxicity of acetaminophen in mice lacking inducible nitric oxide synthase: potential role of tumor necrosis factor-alpha and interleukin-10. Acetaminophen 26-39 nitric oxide synthase 2, inducible Mus musculus 56-87 12392966-4 2002 NOS II knockout mice were found to be less sensitive to the hepatotoxic effects of acetaminophen than wild-type mice. Acetaminophen 83-96 nitric oxide synthase 2, inducible Mus musculus 0-6 12392966-6 2002 In NOS II knockout mice treated with acetaminophen, hepatic expression of TNF-alpha, as well as CTGF, was significantly increased compared to wild-type mice. Acetaminophen 37-50 nitric oxide synthase 2, inducible Mus musculus 3-9 12392966-6 2002 In NOS II knockout mice treated with acetaminophen, hepatic expression of TNF-alpha, as well as CTGF, was significantly increased compared to wild-type mice. Acetaminophen 37-50 tumor necrosis factor Mus musculus 74-83 12392966-6 2002 In NOS II knockout mice treated with acetaminophen, hepatic expression of TNF-alpha, as well as CTGF, was significantly increased compared to wild-type mice. Acetaminophen 37-50 cellular communication network factor 2 Mus musculus 96-100