PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2721538-6 1989 In contrast, the administration of 2 g NAC together with paracetamol resulted in an increase in the AUC of cysteine (+29.2 nmol.ml-1.h) and glutathione (+4.6 nmol.ml-1.h). Glutathione 140-151 X-linked Kx blood group Homo sapiens 39-42 2721538-9 1989 However, NAC supports glutathione synthesis when the demand for glutathione is increased, as during the metabolism of paracetamol. Glutathione 22-33 X-linked Kx blood group Homo sapiens 9-12 2721538-9 1989 However, NAC supports glutathione synthesis when the demand for glutathione is increased, as during the metabolism of paracetamol. Glutathione 64-75 X-linked Kx blood group Homo sapiens 9-12 33331125-4 2021 Other studies indicate that NAC"s antioxidant behavior induces glutathione and in turn modulates cell inflammatory pathways. Glutathione 63-74 X-linked Kx blood group Homo sapiens 28-31 29844459-3 2018 N-acetyl-l-cysteine (NAC) is a glutathione precursor used in the treatment of acetaminophen hepatotoxicity. Glutathione 31-42 X-linked Kx blood group Homo sapiens 21-24 31485293-11 2019 In the absence of oxidation, NAC significantly reduced ROS production (p < 0.001) and increased GSH content (p = 0.02) only in RPE from AMD donors. Glutathione 99-102 X-linked Kx blood group Homo sapiens 29-32 31485293-12 2019 Additionally, NAC-mediated protection from H2O2-induced GSH depletion (p = 0.04) and mitochondrial dysfunction (p < 0.05) was more pronounced in AMD cells compared with No AMD cells. Glutathione 56-59 X-linked Kx blood group Homo sapiens 14-17 30326393-3 2019 Extracellular GSH is unable to be taken into the majority of human cells, and the GSH prodrug N-acetyl-l-cysteine (NAC) does not exhibit promising clinical effects. Glutathione 82-85 X-linked Kx blood group Homo sapiens 115-118 29972340-1 2018 INTRODUCTION: N-acetyl-l-cysteine (NAC), a derivative of the naturally occurring amino acid l-cysteine, is a mucolytic agent that may also act as an antioxidant by providing cysteine intracellularly for increased production of glutathione. Glutathione 227-238 X-linked Kx blood group Homo sapiens 35-38 27722780-6 2018 NAC treatment increased GSH content and GSH-to-oxidized GSH ratio in the liver of IUGR-NAC group, most likely owing to the improved activities of gamma-glutamine-cysteine ligase, gamma-glutamine-cysteine synthetase, and glutathione reductase. Glutathione 24-27 X-linked Kx blood group Homo sapiens 0-3 27722780-6 2018 NAC treatment increased GSH content and GSH-to-oxidized GSH ratio in the liver of IUGR-NAC group, most likely owing to the improved activities of gamma-glutamine-cysteine ligase, gamma-glutamine-cysteine synthetase, and glutathione reductase. Glutathione 24-27 X-linked Kx blood group Homo sapiens 82-96 27722780-6 2018 NAC treatment increased GSH content and GSH-to-oxidized GSH ratio in the liver of IUGR-NAC group, most likely owing to the improved activities of gamma-glutamine-cysteine ligase, gamma-glutamine-cysteine synthetase, and glutathione reductase. Glutathione 40-43 X-linked Kx blood group Homo sapiens 0-3 27722780-6 2018 NAC treatment increased GSH content and GSH-to-oxidized GSH ratio in the liver of IUGR-NAC group, most likely owing to the improved activities of gamma-glutamine-cysteine ligase, gamma-glutamine-cysteine synthetase, and glutathione reductase. Glutathione 40-43 X-linked Kx blood group Homo sapiens 82-96 27722780-6 2018 NAC treatment increased GSH content and GSH-to-oxidized GSH ratio in the liver of IUGR-NAC group, most likely owing to the improved activities of gamma-glutamine-cysteine ligase, gamma-glutamine-cysteine synthetase, and glutathione reductase. Glutathione 40-43 X-linked Kx blood group Homo sapiens 0-3 27722780-6 2018 NAC treatment increased GSH content and GSH-to-oxidized GSH ratio in the liver of IUGR-NAC group, most likely owing to the improved activities of gamma-glutamine-cysteine ligase, gamma-glutamine-cysteine synthetase, and glutathione reductase. Glutathione 40-43 X-linked Kx blood group Homo sapiens 82-96 27722780-9 2018 CONCLUSIONS: NAC may have beneficial effects in improving GSH synthesis and cellular homeostasis in the liver of IUGR suckling piglets. Glutathione 58-61 X-linked Kx blood group Homo sapiens 13-16 27738742-11 2017 Interestingly, glutathione, although being highly related to NAC, did not show an effect on hTRPA1 channel activity. Glutathione 15-26 X-linked Kx blood group Homo sapiens 61-64 29568662-0 2018 S-Nitroso-N-acetyl-L-cysteine ethyl ester (SNACET) and N-acetyl-L-cysteine ethyl ester (NACET)-Cysteine-based drug candidates with unique pharmacological profiles for oral use as NO, H2S and GSH suppliers and as antioxidants: Results and overview. Glutathione 191-194 X-linked Kx blood group Homo sapiens 10-29 29568662-16 2018 NACET, with high oral bioavailability, is a strong antioxidant and abundant precursor of GSH, unlike its free acid N-acetyl-L-cysteine (NAC). Glutathione 89-92 X-linked Kx blood group Homo sapiens 0-3 28830914-5 2017 Although NAC is thought to be a glutathione precursor, NAC protected primary astrocytes from the toxicity of the proteasome inhibitor MG132 without eliciting any increase in glutathione. Glutathione 32-43 X-linked Kx blood group Homo sapiens 9-12 28359953-13 2017 NAC and GSH prevent acrolein- and CSE-induced exosome release, which may contribute to the clinical benefits of NAC treatment. Glutathione 8-11 X-linked Kx blood group Homo sapiens 112-115 27488560-6 2016 The dramatic response to NAC therapy supports the idea that glutathione depletion plays a key role in the pathogenesis of hawkinsinuria. Glutathione 60-71 X-linked Kx blood group Homo sapiens 25-28 27990559-6 2017 In addition, NAC restores levels of neuronal glutathione (GSH), a potent antioxidant, by providing a cell-permeable source of cysteine. Glutathione 45-56 X-linked Kx blood group Homo sapiens 13-16 27990559-6 2017 In addition, NAC restores levels of neuronal glutathione (GSH), a potent antioxidant, by providing a cell-permeable source of cysteine. Glutathione 58-61 X-linked Kx blood group Homo sapiens 13-16 27990559-7 2017 Thus, we hypothesized that NAC treatment can reduce neuronal cell death, not only by increasing GSH concentration but also by zinc chelation. Glutathione 96-99 X-linked Kx blood group Homo sapiens 27-30 27990559-8 2017 As a result, we found that NAC decreased the oxidative stress, zinc release and translocation, and improved the level of glutathione. Glutathione 121-132 X-linked Kx blood group Homo sapiens 27-30 26879220-1 2016 The glutathione precursor N-acetyl-L-cysteine (NAC) is currently being tested on Parkinson"s patients for its neuroprotective properties. Glutathione 4-15 X-linked Kx blood group Homo sapiens 47-50 26951077-5 2016 NAC is a glutathione precursor and exerts its effect after conversion to glutathione, and presumably it has its own biological activity. Glutathione 9-20 X-linked Kx blood group Homo sapiens 0-3 26951077-5 2016 NAC is a glutathione precursor and exerts its effect after conversion to glutathione, and presumably it has its own biological activity. Glutathione 73-84 X-linked Kx blood group Homo sapiens 0-3 26879220-2 2016 Our studies have shown that NAC can elicit protection in glutathione-independent manners in vitro. Glutathione 57-68 X-linked Kx blood group Homo sapiens 28-31 26903865-6 2016 These responses were significantly suppressed by pretreatment with the ROS scavengers N-acetyl-L-cysteine (NAC) and 4,5-dihydroxy-1,3-benzene disulfonic acid disodium salt monohydrate (Tiron), and also by preincubation of cells with the glutathione inducer Dimethylfumarate (DMF). Glutathione 237-248 X-linked Kx blood group Homo sapiens 107-110 27123209-3 2016 N-acetyl-L-cysteine (NAC), an antioxidant that scavenges free radicals, is considered a supplement to alleviate glutathione (GSH) depletion during oxidative stress. Glutathione 112-123 X-linked Kx blood group Homo sapiens 21-24 27123209-3 2016 N-acetyl-L-cysteine (NAC), an antioxidant that scavenges free radicals, is considered a supplement to alleviate glutathione (GSH) depletion during oxidative stress. Glutathione 125-128 X-linked Kx blood group Homo sapiens 21-24 26567752-5 2016 N-acetyl-l-cysteine (NAC) acts as a precursor for the substrate cysteine in synthesis of GSH and also as a mucolytic and anti-inflammatory agent. Glutathione 89-92 X-linked Kx blood group Homo sapiens 21-24 26386189-7 2015 Addition of N-acetyl-l-cysteine (NAC) to the oocyte maturation media reversed the ZEA-induced inhibition of polar body extrusion (from 69% to 81%), up-regulated ROS (from 7.9 to 6.5), down-regulated GSH content (from 0.16 to 0.82 pmol/oocyte) and recovered cumulus cells expansion in morphology and mRNA level. Glutathione 199-202 X-linked Kx blood group Homo sapiens 33-36 23585825-8 2013 Supplement of NAC (a GSH precursor) or GSH recapitulated the effect of Nrf2, suggesting the increase of cellular GSH level is responsible for Nrf2 effect on LC3B and autophagosome. Glutathione 21-24 X-linked Kx blood group Homo sapiens 14-17 25572414-7 2015 Antioxidants, N-acetyl-L-cysteine (NAC) and butylated hydroxyanisole (BHA), were applied to restore GSH content and reduce production of ROS. Glutathione 100-103 X-linked Kx blood group Homo sapiens 35-38 25572414-12 2015 NAC reversed cell death and molecular changes induced by ATO via restoring GSH and reducing ROS content. Glutathione 75-78 X-linked Kx blood group Homo sapiens 0-3 24080471-1 2014 N-acetyl-l-cysteine (NAC) has long been used therapeutically for the treatment of acetaminophen (paracetamol) overdose, acting as a precursor for the substrate (l-cysteine) in synthesis of hepatic glutathione (GSH) depleted through drug conjugation. Glutathione 197-208 X-linked Kx blood group Homo sapiens 21-24 24080471-1 2014 N-acetyl-l-cysteine (NAC) has long been used therapeutically for the treatment of acetaminophen (paracetamol) overdose, acting as a precursor for the substrate (l-cysteine) in synthesis of hepatic glutathione (GSH) depleted through drug conjugation. Glutathione 210-213 X-linked Kx blood group Homo sapiens 21-24 24080471-5 2014 This review seeks to re-evaluate the mechanism of action of NAC as a precursor for GSH synthesis in the context of its activity as an "antioxidant". Glutathione 83-86 X-linked Kx blood group Homo sapiens 60-63 24080471-6 2014 Results from recent studies are examined to establish whether the pre-requisites for effective NAC-induced antioxidant activity (i.e. GSH depletion and the presence of functional metabolic pathways for conversion of NAC to GSH) have received adequate consideration in the interpretation of the data. Glutathione 134-137 X-linked Kx blood group Homo sapiens 95-98 24080471-6 2014 Results from recent studies are examined to establish whether the pre-requisites for effective NAC-induced antioxidant activity (i.e. GSH depletion and the presence of functional metabolic pathways for conversion of NAC to GSH) have received adequate consideration in the interpretation of the data. Glutathione 223-226 X-linked Kx blood group Homo sapiens 95-98 24080471-7 2014 A key conclusion is a reinforcement of the concept that NAC should not be considered to be a powerful antioxidant in its own right: its strength is the targeted replenishment of GSH in deficient cells and it is likely to be ineffective in cells replete in GSH. Glutathione 178-181 X-linked Kx blood group Homo sapiens 56-59 24080471-7 2014 A key conclusion is a reinforcement of the concept that NAC should not be considered to be a powerful antioxidant in its own right: its strength is the targeted replenishment of GSH in deficient cells and it is likely to be ineffective in cells replete in GSH. Glutathione 256-259 X-linked Kx blood group Homo sapiens 56-59 24386148-6 2013 It was also found by MTT assay that NAC, which maintained the level of GSH in cells, could protect cells from death. Glutathione 71-74 X-linked Kx blood group Homo sapiens 36-39 23254439-10 2013 Z-VAD and N-acetyl cysteine (NAC; a well-known antioxidant) attenuated apoptotic cell death and GSH depletion in H(2)O(2)-treated CPAECs. Glutathione 96-99 X-linked Kx blood group Homo sapiens 29-32 23902724-8 2013 Furthermore, PCV2 replication in PK15 cells was significantly impaired after the elevation of intracellular GSH through treatment with the antioxidant N-acetyl-l-cysteine (NAC), a precursor in GSH synthesis. Glutathione 108-111 X-linked Kx blood group Homo sapiens 172-175 23352441-7 2013 Phagocytosis, the loss of MMP, autophagy and the activated signaling pathways were all suppressed by ROS scavenger N-acetyl-l-cysteine (NAC), H2O2 scavenger catalase or OH scavenger glutathione (GSH). Glutathione 182-193 X-linked Kx blood group Homo sapiens 136-139 23352441-7 2013 Phagocytosis, the loss of MMP, autophagy and the activated signaling pathways were all suppressed by ROS scavenger N-acetyl-l-cysteine (NAC), H2O2 scavenger catalase or OH scavenger glutathione (GSH). Glutathione 195-198 X-linked Kx blood group Homo sapiens 136-139 23533997-8 2013 This alantolactone-induced apoptosis and GSH depletion were effectively inhibited or abrogated by a thiol antioxidant, N-acetyl-L-cysteine (NAC). Glutathione 41-44 X-linked Kx blood group Homo sapiens 140-143 23902724-8 2013 Furthermore, PCV2 replication in PK15 cells was significantly impaired after the elevation of intracellular GSH through treatment with the antioxidant N-acetyl-l-cysteine (NAC), a precursor in GSH synthesis. Glutathione 193-196 X-linked Kx blood group Homo sapiens 172-175 22556393-10 2012 Elucidating the molecular mechanisms involved in the GSH-dependent and GSH-independent salutary effects of NAC should identify novel therapeutic targets for myocardial proteinopathies recently appreciated in human cardiomyopathies. Glutathione 53-56 X-linked Kx blood group Homo sapiens 107-110 22609960-7 2012 Treatment with a thiol antioxidant, NAC, showed the recovery of GSH depletion and the reduction of reactive oxygen species levels in MMPT-treated cells, which were accompanied by the inhibition of apoptosis. Glutathione 64-67 X-linked Kx blood group Homo sapiens 36-39 22584220-3 2012 Our results demonstrated that formation of the AM was greatly affected by the reductant used and the relative amounts of the AM formed were increased in the following order: NAC (17%) < l-Cys (53%) < ascorbic acid (61%) < GSH (100%). Glutathione 231-234 X-linked Kx blood group Homo sapiens 174-177 22940535-10 2012 NAC enhanced GSH levels and antioxidant capacity in the NTera-2 and NCCIT cells. Glutathione 13-16 X-linked Kx blood group Homo sapiens 0-3 23018672-2 2012 Previous research indicates that NAC serves as a precursor to L-cysteine (Cys), the rate-limiting substrate in the biosynthesis of glutathione (GSH), a potent, endogenous antioxidant. Glutathione 131-142 X-linked Kx blood group Homo sapiens 33-36 23018672-2 2012 Previous research indicates that NAC serves as a precursor to L-cysteine (Cys), the rate-limiting substrate in the biosynthesis of glutathione (GSH), a potent, endogenous antioxidant. Glutathione 144-147 X-linked Kx blood group Homo sapiens 33-36 23018672-3 2012 We hypothesized that NAC acts by liberating protein-bound Cys in plasma in an NAC concentration-dependent manner, which increases unbound Cys available for GSH biosynthesis. Glutathione 156-159 X-linked Kx blood group Homo sapiens 21-24 23018672-3 2012 We hypothesized that NAC acts by liberating protein-bound Cys in plasma in an NAC concentration-dependent manner, which increases unbound Cys available for GSH biosynthesis. Glutathione 156-159 X-linked Kx blood group Homo sapiens 78-81 22677204-7 2012 Also, during the treatment with AG and NAC, GSH concentration was increased compared to the untreated animals (p<0.05). Glutathione 44-47 X-linked Kx blood group Homo sapiens 39-42 22556393-10 2012 Elucidating the molecular mechanisms involved in the GSH-dependent and GSH-independent salutary effects of NAC should identify novel therapeutic targets for myocardial proteinopathies recently appreciated in human cardiomyopathies. Glutathione 71-74 X-linked Kx blood group Homo sapiens 107-110 21982895-4 2011 It was found that GSH-quercetin reacts with the thiol N-acetyl-L-cysteine (NAC) to form NAC-quercetin, whereas GSH-monoHER does not react with NAC. Glutathione 18-21 X-linked Kx blood group Homo sapiens 75-78 22487454-9 2012 The observed increase in current density was prevented by treatment with NAC, a precursor to GSH synthesis. Glutathione 93-96 X-linked Kx blood group Homo sapiens 73-76 20712400-5 2011 Moreover, a recent double-blind, placebo-controlled study demonstrated that add-on of N-acetyl-l-cysteine (NAC), a precursor of GSH, to antipsychotics improved the negative symptoms and reduced the side effects (akathisia) in patients with chronic schizophrenia. Glutathione 128-131 X-linked Kx blood group Homo sapiens 107-110 21982895-4 2011 It was found that GSH-quercetin reacts with the thiol N-acetyl-L-cysteine (NAC) to form NAC-quercetin, whereas GSH-monoHER does not react with NAC. Glutathione 18-21 X-linked Kx blood group Homo sapiens 88-91 21982895-4 2011 It was found that GSH-quercetin reacts with the thiol N-acetyl-L-cysteine (NAC) to form NAC-quercetin, whereas GSH-monoHER does not react with NAC. Glutathione 18-21 X-linked Kx blood group Homo sapiens 88-91 21337541-1 2011 N-acetyl-L-cysteine (NAC) is a thiol antioxidant that stimulates glutathione synthesis in cells. Glutathione 65-76 X-linked Kx blood group Homo sapiens 21-24 21641992-6 2011 Furthermore, pretreatment with NAC, a precursor of intracellular GSH, effectively abrogated gelomulide K-induced caspase-independent cell death and autophagy, suggesting that ROS-mediated downstream signaling is essential to the anticancer effects of gelomulide K. Glutathione 65-68 X-linked Kx blood group Homo sapiens 31-34 20164428-2 2010 In the current study, we demonstrate that alteration of glutathione-redox balance in macrophages by GSH donors like cell-permeable glutathione ethyl ester reduced or N-acetyl-L-cysteine (NAC) can differentially regulate production of IL-12 cytokine in macrophages. Glutathione 56-67 X-linked Kx blood group Homo sapiens 187-190 21135414-9 2011 However, although NAC is frequently utilized as a glutathione (GSH) precursor, the cytoprotection afforded by NAC in HK-2 cells was not a consequence of increased GSH levels. Glutathione 50-61 X-linked Kx blood group Homo sapiens 18-21 21135414-9 2011 However, although NAC is frequently utilized as a glutathione (GSH) precursor, the cytoprotection afforded by NAC in HK-2 cells was not a consequence of increased GSH levels. Glutathione 63-66 X-linked Kx blood group Homo sapiens 18-21 21550026-5 2011 N-acetyl-l-cysteine (NAC), a precursor of glutathione, reduced TNF-alpha secretion and increased [GSH]. Glutathione 42-53 X-linked Kx blood group Homo sapiens 21-24 21550026-5 2011 N-acetyl-l-cysteine (NAC), a precursor of glutathione, reduced TNF-alpha secretion and increased [GSH]. Glutathione 98-101 X-linked Kx blood group Homo sapiens 21-24 20164428-2 2010 In the current study, we demonstrate that alteration of glutathione-redox balance in macrophages by GSH donors like cell-permeable glutathione ethyl ester reduced or N-acetyl-L-cysteine (NAC) can differentially regulate production of IL-12 cytokine in macrophages. Glutathione 100-103 X-linked Kx blood group Homo sapiens 187-190 20663290-4 2010 Cellular GSH levels increased following treatment by NAC alone but were severely depleted by co-treatment with NAC and PQQ. Glutathione 9-12 X-linked Kx blood group Homo sapiens 53-56 20663290-4 2010 Cellular GSH levels increased following treatment by NAC alone but were severely depleted by co-treatment with NAC and PQQ. Glutathione 9-12 X-linked Kx blood group Homo sapiens 111-114 21509278-6 2009 CONCLUSION: These results indicate that NAC up-regulated the production of pro-inflammatory cytokines, and down regulated anti-inflammatory cytokine production by PBMC, in a process which may be associated with increased levels of glutathione (GSH). Glutathione 231-242 X-linked Kx blood group Homo sapiens 40-43 19549704-11 2009 Blocking ROS generation with N-acetyl-L-cysteine (NAC) significantly prevented GSH depletion and activation of ERK and JNK but not P38. Glutathione 79-82 X-linked Kx blood group Homo sapiens 50-53 19610656-6 2009 In-vitro incubation studies of intact RBCs with 1-chloro-2,4-dinitrobenzene (CDNB) and N-acetyl-L-cysteine (NAC) were found to significantly alter E(GSSG/2GSH) and/or glutathione oxidation kinetics (e.g., k(GSSG)) relative to normal controls based on their function as a toxic electrophilic compound and a competitive free radical scavenging/reducing agent, respectively. Glutathione 167-178 X-linked Kx blood group Homo sapiens 108-111 18695935-2 2009 Recently it has been proposed that NAC administration may modify the plasma levels of low molecular weight thiols (LMW) like cysteine, homocysteine and glutathione, though it has been still debated if their plasma concentration increases or decreases during the therapy. Glutathione 152-163 X-linked Kx blood group Homo sapiens 35-38 19374849-7 2009 The inhibitory effect of GSHee and NAC on HIF-1 binding activity was reversed by bis (2-chlorethyl)-nitrosourea, an oxidized glutathione (GSSG) reductase inhibitor which increases the concentration of GSSG. Glutathione 125-136 X-linked Kx blood group Homo sapiens 35-38 21509278-6 2009 CONCLUSION: These results indicate that NAC up-regulated the production of pro-inflammatory cytokines, and down regulated anti-inflammatory cytokine production by PBMC, in a process which may be associated with increased levels of glutathione (GSH). Glutathione 244-247 X-linked Kx blood group Homo sapiens 40-43 18193173-3 2008 We incubated five cell lines (hepatoma and lung-derived) with zinc chloride and 2 mmol/l N-acetyl-L-cysteine (NAC) to support glutathione synthesis. Glutathione 126-137 X-linked Kx blood group Homo sapiens 110-113 18437097-8 2008 Postresuscitation NAC treatment significantly attenuated the increase in cortical H2O2, but not NO, concentration during reoxygenation, with lower cerebral oxidized glutathione levels. Glutathione 165-176 X-linked Kx blood group Homo sapiens 18-21 18193173-4 2008 In all but one hepatic cell line, the glutathione content was increased by NAC as compared to the D-enantiomere NADC, whereas NADC did not increase GSH content as compared to not treated controls. Glutathione 38-49 X-linked Kx blood group Homo sapiens 75-78 18193173-9 2008 Furthermore, NAC acted as a GSH precursor only at cysteine medium concentrations of 10 micromol/l or below and therefore might be described as a poor cysteine repletor for glutathione synthesis. Glutathione 28-31 X-linked Kx blood group Homo sapiens 13-16 18193173-9 2008 Furthermore, NAC acted as a GSH precursor only at cysteine medium concentrations of 10 micromol/l or below and therefore might be described as a poor cysteine repletor for glutathione synthesis. Glutathione 172-183 X-linked Kx blood group Homo sapiens 13-16 17977519-7 2008 Furthermore, the addition of NAC that replenish intracellular GSH levels inhibited generation of H(2)O(2) and apoptosis in Th1 clones. Glutathione 62-65 X-linked Kx blood group Homo sapiens 29-32 17450321-1 2008 N-acetyl-L-cysteine (NAC), a precursor of L-cysteine, not only elevates the level of glutathione in both astrocytoma and astrocyte cultures, but also affects the cellular level of sulfane sulfur. Glutathione 85-96 X-linked Kx blood group Homo sapiens 21-24 20020852-3 2008 The GSH synthesis inhibitor L-Buthionine (S, R)-sulfoximine (BSO) significantly potentiated toxicity of clivorine, while GSH and GSH synthesis precursors N-Acetyl-L-cysteine (NAC) and S-adenosyl-L-methionine (SAM) protected cells against toxicity of clivorine. Glutathione 4-7 X-linked Kx blood group Homo sapiens 175-178 17504796-9 2007 NAC (5 mM) increased eosinophil glutathione content. Glutathione 32-43 X-linked Kx blood group Homo sapiens 0-3 17727829-6 2007 N-Acetyl-l-cysteine (NAC) pretreatment resulted in the increase in glutathione concentration, reduction of intracellular ROS, complete inhibition of DNA fragmentation, mitochondrial membrane potential (MMP) collapse, Fas externalization and caspase-8 activation. Glutathione 67-78 X-linked Kx blood group Homo sapiens 21-24 20020861-7 2008 The arsenite-induced HMOX1 expression was attenuated by the promoted glutathione (GSH) synthesis by N-acetyl-L-cysteine (NAC). Glutathione 69-80 X-linked Kx blood group Homo sapiens 121-124 20020861-7 2008 The arsenite-induced HMOX1 expression was attenuated by the promoted glutathione (GSH) synthesis by N-acetyl-L-cysteine (NAC). Glutathione 82-85 X-linked Kx blood group Homo sapiens 121-124 16497787-9 2006 Pretreatment with the glutathione precursor N-acetyl-l-cysteine (NAC) prevented DNA-strand breakage and apoptosis. Glutathione 22-33 X-linked Kx blood group Homo sapiens 65-68 17468103-1 2007 In murine embryonic fibroblasts, N-acetyl-L-cysteine (NAC), a GSH generating agent, enhances hypoxic apoptosis by blocking the NFkappaB survival pathway (Qanungo, S., Wang, M., and Nieminen, A. L. (2004) J. Biol. Glutathione 62-65 X-linked Kx blood group Homo sapiens 54-57 17456219-8 2007 NAC (1 mm) did not alter the fMLP-induced Ca(2+) signal but augmented the eosinophil content of reduced GSH and inhibited p47(phox)-p67(phox) translocation. Glutathione 104-107 X-linked Kx blood group Homo sapiens 0-3 17084062-8 2007 Furthermore only in one (of three) cell line tested a significant increase in GSH content by NAC as compared to NADC treatment was achieved. Glutathione 78-81 X-linked Kx blood group Homo sapiens 93-96 16167305-1 2006 N-acetyl-l-cysteine (NAC) is a well-known antioxidant that is capable of facilitating glutathione (GSH) biosynthesis and replenishing intracellular GSH under oxidatively challenging circumstances. Glutathione 86-97 X-linked Kx blood group Homo sapiens 21-24 16167305-1 2006 N-acetyl-l-cysteine (NAC) is a well-known antioxidant that is capable of facilitating glutathione (GSH) biosynthesis and replenishing intracellular GSH under oxidatively challenging circumstances. Glutathione 99-102 X-linked Kx blood group Homo sapiens 21-24 16167305-1 2006 N-acetyl-l-cysteine (NAC) is a well-known antioxidant that is capable of facilitating glutathione (GSH) biosynthesis and replenishing intracellular GSH under oxidatively challenging circumstances. Glutathione 148-151 X-linked Kx blood group Homo sapiens 21-24 16176268-6 2005 By contrast, the thiol antioxidants, N-acetyl-L-cysteine (NAC), GSH and dithiothreitol, which not only react with ROS, but also modulate the cellular redox potential by increasing intracellular levels of GSH and/or by acting as thiol reducing agents, afford almost complete protection and inhibit the progression of hA-evoked apoptosis. Glutathione 204-207 X-linked Kx blood group Homo sapiens 58-61 16298762-4 2006 Both, LA and NAC, markedly reduced the increase in cell oxidants and the reduction in glutathione concentrations in the zinc deficient cells. Glutathione 86-97 X-linked Kx blood group Homo sapiens 13-16 15934011-6 2005 The addition of glutathione (GSH) precursor NAC led to decrease the induction of COX-2 mRNA gene expression and cytotoxicity by both N2 and Endomethasone (p < 0.05). Glutathione 16-27 X-linked Kx blood group Homo sapiens 44-47 12900770-7 2003 According to recent studies using cell lines and animal models N-acetyl-L-cysteine (NAC), a GSH precursor, does not hamper the myeloablative effect of busulfan during conditioning. Glutathione 92-95 X-linked Kx blood group Homo sapiens 84-87 15890017-4 2005 Treatment of cells with NAC resulted in significant augmentation of intracellular small-molecular-weight thiols, glutathione and cysteine. Glutathione 113-124 X-linked Kx blood group Homo sapiens 24-27 16127296-2 2005 The antioxidant N-acetyl L-cysteine (NAC), a membrane-permeable aminothiol, is a sulfhydryl reductant reducing oxidised glutathione, as well as being a precursor of intracellular cysteine and glutathione. Glutathione 120-131 X-linked Kx blood group Homo sapiens 37-40 16127296-2 2005 The antioxidant N-acetyl L-cysteine (NAC), a membrane-permeable aminothiol, is a sulfhydryl reductant reducing oxidised glutathione, as well as being a precursor of intracellular cysteine and glutathione. Glutathione 192-203 X-linked Kx blood group Homo sapiens 37-40 15375156-7 2004 NAC-mediated enhancement of apoptosis was mimicked by incubating cells with GSH monoester, which increased intracellular GSH similarly to NAC. Glutathione 76-79 X-linked Kx blood group Homo sapiens 0-3 15375156-7 2004 NAC-mediated enhancement of apoptosis was mimicked by incubating cells with GSH monoester, which increased intracellular GSH similarly to NAC. Glutathione 76-79 X-linked Kx blood group Homo sapiens 138-141 15375156-7 2004 NAC-mediated enhancement of apoptosis was mimicked by incubating cells with GSH monoester, which increased intracellular GSH similarly to NAC. Glutathione 121-124 X-linked Kx blood group Homo sapiens 0-3 15375156-11 2004 In conclusion, NAC enhanced hypoxic apoptosis by a mechanism apparently involving GSH-dependent suppression of NFkappaB transactivation. Glutathione 82-85 X-linked Kx blood group Homo sapiens 15-18 14687762-9 2004 Addition of the sulfhydryl compounds; glutathione (GSH), N-acetyl-L-cysteine (NAC), L-cysteine or D-penicillamine significantly enhanced the rate of CN- release. Glutathione 51-54 X-linked Kx blood group Homo sapiens 78-81 14644566-1 2003 The thiol N-acetyl-L-cysteine (NAC) is a source of cysteine for the synthesis of the endogenous antioxidant glutathione (GSH) which is depleted by ultraviolet radiation. Glutathione 108-119 X-linked Kx blood group Homo sapiens 31-34 14644566-1 2003 The thiol N-acetyl-L-cysteine (NAC) is a source of cysteine for the synthesis of the endogenous antioxidant glutathione (GSH) which is depleted by ultraviolet radiation. Glutathione 121-124 X-linked Kx blood group Homo sapiens 31-34 14644566-8 2003 NAC significantly reduced the DNA damage produced in lung fibroblasts depleted of normal GSH protection by the glutamylcysteinyl synthetase inhibitor, L-buthionine-[S,R]-sulfoximine. Glutathione 89-92 X-linked Kx blood group Homo sapiens 0-3 14644566-9 2003 Although the specific mechanism of NAC protection has not yet been elucidated, these results support the hypothesis that NAC may protect the cells directly, by scavenging ROS induced by UVA and visible radiation, and indirectly by donating cysteine for GSH synthesis. Glutathione 253-256 X-linked Kx blood group Homo sapiens 121-124 15853972-9 2005 The addition of glutathione (GSH) precursor NAC inhibited the nicotine-induced HO-1 protein expression (p < 0.05). Glutathione 16-27 X-linked Kx blood group Homo sapiens 44-47 15576159-7 2005 The addition of glutathione (GSH) precursor NAC led to decrease the induction of COX-2 mRNA gene expression and cytotoxicity by both AH26 and Topseal (p<0.05). Glutathione 16-27 X-linked Kx blood group Homo sapiens 44-47 15798812-5 2004 In conclusion, the daily doses of NAC necessary for the total recuperation of plasma cysteine and glutathione levels in HIV-infected patients and the additional benefits following the supplementation of NAC in patients submitted to anti-retroviral therapy, need to be studied further. Glutathione 98-109 X-linked Kx blood group Homo sapiens 34-37 15673194-6 2004 Manganese (Mn)-TBAP, a mitochondria-specific SOD mimetic agent and NAC/GSH (N-acetyl cysteine/ reduced glutathione) reduced the YHT-induced cytotoxicity and decreased the number of the YHT-induced apoptotic cells. Glutathione 103-114 X-linked Kx blood group Homo sapiens 67-70 14640786-5 2003 BSO decreased the cellular GSH level and increased cellular reactive oxygen species (ROS) in PC-3 cells, whereas alpha-lipoic acid and NAC increased the GSH level and decreased cellular ROS. Glutathione 153-156 X-linked Kx blood group Homo sapiens 135-138 14612554-11 2003 Taken together, these results suggest that the biological effects of SFN and SFN-NAC on the induction of ARE-related gene expression and apoptosis could be different from each other; however, the different effects on ARE-related gene expression and apoptosis elicited by SFN can be blocked by the addition of GSH. Glutathione 309-312 X-linked Kx blood group Homo sapiens 81-84 12537962-6 2003 NAC blocked intracellular ROS formation and GSH depletion, but Z-DEVD-fmk did not. Glutathione 44-47 X-linked Kx blood group Homo sapiens 0-3 12584558-10 2003 Nrf2 induces the production of Glutathione (GSH) and we demonstrated that N-acetyl L-cysteine (NAC), a precursor to GSH, protected cells from Fas-mediated killing. Glutathione 31-42 X-linked Kx blood group Homo sapiens 95-98 12584558-10 2003 Nrf2 induces the production of Glutathione (GSH) and we demonstrated that N-acetyl L-cysteine (NAC), a precursor to GSH, protected cells from Fas-mediated killing. Glutathione 116-119 X-linked Kx blood group Homo sapiens 95-98 12404184-6 2002 Incubation of HAECs with high glucose in the presence of 10 mmol/L NAC prevented the drop of intracellular GSH content, and decreased both ROS generation and the number of cells committed to apoptosis. Glutathione 107-110 X-linked Kx blood group Homo sapiens 67-70 12198013-7 2002 RESULTS: From period 1 to period 2 the concentration and the absolute synthesis rate of GSH increased significantly (P < 0.05) in the NAC group but not in the control group. Glutathione 88-91 X-linked Kx blood group Homo sapiens 137-140 12385779-10 2002 In addition, NAC treatment also limited the GSH depletion in OTA-exposed PT- and LLC-PK(1) cells. Glutathione 44-47 X-linked Kx blood group Homo sapiens 13-16 12176728-5 2002 Supplementation of cellular GSH with N-acetyl-l-cysteine (NAC) did not reverse the inhibitory effects of TNF-alpha on troponin I promoter activation and only partially restored creatine kinase activity in TNF-alpha-treated cells. Glutathione 28-31 X-linked Kx blood group Homo sapiens 58-61 12198013-8 2002 The increases in the GSH concentration and synthesis rate were approximately 150% and 510% greater, respectively, in the NAC group than in the control group. Glutathione 21-24 X-linked Kx blood group Homo sapiens 121-124 11516525-7 2001 Pretreatment of fibroblasts with N-acetyl-L-cysteine (NAC), a GSH biosynthesis precursor, prevented both lipid peroxidation and cell death induced by thiram exposure. Glutathione 62-65 X-linked Kx blood group Homo sapiens 54-57 11841837-4 2002 Dethiolation is dependent on the availability of GSH and thiols, since it is inhibited by GSH-depleting agents and improved by N-acetyl-L-cysteine (NAC). Glutathione 49-52 X-linked Kx blood group Homo sapiens 148-151 11841839-6 2002 On the other hand, KE-758 as well as a high concentration of NAC significantly increased the level of intracellular GSH. Glutathione 116-119 X-linked Kx blood group Homo sapiens 61-64 11719447-1 2001 The thiol N-acetyl-L-cysteine (NAC), an analogue and precursor of reduced glutathione, has cancer chemopreventive properties attributable to its nucleophilicity, antioxidant activity, and a variety of other mechanisms. Glutathione 74-85 X-linked Kx blood group Homo sapiens 31-34 12019068-4 2002 In agreement, N-acetyl-L-cysteine (NAC), which is a precursor of glutathione and an ROS scavenger, inhibited the candidacidal activity of hLF(1-11). Glutathione 65-76 X-linked Kx blood group Homo sapiens 35-38 11812921-10 2002 Acrylamide reduced GSH levels in SHE cells, and cotreatment with acrylamide and NAC prevented the acrylamide-induced reduction of GSH. Glutathione 19-22 X-linked Kx blood group Homo sapiens 80-83 11812921-10 2002 Acrylamide reduced GSH levels in SHE cells, and cotreatment with acrylamide and NAC prevented the acrylamide-induced reduction of GSH. Glutathione 130-133 X-linked Kx blood group Homo sapiens 80-83 11298119-11 2001 In addition, the expression of CD30 was down regulated by GSH and NAC, suggesting that CD30 expression is dependent on IL-4, or modified by NAC. Glutathione 58-61 X-linked Kx blood group Homo sapiens 140-143 10813654-11 2000 The major products formed in the reaction of PAT with GSH were of the same structural type as obtained with NAC. Glutathione 54-57 X-linked Kx blood group Homo sapiens 108-111 11298119-1 2001 The thiol antioxidant N-acetyl- L-cysteine (NAC), known as a precursor of glutathione (GSH), is used in AIDS treatment trials, as a chemoprotectant in cancer chemotherapy and in treatment of chronic bronchitis. Glutathione 74-85 X-linked Kx blood group Homo sapiens 44-47 11298119-1 2001 The thiol antioxidant N-acetyl- L-cysteine (NAC), known as a precursor of glutathione (GSH), is used in AIDS treatment trials, as a chemoprotectant in cancer chemotherapy and in treatment of chronic bronchitis. Glutathione 87-90 X-linked Kx blood group Homo sapiens 44-47 10852765-9 2000 In conclusion, the administration of high doses of NAC added to GSH significantly decreased the peroxidative stress of patients with septic shock. Glutathione 64-67 X-linked Kx blood group Homo sapiens 51-54 9277499-8 1997 NAC caused an expected dramatic increase in the reduced glutathione (GSH) levels in EC. Glutathione 56-67 X-linked Kx blood group Homo sapiens 0-3 11228747-5 1999 Pretreatment of BPAECs with N-acetyl-L-cysteine (NAC) or 2-mercaptopropionylglycine (MPG) blocked ROS-induced changes in intracellular GSH and PLD activation. Glutathione 135-138 X-linked Kx blood group Homo sapiens 49-52 11228747-8 1999 Furthermore, NAC blocked diamide- or BSO-mediated changes in GSH levels, PLD activity, and protein tyrosine phosphorylation. Glutathione 61-64 X-linked Kx blood group Homo sapiens 13-16 9659525-6 1998 Furthermore, NAC can easily be deacetylated to cysteine, an important precursor of cellular glutathione synthesis, and thus stimulate the cellular glutathione system. Glutathione 92-103 X-linked Kx blood group Homo sapiens 13-16 9659525-6 1998 Furthermore, NAC can easily be deacetylated to cysteine, an important precursor of cellular glutathione synthesis, and thus stimulate the cellular glutathione system. Glutathione 147-158 X-linked Kx blood group Homo sapiens 13-16 9545559-2 1998 We determined the effects of N-acetyl-L-cysteine (NAC), which increases the intracellular GSH levels, on the induction of HSP70 and MT gene expression in a cultured cell line of human amniotic cells (WISH) exposed to CdCl2. Glutathione 90-93 X-linked Kx blood group Homo sapiens 50-53 9545559-4 1998 The treatment of WISH cells with 1.5 and 30 mM NAC for 2 h increased the intracellular GSH levels by 1.4- and 3.1-fold, respectively. Glutathione 87-90 X-linked Kx blood group Homo sapiens 47-50 10681368-10 2000 In the presence of NAC or GSH, such covalent binding was inhibited and the NAC or GSH adducts were formed. Glutathione 26-29 X-linked Kx blood group Homo sapiens 19-22 10681368-10 2000 In the presence of NAC or GSH, such covalent binding was inhibited and the NAC or GSH adducts were formed. Glutathione 26-29 X-linked Kx blood group Homo sapiens 75-78 10681368-10 2000 In the presence of NAC or GSH, such covalent binding was inhibited and the NAC or GSH adducts were formed. Glutathione 82-85 X-linked Kx blood group Homo sapiens 19-22 9480824-6 1998 On the contrary, the antioxidant N-acetyl-L-cysteine (NAC) fully blocks the dRib-induced apoptosis by preventing GSH depletion, while it also inhibits actin-filament-network disruption and mitochondrial depolarization. Glutathione 113-116 X-linked Kx blood group Homo sapiens 54-57 9277499-8 1997 NAC caused an expected dramatic increase in the reduced glutathione (GSH) levels in EC. Glutathione 69-72 X-linked Kx blood group Homo sapiens 0-3 9277499-11 1997 Our data also demonstrate that NAC increases the GSH-to-GSSG ratio within the EC suggesting one possible mechanism through which this antioxidant inhibits agonist-induced monocyte adhesion to EC. Glutathione 49-52 X-linked Kx blood group Homo sapiens 31-34 9013992-6 1997 Restoration of GSH levels in SF T cells with N-acetyl-L-cysteine (NAC), enhanced mitogenic induced proliferative responses and IL-2 production. Glutathione 15-18 X-linked Kx blood group Homo sapiens 66-69 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). Glutathione 201-212 X-linked Kx blood group Homo sapiens 124-127 9188453-9 1997 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction of transcription factor c-fos all were inhibited by NAC and DPI as well as an antioxidant pyrrolidine dithiocarbamate or reduced glutathione (GSH). Glutathione 214-217 X-linked Kx blood group Homo sapiens 124-127 9043953-3 1997 Increasing the concentration of intracellular GSH by means of N-acetyl-L-cysteine (NAC) and GSH ethyl ester (OEt) resulted in total protection against cell death, while inhibiting GSH synthesis with buthionine sulfoximine (BSO) greatly enhanced cell sensitivity to Fas and CD2 apoptotic signaling. Glutathione 46-49 X-linked Kx blood group Homo sapiens 83-86 7811547-1 1994 N-Acetyl-L-cysteine (NAC) and L-2-oxothiazolidine 4-carboxylate (OTC) are pro-GSH drugs that been proposed for AIDS therapy. Glutathione 78-81 X-linked Kx blood group Homo sapiens 21-24 7996046-3 1994 Buthionine sulfoximine did not affect NAC-mediated enhanced HIV-1 replication, indicating that the NAC-mediated effects are glutathione-independent. Glutathione 124-135 X-linked Kx blood group Homo sapiens 99-102 7811547-4 1994 To test whether this difference is due to GSH conversion efficacies of these compounds, we measured GSH restoration by NAC or OTC in GSH-depleted peripheral blood mononuclear cells (PBMCs), using flow cytometry. Glutathione 100-103 X-linked Kx blood group Homo sapiens 119-122 7811547-4 1994 To test whether this difference is due to GSH conversion efficacies of these compounds, we measured GSH restoration by NAC or OTC in GSH-depleted peripheral blood mononuclear cells (PBMCs), using flow cytometry. Glutathione 100-103 X-linked Kx blood group Homo sapiens 119-122 7811547-5 1994 In isolated PBMCs, NAC fully replenishes depleted intracellular GSH whereas OTC only minimally replenishes GSH. Glutathione 64-67 X-linked Kx blood group Homo sapiens 19-22 7811547-6 1994 This ability to replenish GSH in vitro and its ability to scavenge free radicals directly explain why NAC has more potent antiviral activities in vitro. Glutathione 26-29 X-linked Kx blood group Homo sapiens 102-105 7915123-3 1994 We tested the effects of BHA, a phenolic, lipid-soluble, chain-breaking antioxidant, and NAC, a known glutathione precursor with some direct free-radical scavenging properties as well, on the regulation of HIV-1 expression in latently infected U1 cells and in productively and chronically infected U937 cells. Glutathione 102-113 X-linked Kx blood group Homo sapiens 89-92 7828989-7 1994 The concentrations of alpha-tocopherol and glutathione in the blood of NAC patients were in contrast not substantially different from those of healthy controls. Glutathione 43-54 X-linked Kx blood group Homo sapiens 71-74 8194136-3 1994 We confirmed that N-acetyl-L-cysteine (NAC), a cysteine prodrug which maintains intracellular GSH levels during oxidative stress, inhibits in the chronically infected U1 cells, the stimulation of HIV replication induced by phorbol 12-myristate 13-acetate (PMA), interleukin-6 (IL-6) or granulocyte-macrophage colony stimulating factor (GM-CSF). Glutathione 94-97 X-linked Kx blood group Homo sapiens 39-42 8194136-9 1994 GSH assays showed that treatment of U937 and Jurkat T-cells with NAC and OTC moderately increased the GSH level, while HC led to a significantly higher increase of the thiol level. Glutathione 0-3 X-linked Kx blood group Homo sapiens 65-68 8194136-9 1994 GSH assays showed that treatment of U937 and Jurkat T-cells with NAC and OTC moderately increased the GSH level, while HC led to a significantly higher increase of the thiol level. Glutathione 102-105 X-linked Kx blood group Homo sapiens 65-68 7953744-7 1994 Intracellular GSH was increased by incubation with rADF for 24 h, as it is with 2-ME and NAC. Glutathione 14-17 X-linked Kx blood group Homo sapiens 89-92 8238538-2 1993 Since N-acetyl-L-cysteine (NAC) increases glutathione (GSH) levels in vivo and scavenges oxygen radicals in vitro, we tested the effect of NAC given intravenously on lung changes following intratracheal IL-1 administration. Glutathione 42-53 X-linked Kx blood group Homo sapiens 27-30 8238538-2 1993 Since N-acetyl-L-cysteine (NAC) increases glutathione (GSH) levels in vivo and scavenges oxygen radicals in vitro, we tested the effect of NAC given intravenously on lung changes following intratracheal IL-1 administration. Glutathione 55-58 X-linked Kx blood group Homo sapiens 27-30 8238538-5 1993 The latter findings are consistent with the possibility that NAC is enhancing GSH or other sulfhydryls and, as a result, reducing oxidative stress due to H2O2 or H2O2-derived products. Glutathione 78-81 X-linked Kx blood group Homo sapiens 61-64 1530678-9 1992 NAC produced significant increases of plasma cysteine concentrations, and a slight but insignificantly increase of plasma glutathione. Glutathione 122-133 X-linked Kx blood group Homo sapiens 0-3 8148757-2 1993 It has been postulated that NAC may protect lung cells from inhaled oxidants or oxidants produced by inflammatory leukocytes by increasing intra and extra cellular GSH. Glutathione 164-167 X-linked Kx blood group Homo sapiens 28-31 2112750-2 1990 NAC, which replenishes intracellular glutathione, effectively inhibits the tumor necrosis factor alpha- or phorbol ester-stimulated replication of HIV in acutely infected cell cultures. Glutathione 37-48 X-linked Kx blood group Homo sapiens 0-3