PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11476185-7 2001 In these animals, CCl4 increased the hepatic glutathione level instead while the NOS activity remained unchanged. Glutathione 45-56 chemokine (C-C motif) ligand 4 Mus musculus 18-22 9585092-3 1998 Increases in hepatic lipid peroxide (LPO) concentrations and decreases in hepatic GSH concentrations after the CCl4 injection were significantly diminished by the gamma-GCE (160 micromol/kg) administration, but not by the same dose of GSH. Glutathione 82-85 chemokine (C-C motif) ligand 4 Mus musculus 111-115 10999435-6 2000 A. lappa reversed the decrease in GSH and P-450 induced by CCl4 and acetaminophen. Glutathione 34-37 chemokine (C-C motif) ligand 4 Mus musculus 59-63 10375774-0 1998 Structure-activity relationship of schisandrins in enhancing liver mitochondrial glutathione status in CCl4-poisoned mice. Glutathione 81-92 chemokine (C-C motif) ligand 4 Mus musculus 103-107 9635418-4 1998 A decrease in hepatic GSH concentration after the CCl4 injection was significantly diminished by the gamma-GCE administration, but not by the GSH administration. Glutathione 22-25 chemokine (C-C motif) ligand 4 Mus musculus 50-54 9635418-6 1998 These results indicate that gamma-GCE can attenuate CCl4-induced hepatic TG accumulation in mice through the maintenance of hepatic GSH level. Glutathione 132-135 chemokine (C-C motif) ligand 4 Mus musculus 52-56 10821428-8 2000 The difference in hepatoprotective action against CCl4 toxicity between Sch B and DDB may therefore be related to their ability to maintain hepatic mitochondrial glutathione redox status under oxidative stress condition. Glutathione 162-173 chemokine (C-C motif) ligand 4 Mus musculus 50-54 9703894-0 1998 Elevation of mouse liver glutathione level by low-dose gamma-ray irradiation and its effect on CCl4-induced liver damage. Glutathione 25-36 chemokine (C-C motif) ligand 4 Mus musculus 95-99 9703894-2 1998 The liver GSH level increased soon after irradiation with 50 cGy of gamma-rays, reached a maximum at around 12 post-treatment, and returned almost to the control level by 24 h. The activities of glutathione reductase, and glutathione peroxidase also showed the same pattern of change, while the activity of gamma-glutamylcysteine synthetase showed a gradual increase up to 24 h. The effect of pre-irradiation on CCl4-induced liver damage was also investigated. Glutathione 10-13 chemokine (C-C motif) ligand 4 Mus musculus 412-416 9585092-5 1998 These results indicate that gamma-GCE attenuates the progression of CCl4-induced acute liver injury in mice through the maintenance of hepatic GSH levels, leading to inhibition of hepatic LPO formation, which could be due to an efficient utilization of GSH converted from gamma-GCE in the liver cells. Glutathione 143-146 chemokine (C-C motif) ligand 4 Mus musculus 68-72 9585092-5 1998 These results indicate that gamma-GCE attenuates the progression of CCl4-induced acute liver injury in mice through the maintenance of hepatic GSH levels, leading to inhibition of hepatic LPO formation, which could be due to an efficient utilization of GSH converted from gamma-GCE in the liver cells. Glutathione 253-256 chemokine (C-C motif) ligand 4 Mus musculus 68-72 8891674-7 1996 While the CCl4 intoxication greatly impaired mitochondrial glutathione redox status, the beneficial effect of Sch B treatment became more evident after CCl4 challenge. Glutathione 59-70 chemokine (C-C motif) ligand 4 Mus musculus 10-14 9465504-11 1998 Feeding of Pk extract in CCl4-treated mice caused significantly less alteration of serum ALT, AST, liver GSH [8.9 (0.7) micrograms/mg protein], -SH, G6PD, catalase and membrane-bound Na+/K+ ATPase [270.8 (21.3) nmole pi released/min/mg protein]. Glutathione 105-108 chemokine (C-C motif) ligand 4 Mus musculus 25-29 9065729-15 1997 Whereas AAP or CCl4 treatment resulted in 70-80% reduction in hepatic GSH levels, pretreatment of mice with 2-AP caused a 40-210% elevation in hepatic GSH levels, as compared with either AAP or CCl4 alone. Glutathione 70-73 chemokine (C-C motif) ligand 4 Mus musculus 15-19 8986130-5 1996 The differential effect of Sch B and BHT treatment on hepatic mitochondrial glutathione status became more apparent after carbon tetrachloride (CCl4) challenge. Glutathione 76-87 chemokine (C-C motif) ligand 4 Mus musculus 144-148 8986130-6 1996 Pretreatment with Sch B could sustain the hepatic mitochondrial GSH level in CCl4-intoxicated mice and protect against CCl4 hepatotoxicity. Glutathione 64-67 chemokine (C-C motif) ligand 4 Mus musculus 77-81 8884991-4 1996 Hepatic LPO level slightly increased once during the first 4 hr after CCl4 treatment and a marked increase in the level occurred later than 12 h, while serum LPO level increased later than 12 h. Hepatic GSH level decreased rapidly during the first 4 hr after CCl4 treatment and the decreased level recovered slowly thereafter, although the recovered level did not reach the control level. Glutathione 203-206 chemokine (C-C motif) ligand 4 Mus musculus 70-74 8884991-4 1996 Hepatic LPO level slightly increased once during the first 4 hr after CCl4 treatment and a marked increase in the level occurred later than 12 h, while serum LPO level increased later than 12 h. Hepatic GSH level decreased rapidly during the first 4 hr after CCl4 treatment and the decreased level recovered slowly thereafter, although the recovered level did not reach the control level. Glutathione 203-206 chemokine (C-C motif) ligand 4 Mus musculus 259-263 8135659-4 1993 The ascorbate esters markedly attenuated CCl4-induced alterations such as reductions in ascorbate content and hepatic glutathione S-transferase (GST) activity, and increases in glutathione and calcium content and serum GST activity. Glutathione 118-129 chemokine (C-C motif) ligand 4 Mus musculus 41-45 1490281-2 1992 against the hepatotoxic effects of CCl4 and T1-acetate, which were manifested by increased peroxidation of lipids and increased depletion of reduced glutathion in liver homogenates. Glutathione 149-159 chemokine (C-C motif) ligand 4 Mus musculus 35-39 34207230-4 2021 Our results showed that baicalein or Fer-1 supplementation significantly attenuated CCl4 exposure-induced elevations of serum alanine aminotransferase and aspartate aminotransferase, and malondialdehyde levels in the liver tissues and unregulated glutathione levels. Glutathione 247-258 chemokine (C-C motif) ligand 4 Mus musculus 84-88 1598594-4 1992 (3) HSS could restore the liver glutathione contents lowered by CCl4-intoxication. Glutathione 32-43 chemokine (C-C motif) ligand 4 Mus musculus 64-68 1442065-7 1992 Analyzing through multiple linear correlation, we showed that the lowering of SGPT was negatively related to the increase of GSH, positively related to the decrease of MDA in mice given CCl4 or acetaminophen in combination with ASI or SK. Glutathione 125-128 chemokine (C-C motif) ligand 4 Mus musculus 186-190 32940351-10 2020 Moreover, the RAFF pretreatment also significantly decreased the liver malondialdehyde activity and prevented the CCl4 -induced decrease in liver superoxide dismutase, glutathione peroxidase, catalase, and reduced glutathione levels. Glutathione 168-179 chemokine (C-C motif) ligand 4 Mus musculus 114-118 4085456-3 1985 A significant decrease in the SOD and GSH-Px activities in liver extracts and an increase of serum ALP of hepatic origin were found in CCl4-treated animals. Glutathione 38-41 chemokine (C-C motif) ligand 4 Mus musculus 135-139 33308125-7 2021 RESULTS: Administration of CCL4 resulted in oxidative dysregulation, including significant reductions in reduced glutathione and concomitant elevations in the level of malondialdehyde (MDA). Glutathione 113-124 chemokine (C-C motif) ligand 4 Mus musculus 27-31 3816733-6 1986 The addition of diethyl maleate (0.25 mM), which depletes intracellular glutathione (GSH)-potentiated CHCl3 and CCl4 toxicity. Glutathione 72-83 chemokine (C-C motif) ligand 4 Mus musculus 112-116 3816733-6 1986 The addition of diethyl maleate (0.25 mM), which depletes intracellular glutathione (GSH)-potentiated CHCl3 and CCl4 toxicity. Glutathione 85-88 chemokine (C-C motif) ligand 4 Mus musculus 112-116 3816733-8 1986 These results suggest that: in mouse hepatocytes, both CHCl3 and CCl4 are metabolized to toxic components by the MFOS; GSH plays a role in detoxifying those metabolites; free radicals are produced during the metabolism of CHCl3 and CCl4; and free radicals may be important mediators of the toxicity of these two halomethanes. Glutathione 119-122 chemokine (C-C motif) ligand 4 Mus musculus 65-69 3816733-8 1986 These results suggest that: in mouse hepatocytes, both CHCl3 and CCl4 are metabolized to toxic components by the MFOS; GSH plays a role in detoxifying those metabolites; free radicals are produced during the metabolism of CHCl3 and CCl4; and free radicals may be important mediators of the toxicity of these two halomethanes. Glutathione 119-122 chemokine (C-C motif) ligand 4 Mus musculus 232-236 32535387-7 2020 The results showed that in WT mice DNLA reduced CCl4-induced liver injury, accompanied by a significant reduction in CCl4-induced mitochondrial oxidative stress as evidenced by a decrease in mitochondrial H2O2 content and MDA production, and a marked increase in GSH level and Mn-SOD activity. Glutathione 263-266 chemokine (C-C motif) ligand 4 Mus musculus 117-121 32121508-7 2020 However, CCl4 markedly reduced the hepatic GSH levels only in the weaning mice. Glutathione 43-46 chemokine (C-C motif) ligand 4 Mus musculus 9-13 32544869-5 2020 In addition, Sal alleviated CCl4-primed oxidative stress and inflammatory response by restoring hepatic glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and inhibiting cytokines. Glutathione 104-115 chemokine (C-C motif) ligand 4 Mus musculus 28-32 32544869-5 2020 In addition, Sal alleviated CCl4-primed oxidative stress and inflammatory response by restoring hepatic glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and inhibiting cytokines. Glutathione 117-120 chemokine (C-C motif) ligand 4 Mus musculus 28-32 30501137-2 2020 The results showed that the renal damage induced by CCl4 was associated with a rise in oxidative stress monitored by a significant increase of TBARS and PCO levels (+89% and +136% respectively, p < .001) and a significant decrease of GSH level (-68%, p < .001) and antioxidants enzymes such as SOD, CAT, and GPX activities (-41.7%, -47.8%, and -50.5%; p < .001, respectively). Glutathione 234-237 chemokine (C-C motif) ligand 4 Mus musculus 52-56 31193831-7 2019 The of aminotransferase serum activity and malondialdehyde hepatic activity were elevated (P < 0.015) after treatment with CCl4, while the related liver enzymatic activities and glutathione concentration were lower. Glutathione 181-192 chemokine (C-C motif) ligand 4 Mus musculus 126-130 31168820-6 2019 Oral administration of CuA-SEN to CCl4 -induced hepatotoxicity mice markedly increased the levels of superoxide dismutase, glutathione and catalase in serum. Glutathione 123-134 chemokine (C-C motif) ligand 4 Mus musculus 34-38 30322375-6 2018 RESULTS: CCl4 administration increased liver weight, decreased body weight, elevated plasma alanine aminotransferase, and aspartate aminotransferase and increased liver oxidative stress (malondialdehyde and glutathione). Glutathione 207-218 chemokine (C-C motif) ligand 4 Mus musculus 9-13 30713662-4 2019 In addition, exposure to APAP or CCl4 resulted in an increased content of malonaldehyde as well as a decreased ratio of reduced to oxidized glutathione, and a decreased level of superoxide dismutase and catalase activity in the liver (p < 0.05); however, pretreatment with DAS restored the perturbations of the antioxidant system in the liver. Glutathione 140-151 chemokine (C-C motif) ligand 4 Mus musculus 33-37 30142916-9 2018 By evaluating the liver catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) activity, and further using a single agent to evaluate the oxidative stress in CCl4-induced hepatotoxicity by immunofluorescence staining, maltol dramatically attenuated the reduction levels of hepatic CAT, GSH and SOD, and the over-expression levels of CYP2E1 and HO-1. Glutathione 293-296 chemokine (C-C motif) ligand 4 Mus musculus 165-169 30150561-7 2018 The CCl4-induced oxidative stress in liver was significantly ameliorated by eckol, which was characterized by reduced malondialdehyde (MDA) formations, and enhanced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) content. Glutathione 193-204 chemokine (C-C motif) ligand 4 Mus musculus 4-8 30150561-7 2018 The CCl4-induced oxidative stress in liver was significantly ameliorated by eckol, which was characterized by reduced malondialdehyde (MDA) formations, and enhanced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) content. Glutathione 217-220 chemokine (C-C motif) ligand 4 Mus musculus 4-8 29108440-2 2018 Administration of a single dose of CCl4 caused cardio toxicity as monitored by an increase in lipid peroxidation (thiobarbituric acid reactive substances), protein carbonyl level and antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione and vitamin C) in the heart tissue. Glutathione 236-247 chemokine (C-C motif) ligand 4 Mus musculus 35-39 27151496-12 2016 Isorhamnetin attenuated the CCl4-induced increase in the number of 4-hydroxynonenal and nitrotyrosine-positive cells, and prevented glutathione depletion. Glutathione 132-143 chemokine (C-C motif) ligand 4 Mus musculus 28-32 29549726-6 2018 CCl4 led to oxidative stress, supported by the reduced superoxide dismutase (SOD) activity and glutathione (GSH) levels, as well as enhanced malondialdehyde (MDA) and O2- levels in liver samples. Glutathione 95-106 chemokine (C-C motif) ligand 4 Mus musculus 0-4 29549726-6 2018 CCl4 led to oxidative stress, supported by the reduced superoxide dismutase (SOD) activity and glutathione (GSH) levels, as well as enhanced malondialdehyde (MDA) and O2- levels in liver samples. Glutathione 108-111 chemokine (C-C motif) ligand 4 Mus musculus 0-4 28396147-5 2017 Geraniin significantly reduced CCl4 induced lipid peroxidation, increase in amount of glutathione, glutathione reductase and Heme oxygenase-1 (HO-1). Glutathione 86-97 chemokine (C-C motif) ligand 4 Mus musculus 31-35 27746874-6 2016 RESULTS: CCl4-induced hepatotoxicity was manifested by an increase in the levels of ALT, AST, MDA, IL-6, CRP, and TNF-alpha, and a decrease in the SOD level and GSH/GSSG ratio in the serum. Glutathione 161-164 chemokine (C-C motif) ligand 4 Mus musculus 9-13 29636837-3 2018 The CCl4 treatment has significantly increased TBARS levels and reduced the antioxidant enzyme such as GSH, GPx, GR, GST, CAT, and SOD in group 2 compared to group 1, while the Zingerone treatment showed significant reduction in TBARS levels and increased the antioxidant enzymes in group 3 (CCl4 + Zingerone) as compared to group 2. Glutathione 103-106 chemokine (C-C motif) ligand 4 Mus musculus 4-8 29351226-4 2018 Curcumin pre-treatment at 50, 100 and 200 mg/kg significantly ameliorated CCl4-induced oxidative stress, characterized by decreased malondialdehyde (MDA) formations, and increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) content, followed by a decrease in caspase-9 and -3 activities. Glutathione 238-249 chemokine (C-C motif) ligand 4 Mus musculus 74-78 29351226-4 2018 Curcumin pre-treatment at 50, 100 and 200 mg/kg significantly ameliorated CCl4-induced oxidative stress, characterized by decreased malondialdehyde (MDA) formations, and increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) content, followed by a decrease in caspase-9 and -3 activities. Glutathione 251-254 chemokine (C-C motif) ligand 4 Mus musculus 74-78 29080450-4 2018 The exposure to a single dose of CCl4 caused cardiotoxicity expressed by an increase in lipid peroxidation (TBARS), protein carbonyls (PC) levels and in antioxidant markers (superoxide dismutase (SOD), catalase (CAT), gluthathione peroxidase (GPx), glutathione (GSH) and Vitamin C levels) in the CCl4-treated group when compared with the untreated group. Glutathione 262-265 chemokine (C-C motif) ligand 4 Mus musculus 33-37 28448545-3 2017 As seen previously, mice injected with CCl4 exhibited increased plasma levels of alanine aminotransferase, aspartate aminotransferase, and creatinine; transient body weight loss; and increased lipid peroxidation along with decreased total antioxidant power, glutathione, ATP, and NADPH. Glutathione 258-269 chemokine (C-C motif) ligand 4 Mus musculus 39-43 28246539-6 2017 Pretreatment with SLE not only decreased the content of MDA but increased SOD, GSH, and GSH-Px activities in the liver, suggesting that SLE attenuated CCl4-induced oxidative stress. Glutathione 88-91 chemokine (C-C motif) ligand 4 Mus musculus 151-155 27384427-5 2016 Acute liver injury, induced by CCl4, was evident from histological changes, such as cell necrosis, inflammation and apoptosis, and a concomitant reduction of glutathione (GSH) and GSH redox enzyme activities in the liver. Glutathione 158-169 chemokine (C-C motif) ligand 4 Mus musculus 31-35 27384427-5 2016 Acute liver injury, induced by CCl4, was evident from histological changes, such as cell necrosis, inflammation and apoptosis, and a concomitant reduction of glutathione (GSH) and GSH redox enzyme activities in the liver. Glutathione 171-174 chemokine (C-C motif) ligand 4 Mus musculus 31-35 27384427-5 2016 Acute liver injury, induced by CCl4, was evident from histological changes, such as cell necrosis, inflammation and apoptosis, and a concomitant reduction of glutathione (GSH) and GSH redox enzyme activities in the liver. Glutathione 180-183 chemokine (C-C motif) ligand 4 Mus musculus 31-35 25783052-6 2015 In addition, PC significantly counteracted the increase in glutathione levels and glutathione-S-transferase activity induced by CCl4. Glutathione 59-70 chemokine (C-C motif) ligand 4 Mus musculus 128-132 26441060-5 2016 In addition, tempol significantly ameliorated CCl4-induced lipid peroxidation and GSH depletion, and improved catalase activity. Glutathione 82-85 chemokine (C-C motif) ligand 4 Mus musculus 46-50 24611872-4 2014 After 24 h of CCl4 administration, an increase in the levels of transaminases aspartate aminotransferase and alanine aminotransferase activities and malondialdehyde concentration occurred and a significant decrease in superoxide dismutase, catalase glutathione-peroxidase activities, and glutathione levels was detected as well. Glutathione 249-260 chemokine (C-C motif) ligand 4 Mus musculus 14-18 25709018-7 2015 Mechanistic study results indicate that the administration of the CCl4- or APAP-injured mice with HJP enhanced SOD and GSH-Px and decreased MDA, indicating that anti-oxidation and detoxification could be the pathways for the liver protection observed. Glutathione 119-122 chemokine (C-C motif) ligand 4 Mus musculus 66-70 25471833-4 2014 Quercetin decreased the CCl4-increased malondialdehyde (MDA) and reduced the glutathione (GSH) amounts in the liver. Glutathione 77-88 chemokine (C-C motif) ligand 4 Mus musculus 24-28 25471833-4 2014 Quercetin decreased the CCl4-increased malondialdehyde (MDA) and reduced the glutathione (GSH) amounts in the liver. Glutathione 90-93 chemokine (C-C motif) ligand 4 Mus musculus 24-28 25338212-5 2014 In contrast, a significant reduction (p < 0.001) in glutathione and superoxide dismutase contents as well as the total protein level was evident in the CCl4-intoxicated mice. Glutathione 55-66 chemokine (C-C motif) ligand 4 Mus musculus 155-159 24726765-6 2014 Mechanistic studies revealed that blockade of HMGB1 attenuated CCl4-induced MDA accumulation along with improved SOD and GSH activity. Glutathione 121-124 chemokine (C-C motif) ligand 4 Mus musculus 63-67 21428416-5 2011 Lipid peroxidation was increased and hepatic glutathione content was decreased significantly after CCl4 treatment, and these changes were reduced by administration of 1. Glutathione 45-56 chemokine (C-C motif) ligand 4 Mus musculus 99-103 22634310-7 2012 CCl(4)-intoxication also enhanced hepatic lipid peroxidation, decreased hepatic GSH level and inhibited the activities of antioxidant enzymes. Glutathione 80-83 chemokine (C-C motif) ligand 4 Mus musculus 0-6 22515645-3 2012 Pretreatment with EAF (1000 mg/kg bw) prior to CCl4 administration significantly (p < 0.001) decreased the CCl4-elevated levels of serum AST, ALT, alkaline phosphatase, total bilirubin, and hepatic MDA in mice and prevented the increases in GSH, SOD, and CAT caused by CCl4. Glutathione 244-247 chemokine (C-C motif) ligand 4 Mus musculus 110-114 22515645-3 2012 Pretreatment with EAF (1000 mg/kg bw) prior to CCl4 administration significantly (p < 0.001) decreased the CCl4-elevated levels of serum AST, ALT, alkaline phosphatase, total bilirubin, and hepatic MDA in mice and prevented the increases in GSH, SOD, and CAT caused by CCl4. Glutathione 244-247 chemokine (C-C motif) ligand 4 Mus musculus 110-114 24803985-3 2014 Results showed that the group injected with CCL4 exhibited significantly higher levels of oxidative stress markers, MDA, and significantly lower concentrations of GSH, SOD and catalase. Glutathione 163-166 chemokine (C-C motif) ligand 4 Mus musculus 44-48 24137268-9 2013 The treatment with CCl4 was observed to increase the levels of aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH) and malondialdehyde (MDA) and decrease the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (Gpx) in the liver tissues of the mice. Glutathione 245-256 chemokine (C-C motif) ligand 4 Mus musculus 19-23 24137268-9 2013 The treatment with CCl4 was observed to increase the levels of aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH) and malondialdehyde (MDA) and decrease the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (Gpx) in the liver tissues of the mice. Glutathione 258-261 chemokine (C-C motif) ligand 4 Mus musculus 19-23 23611112-8 2013 However, the multiple administration of CCl4 to obese mice reduced the ratio of reduced glutathione to oxidized glutathione, superoxide dismutase activity and mitochondrial DNA copy number, leading to the development of chronic oxidative stress, increased numbers of apoptotic cells and increased levels of both tumour necrosis factor-alpha and transforming growth factor-beta mRNA. Glutathione 88-99 chemokine (C-C motif) ligand 4 Mus musculus 40-44 23611112-8 2013 However, the multiple administration of CCl4 to obese mice reduced the ratio of reduced glutathione to oxidized glutathione, superoxide dismutase activity and mitochondrial DNA copy number, leading to the development of chronic oxidative stress, increased numbers of apoptotic cells and increased levels of both tumour necrosis factor-alpha and transforming growth factor-beta mRNA. Glutathione 112-123 chemokine (C-C motif) ligand 4 Mus musculus 40-44 19242656-4 2009 The development of CCl4-induced acute liver failure altered the redox state with a decreased hepatic GSH and increased formation of lipid peroxidative products, which were partially normalized by treatment with heparin-SOD or heparin + SOD. Glutathione 101-104 chemokine (C-C motif) ligand 4 Mus musculus 19-23 20093790-5 2010 Hepatic glutathione contents were significantly decreased and lipid peroxidation was increased after CCl4 treatment. Glutathione 8-19 chemokine (C-C motif) ligand 4 Mus musculus 101-105 19899326-9 2009 Furthermore, CCl4-intoxication decreased the levels of renal reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) by 44, 56 and 43%, respectively. Glutathione 69-80 chemokine (C-C motif) ligand 4 Mus musculus 13-17 19899326-9 2009 Furthermore, CCl4-intoxication decreased the levels of renal reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) by 44, 56 and 43%, respectively. Glutathione 82-85 chemokine (C-C motif) ligand 4 Mus musculus 13-17 17086479-4 2007 Hepatic glutathione and taurine concentrations after CCl4 challenge were increased markedly by beta-alanine intake. Glutathione 8-19 chemokine (C-C motif) ligand 4 Mus musculus 53-57 18724385-10 2008 KEY RESULTS: CCl4 injection produced: marked elevation of alanine aminotransferase and aspartate aminotransferase; hepatic membrane lipid peroxidation, assayed by 8-isoprostane levels; and depletion of reduced glutathione and superoxide dismutase. Glutathione 210-221 chemokine (C-C motif) ligand 4 Mus musculus 13-17 17617128-4 2007 RESULTS: A small dose of CCl4 (10 microl/kg of body weight) significantly increased the serum alanine aminotransferase (ALT) level and hepatic malondialdehyde content, decreased hepatic reduced glutathione (GSH) content and induced ultrastructural alterations of hepatic mitochondria in transgenic mice, but not in nontransgenic mice. Glutathione 194-205 chemokine (C-C motif) ligand 4 Mus musculus 25-29 17617128-4 2007 RESULTS: A small dose of CCl4 (10 microl/kg of body weight) significantly increased the serum alanine aminotransferase (ALT) level and hepatic malondialdehyde content, decreased hepatic reduced glutathione (GSH) content and induced ultrastructural alterations of hepatic mitochondria in transgenic mice, but not in nontransgenic mice. Glutathione 207-210 chemokine (C-C motif) ligand 4 Mus musculus 25-29 17617128-7 2007 SNMC protects hepatocytes against CCl4-induced oxidative stress and mitochondrial injury in the presence of HCV proteins by restoring depleted cellular GSH. Glutathione 152-155 chemokine (C-C motif) ligand 4 Mus musculus 34-38 17010209-9 2006 TBARS level was also increased significantly whereas GSH, SOD, CAT and GST levels were decreased in the liver and kidney tissue homogenates of CCl4 treated mice. Glutathione 53-56 chemokine (C-C motif) ligand 4 Mus musculus 143-147