Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The redox status and steroid metabolism of liver of adult male rat exposed to lead (Pb) and cadmium (Cd) either alone or in co-exposure (0.025 mg/kg body weight intraperitoneally/15 days) was studied. Pb and Cd significantly accumulated in the liver. The activity of steroid metabolizing enzymes 17-betahydroxysteroid oxidoreductase and uridine diphosphate-glucuronyltransferase were decreased in experimental animals. 17-beta-Hydroxysteroid dehydrogenase was reduced to 33%, 38%, and 24% on treatment of Pb, Cd, and co-exposure (Pb + Cd). Furthermore, the activity of uridine diphosphate-glucuronosyltransferase was significantly reduced to 27% (Pb exposure), 36% (Cd exposure), and 25% (co-exposure of Pb + Cd). Cd exposure exhibited more toxic effect than Pb, while co-exposure demonstrated the least. The activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase, and glucose-6-phosphate dehydrogenase decreased and glutathione peroxidase increased in mitochondrial and post-mitochondrial fractions. The level of lipid peroxidation increased, and cellular glutathione concentration decreased. Hepatic DNA was decreased, whereas RNA content and the activity of alanine transaminase remained unchanged. Histological studies revealed that only Cd-exposed groups exhibited cytotoxic effect. These results suggest that when Pb and Cd are present together in similar concentrations, they exhibited relatively decreased toxic effect when compared to lead and cadmium in isolation with regard to decreased steroid metabolizing and antioxidant enzyme activities. This seems that the toxic effect of these metals is antagonized by co-exposure due to possible competition amongst Pb and Cd for hepatic accumulation.
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PMID:Lead and cadmium co-exposure mediated toxic insults on hepatic steroid metabolism and antioxidant system of adult male rats. 1965 23

Lambda-cyhalothrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of lambda-cyhalothrin (LTC) to induce oxidative stress, changes in biochemical parameters and enzyme activities in the kidney of male rats and its possible attenuation by Vitamin C (vit C). Renal function, histopathology, tissue malondialdehyde (MDA), protein carbonyl (PCO) levels, antioxidant enzyme activities and reduced glutathione (GSH) levels were evaluated. Exposure of rats to lambda-cyhalothrin, during 3 weeks, caused a significant increase in kidney MDA and protein carbonyl levels (p<0.01) as compared to controls. Co-administration of vitamin C was effective in reducing MDA and PCO levels. The kidney of LTC-treated rats exhibited severe vacuolations, cells infiltration and widened tubular lumen. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) were significantly decreased due to lambda-cyhalothrin exposure. Co-administration of vitamin C ameliorated the increase in enzymatic activities of aminotransferases (AST and ALT), lactate dehydrogenase (LDH), creatinine and urea levels and improved the antioxidant status. These data indicated the protective role of ascorbic acid against lambda-cyhalothrin-induced nephrotoxicity and suggested a significant contribution of its antioxidant property to these beneficial effects.
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PMID:Toxic effects of lambda-cyhalothrin, a synthetic pyrethroid pesticide, on the rat kidney: Involvement of oxidative stress and protective role of ascorbic acid. 1973 94

Changes in water temperature and salinity are responsible for a variety of physiological stress responses in aquatic organisms. Stress induced by these factors was recently associated with enhanced reactive oxygen species (ROS) generation, which caused oxidative damage. In the present study, we investigated the time-related effects of changes in water temperature and salinity on mRNA expression and the activities of antioxidant enzymes (SOD and CAT) and lipid peroxidation (LPO) in the gills and digestive glands of the ark shell, Scapharca broughtonii. To investigate physiological responses, hydrogen peroxide (H(2)O(2)), lysozyme activity, aspartate aminotransferase (AspAT), and alanine aminotransferase (AlaAT) were measured in the hemolymph. Water temperature and salinity changes significantly increased antioxidant enzyme mRNA expression and activity in the digestive glands and gills in a time-dependent manner. H(2)O(2) concentrations increased significantly in the high-temperature and hyposalinity treatments. LPO, AspAT and AlaAT levels also increased significantly in a time-dependent manner, while lysozyme activity decreased. These results suggest that antioxidant enzymes play important roles in reducing oxidative stress in ark shells exposed to changes in water temperature and salinity.
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PMID:Activity of antioxidant enzymes and physiological responses in ark shell, Scapharca broughtonii, exposed to thermal and osmotic stress: effects on hemolymph and biochemical parameters. 1978 26

Gibberellic acid (GA(3)), a plant growth regulator, was largely used in agriculture of many countries including Tunisia. However, its potential hazardous effects on human health were relatively unexplored. The purpose of this study was to investigate the effects of GA(3) on hepatic function in female rats and their pups. Animals were given daily 200 ppm GA(3) in drinking water from the 14th day of pregnancy until day 14 after delivery. It was found that GA(3) induced liver damages as evidenced by the elevation of plasma aminotransferases (ALT, AST), lactate dehydrogenase activities, bilirubin and albumin levels. Hepatotoxicity was objectified by the significant increase of malondialdehyde (MDA) level and a decrease of antioxidant enzyme activities such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione content in liver of suckling pups and their mothers. Impairment of hepatic function corresponded histologically. We have observed blood vessels congestion and leucocytes infiltration, which were more pronounced in hepatocytes of dams than those of suckling pups. Results of this current study suggest that exposure rats to GA(3) induces hepatotoxicity and histopathological changes in liver of female rats and their progeny.
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PMID:Hepatotoxicity induced by gibberellic acid in adult rats and their progeny. 1981 99

To assess liver damages in pregnant and lactating rats and in their suckling pups, wistar female rats were given through drinking water 350 ppm of CoCl(2) (157 ppm Co(2+)) from the 14th day of pregnancy until day 14 after delivery. The effects of cobalt chloride on lipid peroxidation levels, antioxidant enzyme activities, lipid profile and histopathology aspects of liver were evaluated. Biochemical results showed that lipid peroxidation increased significantly in Co-treated rats, as evidenced by high liver thiobarbituric acid-reactive substance (TBARS) levels. Alteration of the antioxidant system in treated group was confirmed by the significant decline of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and reduced glutathione (GSH) content in liver of suckling pups and their mothers. Moreover, CoCl(2) exposure induced an increase in the activities of the aspartate transaminase (AST), alanine transaminase (ALT), lactate deshydrogenase (LDH) and bilirubin levels in pups and their mothers while liver LDH activity and plasma albumin level were significantly decreased. On the other hand, cobalt chloride induced a marked hypoglycemia, a significant decline in triglycerides and total cholesterol levels. Histological studies showed an infiltration of mononuclear cells and vascular congestion in liver of pups and their mothers. Based on the present findings, exposure of rats to CoCl(2) during late pregnancy and early postnatal period affects antioxidant enzyme activities and lipid peroxidation indicating liver damage in mothers and their offspring.
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PMID:Cobalt chloride induces hepatotoxicity in adult rats and their suckling pups. 1981 22

To investigate the effects of atorvastatin and cinnamon on serum lipid profile, oxidative stress, antioxidant capacity, hepatic enzymes activities, nitric oxide (NO) as well as homocysteine (Hcy) in hypercholesterolemic rats, 48 male albino rats, weighing 130-190 gm were divided into 2 groups, normal group fed on basal rat chow diet (n=12) and high cholesterol group (HCD) were fed on 1% cholesterol-enriched diet for 15 day (n=36). Hypercholesterolemic rats were divided into 3 subgroups (n=12 for each) fed the same diet and treated with atorvastatine (HCD+Atorvastatin) or cinnamon extract (HCD+cinnamon) or none treated (HCD) for 3&6 weeks. Serum triglycerides (TG), Total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), ALT, AST, NO, Hcy, hepatic reduced glutathione (GSH), Malondialdehyde (MDA) and antioxidant enzymes, Superoxide dismutase (SOD) and catalase activity were measured. Results showed that HCD increased significantly TG, TC, LDL-C, ALT, AST, Hcy and hepatic MDA, while lowered significantly antioxidant enzyme activities and NO levels. Atorvastatin therapy significantly increased HDL-C, NO and antioxidant activity while decreased LDL-C, MDA and Hcy concentrations. Serum TG, TC, LDL-C, ALT, AST and hepatic MDA levels were significantly lowered meanwhile, serum HDL, NO values and hepatic antioxidant activities were significantly, higher in cinnamon-treated than untreated group. These results indicate that lipid abnormalities, oxidative injury and hyperhomocystienemia were induced by HCD and this study recommend that administration of atorvastatine or cinnamon provided protection against the lipemic-oxidative disorder and act as hypocholesterolemic, hepatoprotective agent and improve cardiovascular function through modulation of oxidative stress, NO and Hcy.
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PMID:Oxidative markers, nitric oxide and homocysteine alteration in hypercholesterolimic rats: role of atorvastatine and cinnamon. 1991 18

Liver ischemia/reperfusion (I/R) injury, which is mainly caused by the generation of reactive oxygen species (ROS) during the reperfusion, remains an important clinical problem associated with liver transplantation and major liver surgery. Therefore, ROS should be detoxified to prevent hepatic I/R-induced injury. Delivery of antioxidant genes into liver is considered to be promising for prevention of hepatic I/R injury; however, therapeutic effects of antioxidant gene transfer to the liver have not been fully examined. The aim of this study was to examine whether adenovirus (Ad) vector-mediated catalase gene transfer in the liver is an effective approach for scavenging ROS and preventing hepatic I/R injury. Intravenous administration of Ad vectors expressing catalase, which is an antioxidant enzyme scavenging H(2)O(2), resulted in a significant increase in catalase activity in the liver. Pre-injection of catalase-expressing Ad vectors dramatically prevented I/R-induced elevation in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and hepatic necrosis. The livers were also protected in another liver injury model, CCl(4)-induced liver injury, by catalase-expressing Ad vectors. Furthermore, the survival rates of mice subjected to both partial hepatectomy and I/R treatment were improved by pre-injection of catalase-expressing Ad vectors. On the other hand, control Ad vectors expressing beta-galactosidase did not show any significant preventive effects in the liver on the models of I/R-induced or CCl(4)-induced hepatic injury described above. These results indicate that hepatic delivery of the catalase gene by Ad vectors is a promising approach for the prevention of oxidative stress-induced liver injury.
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PMID:Prevention of hepatic ischemia-reperfusion injury by pre-administration of catalase-expressing adenovirus vectors. 1995 28

Physical training induces beneficial adaptations; however, exhausting exercise increases reactive oxygen species generation, resulting in damage to DNA and tissues. Pequi (Caryocar brasiliense), a fruit of the Brazilian Cerrado, contains a carotenoid-rich oil. We investigated whether pequi oil had antioxidant effects in runners. Evaluations were made after outdoor races before and after ingestion of 400 mg pequi-oil capsules for 14 days. Blood samples were taken after races and submitted to comet and TBARS assays and biochemical analyses of creatine kinase (CK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). To determine if the protective effects of pequi-oil were influenced by antioxidant enzyme genotypes, MnSOD (-Val9Ala), CAT (-21A/T) and GPX1 (Pro198Leu) gene polymorphisms were also investigated. Pequi oil was efficient in reducing tissue injuries evaluated for AST and ALT, particularly in women, and in reducing DNA damages in both sexes. Except for CK levels, the results were influenced by MnSOD genotypes; heterozygous excess was related to less DNA damage, tissue injury and lipid peroxidation, besides presenting a better response to pequi oil against exercise-induced damage.
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PMID:Dietary carotenoid-rich pequi oil reduces plasma lipid peroxidation and DNA damage in runners and evidence for an association with MnSOD genetic variant -Val9Ala. 2008 61

Sea tangle has long been used as Korean folk remedy to promote material health, and is one of the popular dietary supplement. This study was designed to evaluate the protective effect of fermented sea tangle (FST) against ethanol and carbon tetrachloride (CCl(4))-induced hepatotoxicity in rats. Sprague-Dawley rats were orally treated with FST (25, 250, 2500 mg/kg/day) with administration of ethanol (5 mL/kg) for 13 weeks and the single intraperitoneal (i.p.) dose of 50% CCl(4) (5 mL/kg/day, CCl(4) in olive oil) at 12 week, and repeated i.p. dose of 20% CCl(4) (2 mL/kg/day) for 1 week. Hepatotoxicity was evaluated by measuring the serum levels of glutamic pyruvate transaminase (GPT), gamma glutamyl transpeptidase (gamma-GT) and malondialdehyde (MDA) as well as the tissue levels of antioxidant enzyme such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Ethanol and CCl(4)-induced the rat liver damage, and significantly increased (p<0.05) the GPT, gamma-GT and MDA levels, and decreased the SOD, CAT and GPx levels. However, treatment with FST could decrease serum GPT, gamma-GT, and MDA levels significantly in plasma, and increase the activities of SOD, CAT, and GPx in liver tissues compared with ethanol and CCl(4)-treated group.
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PMID:Protective effect of fermented sea tangle against ethanol and carbon tetrachloride-induced hepatic damage in Sprague-Dawley rats. 2013 53

Recent studies reported that 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors have pleotropic effects independent of their lipid-lowering properties. The present study was undertaken to determine whether treatment with rosuvastatin (RO) would be beneficial in a rat model of bile duct ligation (BDL). Animals were divided into three groups: a sham group (group I), a BDL group treated with vehicle (group II), and a BDL group treated with RO (10 mg/kg) (group III). Serum levels of total bilirubin, gamma-glutamyl transpeptidase, alanine aminotransferase, and aspartate aminotransferase decreased significantly in group III when compared to group II. Lipid peroxides and NO levels of group III were found to be significantly lower than those of group II. Antioxidant enzymes (superoxide dismutase, glutathione-S-transferase, and catalase) activity in liver tissues markedly decreased in group II, whereas treatment with RO preserved antioxidant enzyme activity. DT-diaphorase activity in group II was significantly higher than that in group III. The histopathological results showed multiple numbers of newly formed bile ductules with inflammatory cells infiltration in group II. These pathological changes were improved in group III. Our data indicate that RO ameliorates hepatic injury, inflammation, lipid peroxidation and increases antioxidant enzymes activity in rats subjected to BDL. RO may have a beneficial effect on treatment of cholestatic liver diseases.
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PMID:Effect of rosuvastatin on cholestasis-induced hepatic injury in rat livers. 2014 76


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