Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was performed to compare the effect of liver protection of fine saengshik (FS) and superfine saengshik (SS) and uncooked and powdered grains and vegetables, produced by the different mill technique on the acute hepatotoxicity induced by CCl(4) in mouse. As the result of particle size distribution in number, particles included under 0.955 microm dia were 7.02% and 68.92% respectively. Hematological and serological examination showed that AST (P < 0.05) and ALT (P < 0.05) of SS + CCl(4) group decreased significantly compared with those of FS + CCl(4) group. On the examination of antioxidant effect, water extract of SS showed a higher superoxide dismutase (SOD)-like activity on the condition of the HX/XOD system than that of FS (P < 0.001). Also, the glutathione peroxidase (P < 0.01) and glutathione reductase (P < 0.05) activities in liver showed a significant difference between FS + CCl(4) and SS + CCl(4) groups. On the histological observation of liver, SS + CCl(4) group showed a mild reversible hepatocytic change and infiltration of inflammatory cells around the central veins, whereas FS + CCl(4) group showed severe agglutination necrosis by CCl(4) toxicity. These results suggest that superfine saengshik significantly improves liver protection effect compared with fine saengshik; its major mechanism is supposed to be the improved antioxidant effect of saengshik by reduced size of particles.
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PMID:Superfine saengshik improves liver protecting effect compared with fine saengshik in an animal model. 1932 52

Tamoxifen (TAM) is widely used in the treatment and prevention of breast cancer. Adverse effects of TAM include hepatotoxicity. Caffeic acid phenethyl ester (CAPE), an active component of propolis, has been used in folk medicine for diverse ailments. In the current study, the protective effects of CAPE against TAM-induced hepatotoxicity in female rats were evaluated. TAM (45 mg/kg/day, i.p., for 10 consecutive days) resulted in an elevation of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), depletion of liver reduced glutathione (GSH) and accumulation of oxidized glutathione (GSSG) and lipid peroxidation (LPO). Also, TAM treatment resulted in inhibition of hepatic activity of glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT). Further, it raised liver tumor necrosis factor-alpha (TNF-alpha) level and induced histopathological changes. Pretreatment with CAPE (2.84 mg/kg/day; i.p., for 20 consecutive days, starting 10 days before TAM injection) significantly prevented the elevation in serum activity of the assessed enzymes. CAPE significantly inhibited TAM-induced hepatic GSH depletion and GSSG and LPO accumulation. Consistently, CAPE normalized the activity of GR, GPx, SOD and CAT, inhibited the rise in TNF-alpha and ameliorated the histopathological changes. In conclusion, CAPE protects against TAM-induced hepatotoxicity.
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PMID:Caffeic acid phenethyl ester protects against tamoxifen-induced hepatotoxicity in rats. 1939 97

The present study examined the protective effects of seabuckthorn (Hippophae rhamnoides L., SBT) seed oil on carbon tetrachloride (CCl(4))-induced hepatic damage in male ICR mice. Our results showed that oral administration of SBT seed oil at doses of 0.26, 1.30, and 2.60 mg/kg for 8 weeks significantly reduced the elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), triglyceride (TG), and cholesterol at least 13% in serum, and the level of malondialdehyde (MDA) in liver at least 22%, that was induced by CCl(4) (1 mL/kg) in mice. Moreover, the treatment of SBT seed oil was also found to significantly increase the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rd), and GSH content in liver up to 134%. Our study found that the optimal dose of SBT seed oil was 0.26 mg/kg, as the minimum amount exhibiting the greatest hepatoprotective effects on CCl(4)-induced liver injury. Overall, the hepatoprotective effect of SBT seed oil at all tested doses was found to be comparable to that of silymarin (200 mg/kg) and have been supported by the evaluation of the liver histopathology in mice.
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PMID:Protective effects of seabuckthorn (Hippophae rhamnoides L.) seed oil against carbon tetrachloride-induced hepatotoxicity in mice. 1952 9

In the present study, alteration in antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) and marker enzymes of tissue damage alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) with laboratory exposure to wastewaters from Aligarh (AWW) and Saharanpur (SWW) were investigated in rat liver and kidney. Levels of malondialdehyde (MDA), reduced glutathione (GSH) and hydrogen peroxide (H(2)O(2)) were also determined. A profound enhancement of 5 and 2.5-folds in MDA level was recorded in the liver and kidney respectively as a result of oral administration of SWW to the rats. Exposure to both AWW and SWW resulted in 3-4-fold increase in GR activity and 3-fold increase in SOD and ALT activity in the hepatic tissue compared to control values. Ingestion of AWW and SWW resulted in 3.5-fold rise in renal AST levels whereas AWW caused 75% decline in GST activity in kidney of treated rats. Results indicate that wastewater (AWW/SWW) caused severe damage to renal and hepatic tissues and the effect seems in part to be mediated by suppression of antioxidant system with GR and SOD as potential candidates for hepatic toxicity biomarkers of wastewaters.
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PMID:Effect of wastewater intake on antioxidant and marker enzymes of tissue damage in rat tissues: implications for the use of biochemical markers. 1959 98

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

We evaluated whether repeated arsenic preexposure can increase acetaminophen-induced hepatic oxidative stress. Rats were exposed to arsenic (25 ppm; rat equivalent concentration of maximum groundwater contamination level) via drinking water for 28 days. Next day, they were given single oral administration of acetaminophen (420 or 1000 mg/kg b.w.). Hepatotoxicity was evaluated by assessing serum biomarkers, cytochrome-P450 (CYP) content, CYP3A4- and CYP2E1-dependent enzymes, lipid peroxidation and antioxidants. Arsenic or acetaminophen increased serum ALT and AST activities and depleted CYP. Arsenic decreased, but acetaminophen increased CYP-dependent enzyme activities. These agents independently increased lipid peroxidation and decreased antioxidants. Arsenic did not alter the effects of acetaminophen on serum biomarkers, caused further CYP depletion and decreased acetaminophen-mediated induction of drug-metabolizing enzymes. Arsenic enhanced the lower dose of acetaminophen-mediated lipid peroxidation and glutathione depletion with no further alterations in enzymatic antioxidants. However, arsenic attenuated the higher dose-mediated lipid peroxidation and glutathione depletion with improvement in glutathione peroxidase and glutathione reductase activities, further decrease in catalase and no alterations in superoxide dismutase and glutathione-S-transferase activities. Results show that arsenic preexposure increased the susceptibility of rats to hepatic oxidative stress induced by the lower dose of acetaminophen, but reduced the oxidative stress induced by the higher dose.
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PMID:Influence of repeated preexposure to arsenic on acetaminophen-induced oxidative stress in liver of male rats. 1993 28

This study investigates the hepatoprotective activity of ethanol extract from Shidagonglao roots (SDGL(EtOH)). The hepatoprotective effect of SDGL(EtOH) (20, 100 and 500 mg/kg) was analyzed on carbon tetrachloride (CCl(4))-induced acute liver injury. Rats pretreated orally with SDGL(EtOH) (100 and 500 mg/kg) and silymarin (200 mg/kg) for 3 consecutive days prior to the administration of a single dose of 50% CCl(4) (0.10 ml/100 g of bw, ip) significantly prevented the increases in the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in CCl(4)-treated rats. Histological analysis also showed that SDGL(EtOH) (100 and 500 mg/kg) and silymarin reduced the incidence of liver lesions including vacuole formation, neutrophil infiltration and necrosis of hepatocytes induced by CCl(4) in rats. Moreover, the SDGL(EtOH) (100 and 500 mg/kg) increased the activities of anti-oxidative enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GRd) and decreased malondialdehyde (MDA) level in liver, as compared to those in the CCl(4)-treated group. Furthermore, SDGL(EtOH) (100 and 500 mg/kg) and silymarin attenuated the increased levels of tumor necrosis factor-alpha (TNF-alpha) in serum and nitric oxide (NO) in liver as compared to the CCl(4)-treated group. The hepatoprotective mechanisms of SDGL(EtOH) are likely related to inhibition of TNF-alpha, MDA and NO productions via increasing the activities of antioxidant enzymes (SOD, GPx and GRd). These experimental results suggest that SDGL(EtOH) can attenuate CCl(4)-induced acute liver injury in rats.
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PMID:Hepatoprotective effect of shidagonglao on acute liver injury induced by carbon tetrachloride. 1993 18

The protective effect of aspartate and glutamate in isoproterenol induced myocardial infarction (MI) was investigated in experimental animals. Male albino wistar rats were pretreated with aspartate [100mg (kg body weight)-1 day-1] or glutamate [100mg (kg body weight)-1 day-1] intraperitoneally for a period of 7 days. Following amino acid treatment, MI was induced in rats by subcutaneous injection of isoproterenol [200mg (kg body weight)-1 day-1] for 2 days. After 24h following the last injection, the animals were sacrificed and the biochemical analysis was carried out. The activities of cardiac marker enzymes (alanine transaminase, aspartate transaminase, lactate dehydrogenase and creatine phosphokinase) were increased significantly (P<0.05) in the serum of MI induced rats as compared to control rats. The levels of glutathione and mitochondrial ATP and the activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase and glutathione reductase) were decreased whereas lipid peroxides increased significantly (P<0.05) in the heart of MI induced rats as compared to control rats. However, pretreatment with aspartate or glutamate to MI induced rats significantly (P<0.05) reduced the activities of cardiac marker enzymes and increased the activities of antioxidant enzymes as compared to MI induced rats. Aspartate or glutamate pretreatment also increased the levels of glutathione and mitochondrial ATP while decreased the level of lipid peroxides in the cardiac tissue. The overall effects of aspartate and glutamate in reducing the oxidative stress in MI induced rats are similar. There was no significant difference between the control rats and aspartate or glutamate treated control rats. The present study shows that aspartate and glutamate could reduce oxidative stress in MI induced rats.
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PMID:Aspartate and glutamate prevents isoproterenol-induced cardiac toxicity by alleviating oxidative stress in rats. 1996 69

ABSTRACT Azathioprine (AZA), one of the widely prescribed immunosuppressant drugs in organ transplantation and autoimmune diseases, could cause hepatotoxicity in the course of therapy. The current work was designed to assess the protective role of the dietary flavonoid, quercetin (QE), in oxidative hepatic damage induced by AZA. Adult male Wistar rats were divided into four treatment groups. Two groups were treated with single intraperitoneal injection of AZA (50 mg/kg body weight); one of these groups was pretreated with QE (50 mg/kg body weight) intraperitoneally once a day for 7 days. A vehicle treated control group and a QE control group were also included. Hepatotoxicity, evident from increased levels of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma glutamyl transpeptidase (GGT) in serum 24 h after AZA treatment, was significantly (p < 0.05) normalized by QE pretreatment. AZA administered rats displayed declined levels of endogenous antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)], along with elevated levels of malondialdehyde (MDA). However, pretreatment with QE significantly precluded lipid peroxidation and maintained the activities of antioxidant defenses at a near normal status. Besides, AZA induced oxidative stress and subsequent DNA damage was effectively manifested by QE, which was confirmed by agarose gel electrophoresis. These findings highlight the salubrious effect of QE as a hepatoprotectant in AZA-induced oxidative stress mediated hepatic injury.
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PMID:Mitigation of azathioprine-induced oxidative hepatic injury by the flavonoid quercetin in wistar rats. 2002 Aug 51


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