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)

The study aimed to evaluate the behavior of alpha-glutathione S-transferase (alpha-GST) in the serum of hemodialysis patients with hepatitis C virus (HCV) infection following treatment with high-dose IFN-alpha-2b. Ten patients with detected anti-HCV antibodies and HCV RNA by RT-PCR were selected and treated with high-dose interferon (IFN)-alpha-2b, 10 million units s.c. daily for 2 weeks followed by 3 times per week for 6 additional weeks. Blood samples were obtained from these patients at baseline for plasma alpha-GST and hepatic aminotransferases. Patients were monitored with weekly blood counts and monthly liver enzymes. Biochemical (normal alpha-GST and ALT) and virologic (negative HCV RNA by RT-PCR) responses were observed in 3 (30%) of the 10 patients. At the end of the follow-up (follow-up duration 44 weeks), 3 patients demonstrated long-term biological and virologic responses and 7 had relapses. In the nonresponders plasma AST and ALT approached normal levels on some occasions despite persistent viral RNA. In contrast to transaminases alpha-GST remained distinctly elevated in nonresponders and provided a more clear distinction between the responders and nonresponders. In conclusion, plasma alpha-GST, as a sensitive and reliable marker of response, may have a role in the monitoring of hemodialyzed patients undergoing IFN-alpha-2b therapy.
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PMID:The role of alpha-glutathione S-transferase in the monitoring of hemodialysis patients with hepatitis C virus infection undergoing high-dose interferon-alpha-2b therapy. 1022 80

In this experiment, we studied the different changes in activities and protein levels of each subform of hepatic cytochrome P450 and glutathione S-transferase (GST), in chemical-induced liver injury in rats. Rats were administered 1,1-dichloroethylene (DCE), allyl alcohol (AA), bromobenzene (BB) and N,N-dimethylformamide (DMF) p.o. once every two days for 7 times, and decapitated 18 hr after the last administration. DCE and AA showed stronger hepatic toxicity than BB and DMF, as serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were higher in DCE and AA treated rats than in BB and DMF groups. Anti-cytochrome P450 inhibitable activity of toluene metabolism and/or immunoblot analysis showed that CYP2E1 and CYP2B1/2 were induced by BB and DMF, but not by the other two chemicals; CYP2C11 was greatly decreased by all of the four toxicants; and CYP1A1/2 was slightly reduced by the four treatments. These changes were reflected in testosterone metabolism. Formation of 6 beta- and 7 alpha-hydroxytestosterone from testosterone was enhanced only in DMF-treated rats, whereas that of 2 alpha- and 16 alpha-hydroxytestosterone was reduced by all of the four chemicals. Serum GST activity was increased only in BB and DMF treated rats, but liver cytosolic GST activity was enhanced by all of the four hepatotoxicants, with higher values in BB and DMF groups than in DCE and AA groups. Immunoblot analysis demonstrated that GST Yp was induced by BB and DMF treatments, and Ya and Yc were increased only by BB. GST Yk and Yb1 were not affected by the treatments. The different change patterns of enzymes by a specific toxin and the similar modifying effect on a specific enzyme by different toxins were discussed in relation to the liver damage and to the heterogeneous distribution of enzymes in liver.
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PMID:Different change patterns of the isozymes of cytochrome P450 and glutathione S-transferases in chemically induced liver damage in rat. 1054 60

Mice were fed with high zinc diet (15 g/kg) for 3 weeks. High zinc could cause liver toxicity: 1. inhibiting the activity of GOT and GPT in liver homogenate, reducing GSH and glycogen contents. 2. increasing the activity of aniline hydroxylase and inhibiting the activities of NADPH-cytochrome C reducease, benzo-phytamine-N-demethylase and glutathione S-transferase. The activities of cytochrome P450 and cytochrome b5 were not obviously changed 3. increasing microsomal membrane fluidity in the superficial layers, but not in the deep layers.
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PMID:[Effects of high dietary zinc on liver function, hepatic drug metabolism enzymes and membrane fluidity in mice]. 1068 26

Redox cycling metabolism of diquat catalyzes generation of reactive oxygen species, and diquat-induced acute hepatic necrosis in male Fischer 344 (F344) rats has been studied as a model of oxidant mechanisms of cell killing in vivo. At equal doses of diquat, female F344 rats sustained less hepatic damage than did male rats, as estimated by plasma alanine aminotransferase (ALT) activities after 6 h. Biliary efflux of glutathione disulfide (GSSG) was greater in male than in female rats at each dose of diquat, but even comparable rates of GSSG excretion were associated with less hepatic injury in female rats. Hepatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) were similar in the two genders, and activities of glutathione reductase (GR) and glutathione S-transferase-alpha (GST-alpha) activities were higher in the male rats. Previous studies in male rats have implicated formation of 2,4-dinitrophenylhydrazine (DNPH)-reactive "protein carbonyls" and related iron chelate-catalyzed redox reactions as mechanisms critical to diquat-induced acute cell death in vivo. However, diquat-treated female rats showed higher levels of DNPH-reactive proteins in livers and in bile than did males, both at identical doses of diquat and at doses that produced similar elevations in plasma ALT activities. In female rats, fragmentation of hepatic deoxyribonucleic acids (DNA) was increased by doses of diquat that did not increase plasma ALT activities, and increased fragmentation was observed prior to elevation of plasma ALT activities. In the present studies, hepatic necrosis was most closely associated with DNA fragmentation, although additional studies are needed to determine the mechanisms responsible for and the pathophysiological consequences of the fragmentation.
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PMID:Sex differences in diquat-induced hepatic necrosis and DNA fragmentation in Fischer 344 rats. 1074 47

We previously reported that the mold Monascus anka, traditionally used for fermentation of food, showed antioxidant and hepatoprotective actions against chemically induced liver injuries. In the present study, the antioxidant component of M. anka was isolated and identified. The antioxidant was elucidated to be dimerumic acid. DPPH (1,1-diphenyl-2-picrylhydrazyl) radical was significantly scavenged by the antioxidant whereas hydroxyl radical and superoxide anion were moderately scavenged. When the antioxidant (12 mg/kg) was given to mice prior to carbon tetrachloride (CCl(4), 20 microl/kg, ip) treatment, the CCl(4)-induced liver toxicity in mice seen in an elevation of serum aspartate aminotransferase and alanine aminotransferase activities was depressed, suggesting the hepatoprotective action of the antioxidant. The liver microsomal glutathione S-transferase activity, which is known to be activated by oxidative stress or active metabolites, was increased by CCl(4) treatment and the increase was also depressed by pretreatment with the mold antioxidant. Thus these data confirmed that the dimerumic acid isolated from M. anka is the potential antioxidant and protective against CCl(4)-induced liver injury.
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PMID:Dimerumic acid as an antioxidant of the mold, Monascus anka. 1080 32

Serum concentrations of alpha-glutathione S-transferase (alphaGST) were determined before and after hepatectomy to examine the clinical usefulness of alphaGST as a marker of hepatocellular damage compared with the conventional liver function tests. Prior to hepatectomy, serum alphaGST concentrations correlated significantly with serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). In patients who had a good postoperative course, serum alphaGST concentrations rose significantly to a peak immediately after surgery, followed by a rapid fall to the normal range within 1 week, yielding a monophasic pattern. Serum alphaGST concentrations reached a peak earlier than other parameters of liver function, and peak serum alphaGST concentrations correlated with peak serum concentrations of AST and ALT. The mean decrease rate of serum alphaGST concentration from peak values was significantly more rapid than that of serum AST and ALT, indicating an early return of alphaGST concentrations to the normal range. These findings suggest that serum alphaGST may be a more sensitive marker of hepatocellular damage than transaminases and may therefore be useful for rapid monitoring of the extent and persistence of liver injury after hepatectomy.
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PMID:Serum alpha-glutathione S-transferase: a new marker of hepatocellular damage associated with hepatectomy. 1083 32

Liver steatosis is frequently encountered at organ harvest and, although functionally inapparent in the donor, may seriously affect the functional recovery of the graft after ischemic preservation. The present study was aimed to investigate the diagnostic value of alpha-glutathione S-transferase (GST) in non-ischemic and ischemic livers with or without compensated steatosis. A histologically documented mild to moderate steatosis was induced in livers of male Wistar rats by fasting for 2 days and subsequent feeding of a fat-free diet enriched in carbohydrates. Fatty livers (FL) were retrieved and perfused in vitro for 45 min either immediately or after ischemic preservation at 4 degrees C in HTK solution. Effluate was collected during isolated perfusion and later analysed for liver specific enzymes, including GST. Normal livers (NL) were excised from healthy rats and underwent the same protocol. Non-ischemic livers showed similar enzyme release (FL versus NL) for ALT or GLDH but significant differences in GST. After ischemic preservation of NL, enzyme release increased mildly with respect to the non-ischemic reference values for ALT, remained unchanged for GLDH and rose substantially for GST. In FL, there was a more than 10-fold increase in all parameters, being most pronounced for GLDH as a marker of mitochondrial damage. It is concluded that GST may discriminate between healthy and suboptimal steatotic livers prior to ischemia and that the release of GST upon postischemic reperfusion of normal livers proves to be the most sensitive indicator for hepatocellular injury. However, GST turned out to be less useful for the detection of postischemic reperfusion injury in steatotic grafts.
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PMID:Value of alpha glutathione S-transferase for in vitro evaluation of preservation injury in normal and steatotic livers. 1111 71

The liver injury was induced by intestinal ischemia-reperfusion and the protective effect of erigeron injection (EI) was studied in mice. The results showed that serum alanine transaminase (ALT) and glutathione S-transferase (GST) activity increased while the root of superior mesenteric artery was blocked with non-injury artery clap for 20 minute and reperfusion for 1 hour. EI could protect the above changes induced by intestinal ischemia-reperfusion. EI could reduce the activities of serum ALT and GST, decrease the content of hepatic MDA and significantly increase the activity of SOD. The pathological changes of hepatocytes induced by intestinal ischemia-reperfusion were less in EI groups. These results suggested that EI could protect the liver of mice from injury induced by intestinal ischemia-reperfusion. One of the mechanisms of hepatoprotective action was related to the antioxidative function of erigeron.
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PMID:[Protective effect of erigeron injections on hepatotoxicity induced by intestinal ischemia-reperfusion in mice]. 1132 58

This study examined the effects of 1 degrees C hypo- or hyperthermia on in vivo liver ischemia and reperfusion (I/R) injury in 15 fasted male Wistar rats. Rats were ventilated, and rectal temperature was maintained at 36, 37 (normothermic), or 38 degrees C. In all rats, 70% liver ischemia was induced by clamping the afferent vessels to the median and left lateral lobes for 60 min, and reperfusion was allowed for 90 min. Changes in plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alpha-glutathione S-transferase (alpha-GST) levels were measured, hemodynamics and bile secretion were monitored, and arterial blood-gas analysis was performed. All ventilated rats showed a normal pH, arterial PCO(2), and arterial PO(2). AST, ALT, and alpha-GST levels were significantly higher in the 38 degrees C group when compared with the 36 and 37 degrees C groups after ischemia. No differences in bile secretion were found between all groups. Histopathological alterations were in agreement with AST, ALT, and alpha-GST levels in plasma. We conclude that a decrease of only 1 degrees C in body temperature significantly attenuates liver I/R injury, whereas an increase of 1 degrees C significantly increases liver I/R injury.
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PMID:Pronounced effect of minor changes in body temperature on ischemia and reperfusion injury in rat liver. 1140 39

Extract of Salvia Miltiorrhiza (SM) has been widely used in traditional Chinese medicine for treating liver diseases. Recent experimental evidence indicates that it has anti-tumor potential. In this study, the effect of SM on alfatoxin B1 (AFB1)-induced hepatocarcinogenesis was investigated in male Fischer 344 rats. AFB1 (40 microg/100 g body wt, by gavage) was administered once a week for 24 weeks. In SM treatment group, rats were given SM (0.25g/100g body wt, 5 days/week by gavage) for a total of 28 weeks, including 4 weeks before and 24 weeks during AFB1 exposure. Results showed that the elevation of serum alanine aminotransferase and aspartate aminotransferase activities due to AFB1 dosing was almost completely abolished by the treatment of SM, indicating that SM could prevent AFB1-induced liver cell injury. It was further observed that SM substantially reduced glutathione S-transferase placenta form (GST-P) positive foci formation and GST-P mRNA expression caused by AFB1, which clearly suggests that SM is effective in preventing AFB1-induced hepatocarcinogenesis. Furthermore, the inhibition on AFB1 hepatocarcinigenesis was associated with a corresponding decrease in AFB1-DNA adducts formation as well as AFB1-induced oxidative DNA damage (8-hydroxydeoxyguanosine) in rat liver. Our results also indicate that the protective effect of SM might be mediated through dual mechanisms: (i) the enhancement of AFB1 detoxification pathway, especially the induction of GST-Yc2 mRNA expression, and (ii) the antioxidant property of SM.
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PMID:Protection of salvia miltiorrhiza against aflatoxin-B1-induced hepatocarcinogenesis in Fischer 344 rats dual mechanisms involved. 1144 22


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