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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha-Glutathione S-transferase (alpha-GST; EC 2.5.1.18) has been advocated as a better marker of hepatocellular damage than the transaminases in toxic and autoimmune hepatitis. We have assessed the potential interest of plasma alpha-GST determination in 94 anti-hepatitis C virus-positive patients with histologically proven chronic hepatitis C (34 women, 60 men, ages 40.0 +/- 11.9 years). Blood samples were assayed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase, alkaline phosphatase, and alpha-GST on the same day a liver biopsy was performed. alpha-GST concentrations were significantly above reference values in 64% of patients (compared with 58% for AST, 68% for ALT), and this increase was seen in 52% of patients with normal values for transaminases and a Knodell score > 3. Furthermore, there was a significant correlation between alpha-GST and lobular necrosis score (r = 0.31; P < 0.01). Our findings suggest that association of plasma alpha-GST with ALT may improve the biochemical assessment of liver damage in patients with chronic hepatitis C.
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PMID:Plasma alpha-glutathione S-transferase assessed as a marker of liver damage in patients with chronic hepatitis C. 749 11

In order to validate previous field observations by the authors on whitefish, Coregonus lavaretus L. s.l., a 30-day laboratory experiment with concentrations (0, 1.3, 2.3, 3.5, and 7 vol%) of bleached kraft pulp and paper mill effluent (BKME) simulating those occurring in a polluted lake was conducted. Chlorine dioxide had almost entirely replaced chlorine gas in the bleaching of pulp. As a consequence, the concentrations of adsorbable organic halogens and chlorinated phenolics (CPs) in BKME were significantly lowered compared to earlier studies. This reduction was also seen in the concentrations of CPs in the bile and CPs and extractable organic halogens in the intestinal lipids: the concentrations were low and did not depend on the dilution of BKME. In contrast, the resin acid content of bile decreased with decreasing BKME concentration. The growth of fish was speeded up in all BKME concentrations. However, at the highest BKME concentration (7 vol%) the increase was lowest. The induction of hepatic ethoxyresorufin O-deethylase (EROD) activity revealed strong dose-response relationship with BKME. At 3.5 vol% BKME (corresponding to a distance of 3.3 km from the mill sewer in the field) the EROD activity increased 12-fold. There was a tendency for lower activity of uridinediphosphate glucuronosyltransferase in the liver, but the decrease (34%; P < 0.05) was statistically significant only at 7 vol% BKME. The activity of liver glutathione S-transferase remained unchanged. All dilutions of BKME significantly depressed the concentrations of plasma immunoglobulin M (IgM). Erythrocytic concentrations of nucleotide triphosphates decreased and of sodium increased as the BKME concentration increased. Also some other blood parameters (hematocrit, hemoglobin, plasma glucose, and aspartate aminotransferase) were changed in all BKME exposures, although without obvious dependence on effluent concentration. In conclusion, there was a good agreement between field studies and laboratory experiments using BKME concentrations occurring in the field, confirming close or similar causes for responsive toxicity endpoints.
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PMID:Physiological toxicity of low-chlorine bleached pulp and paper mill effluent on whitefish (Coregonus lavaretus L. s.l.): a laboratory exposure simulating lake pollution. 749 61

Liver and muscle amino acid enzyme activities and plasma proteins, urea, amino acids, glucose, lactate, 3-hydroxybutyrate and acetoacetate concentrations were studied in growing rats undergoing adaptation to high-fat, high-energy diet and glucose gavage. Liver and muscle were used for the estimation of alanine transaminase (GPT, EC 2.6.1.1.), adenylate deaminase (AMD, EC 3.5.4.6.), glutamine synthetase (GST, EC 6.3.1.2) and serine dehydratase (SDH, EC 4.2.1.13) activities, the latter only in liver samples. The most important modifications produced in muscle enzyme activities by glucose gavage were observed in rats fed a cafeteria diet. Glucose gavage affects liver enzyme activities in the same sense than cafeteria diet. Energy plasma components were affected in opposite way by glucose gavage according to diet administered.
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PMID:Changes induced in amino acid-enzymes of developing rats by a high-energy diet and glucose gavage. 768 82

The in vivo effects of human placental extract (1-4 ml/kg) on hepatic lipid peroxidation, blood and liver glutathione (GSH) levels and several enzymes associated with the antioxidant defence mechanism; i.e., catalase, glutathione peroxidase, glutathione reductase and glutathione S-transferase, together with some blood biochemical responses were investigated in rats. At an optimal dose level (4 ml/kg), a single acute intraperitoneal administration of the extract caused a significant enhancement (49.9%; p < 0.001) of lipid peroxidation with a decline in GSH level both in blood (45.1%; p < 0.001) and liver (61.0%; p < 0.001) in comparison to control animals. Activities of catalase, glutathione peroxidase and glutathione reductase were inhibited in a dose-responsive way by the treatment with the extract which also increased the activity of glutathione S-transferase in a dose-dependent manner. The extract was found to be hepatotoxic in terms of elevation of serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, serum lactate dehydrogenase and blood methemoglobin concentration. Results of this study suggest the adverse consequences of the administration of the extract due to its substantial ability to alter normal cellular processes.
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PMID:Elevated lipid peroxidation, decreased glutathione levels and changes in glutathione-related enzymes in rats treated with human placental extract. 821 15

A recent study from our laboratory demonstrated that cyclosporine (CsA), a prototype immunosuppressant, enhanced the growth of carcinogen-induced enzyme altered foci in rat liver, suggesting that CsA may stimulate development of hepatocellular carcinomas. In the present study, we examined (i) whether CsA accelerates development of hepatocellular carcinomas in experimental animals, (ii) whether CsA stimulates the proliferation of resting hepatocyte in vivo and (iii) whether CsA modulates the production of growth factors implicated in liver cell growth, hepatocyte growth factor (HGF), transforming growth factor alpha (TGF alpha) and transforming growth factor beta 1 (TGF beta 1). Foci of hepatocytes, positive for glutathione S-transferase placental form were induced in male F344 rats by a single dose of diethylnitrosamine followed by 7 weeks promotion by a choline-deficient diet. The animals were then divided in two groups, and subsequent development of hepatocellular carcinomas was compared in rats fed a basal diet or a basal diet containing 0.015% CsA. Development of hepatocellular carcinoma was accelerated in the rats maintained on a CsA diet. Feeding a CsA diet as the sole treatment, for 2, 4 and 10 weeks induced significant increases in liver weight, and resulted also in an enhanced incorporation by hepatocytes of 5-bromo-2-deoxy-uridine. Serum levels of glutamate-oxaloacetate transferase, glutamate-pyruvate transferase and lactic dehydrogenase were not altered by feeding a CsA diet. Northern Blot analyses of the expression of HGF, TGF alpha and TGF beta 1 mRNAs in the liver showed similar patterns of expression between rats fed a basal diet and a CsA diet. The levels of HGF mRNA were not altered in the lungs and kidneys of rats fed a CsA diet. These results indicate that CsA stimulates rat liver cell proliferation in vivo without inducing liver cell necrosis, and that this effect may contribute to accelerated development of hepatocellular carcinomas in rats fed a CsA diet. As previously observed with BR 931, a hypolipidemic peroxisome proliferator, stimulation of liver cell growth by CsA did not entail changes in the production of HGF, TGF alpha or TGF beta 1.
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PMID:Cyclosporine stimulates hepatocyte proliferation and accelerates development of hepatocellular carcinomas in rats. 835 42

The contribution of testosterone to the nephrotoxic effects of 1,2-dichloropropane (DCP) was assessed by a series of castration and sex hormone replacement experiments on Wistar rats. The nephrotoxic action of DCP was evaluated by measuring the accumulation of organic anion and release of aspartate aminotransferase into the incubation medium using a renal cortical slice model. Our data show that sex, castration, and testosterone pretreatment are factors that influence the effect of DCP on renal cortical slices of rats Males appear to be more sensitive to nephrotoxic effects of DCP than females, male castration prevents the nephrotoxic effects of DCP, and pretreatment of females and castrated males with testosterone increases the susceptibility to DCP. In this study an attempt was made to evaluate the role of sex differences in the expression of enzymes participating in Phase I and Phase II detoxication reactions in order to explain the differences in sensitivity of the two genders to the nephrotoxic action of DCP. Our results implicate gender-specific expression of cytochrome P-450 in the kidneys as a predominant factor that determines the different susceptibilities of male and female rats to the nephrotoxic effect of DCP. We propose that the oxidation of DCP by CYP IIE1 is the first saturable and limiting step in the metabolic activation of DCP to nephrotoxic metabolites. It appears that, despite the fact that the nephrotoxic effect of DCP is determined mainly by its cysteine-conjugated metabolites, gluthathione (GSH) content and glutathione S-transferase (GST) activity in kidney are not directly related to increased androgen-related susceptibility to DCP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of sex-related differences in nephrotoxicity of 1.2-dichloropropane in rats. 857 Aug 64

A choline deficient L-amino acid defined (CDAA) diet led to the development of liver cirrhosis in male Wistar rats after 16 weeks. A new prolyl 4-hydroxylase inhibitor, 2,4-pyridine dicarboxylic acid bis [(2-methoxyethyl amide)] (HOE 077), prevented liver fibrosis in a dose-dependent manner without a reduction in increased serum alanine aminotransferase and aspartate aminotransferase in parallel with a reduction in preneoplastic enzyme-altered lesions stained with anti-glutathione S-transferase placental form antibody. HOE 077 reduced the increase in serum procollagen III peptide (PIIIP) in a dose-dependent manner and in proportion to the reduction in mRNA expression of type III procollagen in the liver of rats fed a CDAA diet.
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PMID:New prolyl 4-hydroxylase inhibitor reduces procollagen gene expression and enzyme-altered lesions in rat liver cirrhosis. 858 46

We found that NADPH-dependent ubiquinone reductase (NADPH-UQ reductase) in rat liver cytosol reduces ubiquinone (UQ) to ubiquinol (UQH2) in lipid membranes and consequently inhibits lipid peroxidation [Takahashi T., et al., Biochem. J., 309, 883-890 (1995)]. Here we examined whether or not this UQH2-regenerating system functions as a cellular antioxidant defense in animals. Rats were given UQ-10 for 2 weeks, and were then exposed to carbon tetrachloride (CCl4). The UQ-10 supplement increased only in the NADPH-UQ reductase and the UQH2-10 pool of rat liver without any appreciable change in the levels of other antioxidant factors. On the other hand, CCl4 markedly increased plasma aspartate aminotransferase and alanine aminotransferase, liver weight and thiobarbituric acid reacting substances formation, which are indicators of CCl4-hepatitis, and it decreased the liver levels of L-ascorbic acid, reduced form of glutathione (GSH), alpha-tocopherol, NADPH-UQ reductase and glutathione S-transferase. However, all the above indicators of CCl4-induced hepatitis were significantly improved in rats given UQ-10. Furthermore, alpha-tocopherol, but neither L-ascorbic acid nor GSH, was significantly saved. UQ-10 supplement also was recovered glutathione S-transferase and NADPH-UQ reductase activities slightly. These results indicated that UQ-10 given to rats increased the cellular UQH2-10 pool and cytosolic NADPH-UQ reductase activity in their livers, resulting in the inhibition of lipid peroxidation in the biomembranes, and consequently protected the rats from the CCl4-hepatotoxicity.
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PMID:Cellular antioxidant defense by a ubiquinol-regenerating system coupled with cytosolic NADPH-dependent ubiquinone reductase: protective effect against carbon tetrachloride-induced hepatotoxicity in the rat. 887 5

Recent data suggest that plasma levels of the phase II detoxification enzyme glutathione S-transferase alpha may be a sensitive indicator of hepatocellular integrity in acute liver disorders but little information is available in chronic hepatic disorders. Using a newly developed enzyme linked immunosorbent assay, glutathione S-transferase A1-1 (GSTA1-1) levels were measured in 279 plasma samples from patients with chronic liver disorders. Results were categorized as normal or elevated plasma GSTA1-1 and normal or elevated plasma aspartate aminotransferase (AST) levels. In 24 patients with alcoholic liver cirrhosis, plasma GSTA1-1 levels were not significantly different from a group of 350 healthy controls and only one patient (4%) had an elevated GSTA1-1 level while 10 (42%) patients had elevated AST activities. In samples from patients with primary biliary cirrhosis (n = 150), primary sclerosing cholangitis (n = 26) or chronic hepatitis (n = 79) significantly (P < 0.0001) elevated plasma GSTA1-1 concentrations were detected in 25 (17%), 7 (27%) and 17 (22%) of the samples, respectively. AST activities were increased in a higher percentage of samples in all three disorders: 89%, 88%, and 57%, respectively. Plasma GSTA1-1 and AST levels were significantly correlated (P < 0.005) in the above mentioned disorders but not in alcoholic liver cirrhosis. It is concluded that plasma GSTA1-1 is not a sensitive parameter for the detection of hepatocellular damage in chronic liver disorders.
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PMID:Plasma glutathione S-transferase alpha 1-1 levels in patients with chronic liver disorders. 904 44

A controlled test of the efficacy of triclabendazole against all stages (early immature, late immature and mature) of Fasciola hepatica has been performed in experimentally infected goats. The influence of triclabendazole treatment on the pathophysiology of the disease, in terms of haematological parameters and serum enzyme levels, and in the dynamics of production of specific antibodies to excretory/secretory products (ESP) of F. hepatica were also examined. Goats were orally infected with 200 viable metacercarie and treated at 4, 8 and 16 weeks postinfection (PI) with triclabendazole at the dose rate of 10 mg kg-1 body weight. The drug can be regarded as highly effective against mature (100%) and late immature (99.2%) flukes and effective against early immature flukes (94.9%). A moderate anaemia was found associated with the presence of late immature and mature flukes in bile ducts. Treatment with triclabendazole, by eliminating most of these flukes, largely reduced haematological alterations. Serum levels of the enzymes aspartate aminotransferase, lactate dehydrogenase and gamma-glutathione transferase reflected hepatic damage during goat fasciolosis. Early treatment (at 4 weeks PI) prevents the development of both parenchyma and bile ducts lesions; treatment at 8 weeks PI only prevents bile ducts lesions and treatment at 16 weeks PI has no appreciable effect on the development of the main hepatic lesions. The antibody response to F. hepatica ESP, as measured by enzyme-linked immunosorbent assay, was also affected by treatment with triclabendazole. In all treated animals a peak in antibody levels was observed between weeks 9 and 13, followed by a drop whose magnitude depended on the efficacy of treatment. In those animals in which triclabendazole was highly effective, antibody levels fell back to negative values similar to those recorded preinoculation at 18-21 weeks PI.
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PMID:Triclabendazole treatment in experimental goat fasciolosis: anthelmintic efficacy and influence in antibody response and pathophysiology of the disease. 906 52


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