Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.5.1.18 (glutathione S-transferase)
 22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence and phenotype of preneoplastic and neoplastic liver lesions appearing in LEC rats after recovery from severe hereditary hepatitis were studied in comparison with the liver lesions appearing in chemical liver carcinogenesis. The livers of 168 rats (90 male, 78 female) were stained for seven histochemical markers at different time periods from the 20th week to the 122nd week of life. Glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and non-specific esterase (ES) were used as negative markers. Gamma-glutamyltransferase (GGT), glutathione S-transferase placental form (GSTP), esterase isozyme L-1 (L1) and alpha-fetoprotein (AFP) were used as positive markers. The study on the incidence of liver lesions in the LEC rats revealed sequential development of liver foci, nodules and hepatocellular carcinomas (HCCs) similar to those seen in chemically induced liver carcinogenesis. These lesions appeared earlier and more frequently in male LEC rats than in female ones, suggesting the importance of hormonal environment in spontaneous HCC development. The histochemical analysis of spontaneous liver lesions in LEC rats showed that GSTP was the most reliable positive marker as previously reported in chemical liver carcinogenesis. There was no essential difference in the expression of the markers in spontaneous and chemically induced liver lesions except for L1, which is considered to be related to xenobiotic metabolism. The results of this study suggest that both spontaneous and chemically induced liver cancer may develop by passing through phenotypically similar preneoplastic processes. In addition, the LEC rat uniquely showed chronic liver damage (hepatocyte death and regeneration) at the promotion stage of carcinogenesis. Such a natural history of HCC development in LEC rats is similar to that of human HCC which is frequently associated with chronic liver damage. Thus, the LEC rat provides a useful model for studying the process and underlying mechanisms of human liver cancer development.
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PMID:Phenotype of preneoplastic and neoplastic liver lesions during spontaneous liver carcinogenesis of LEC rats. 169 69

Elevated levels of serum enzymes are frequently associated not only with alcohol-related organ damage but also with excessive alcohol consumption and alcoholism without significant tissue injury. However, both in the early detection of alcoholism as well as also in the diagnosis of alcohol-related diseases the sensitivities and specificities of these enzyme markers vary considerably. They may be influenced by nonalcohol-related diseases, enzyme-inducing drugs, nutritional factors, metabolic disorders, age, smoking, etc. Consequently, we have neither a single laboratory test--enzyme marker--nor a test combination that is reliable enough for the exact diagnosis between alcohol- and nonalcohol-related organ damage. In most cases it is possible to determine the tissue from which the elevated enzyme is derived, but only occasionally enzyme changes reflect the quantity of the tissue injury. Gamma-glutamyltransferase (GGT) is the most widely used laboratory marker of alcoholism and heavy drinking, detecting 34-85% of problem drinkers and alcoholics. However, the unspecificity of increased serum GGT limits its use for general screening purposes. Its value in the follow-up of various treatment programs, however, is well established. An elevated level of serum aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in an alcoholic or a heavy consumer indicates alcohol-induced organ damage. The use of test combinations significantly improves the information received with single serum enzyme determinations. An ASAT/ALAT ratio greater than 1.5 can be considered as highly suggestive for the alcoholic etiology of the liver injury. Still better discrimination between alcoholic and nonalcoholic origin of the liver disease may be achieved by the determination of the ratio of GGT to alkaline phosphatase. If this ratio exceeds 1.4 the specificity of the finding in favor for alcoholic liver injury is 78%. The determination of the mitochondrial isoenzyme of ASAT also improves the diagnostic value of ASAT determination. The ratio of mitochondrial isoenzyme to total over 4 is highly suggestive for alcohol-related liver injury. In general, however, the determination of serum activities of other enzymes such as ornithine carbamyl transferase, lactate dehydrogenase, isocitrate dehydrogenase, sorbitol dehydrogenase, alcohol dehydrogenase, guanase, aldolase, alkaline phosphatase or glutathione S-transferase do not significantly improve the diagnostic information obtained with more conventional laboratory markers of liver injury.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of enzymes for the diagnosis of alcohol-related organ damage. 243 6

Groups of 8 6-w-old female Sprague-Dawley rats were initiated with 30 mg diethylnitrosamine (DEN)/kg. Control and initiated groups were fed a semipurified diet or diets supplemented with Fusarium proliferatum-contaminated corn to contain 20 or 50 mg fumonisin B1 (FB1)/kg. Histochemical staining for gamma-glutamyltransferase (GGT) and immunochemical staining for placental glutathione S-transferase (PGST), markers of altered hepatic foci (AHF), were performed on serial frozen hepatic sections. Gamma-glutamyltransferase -(+) AHF were not found in any group. Dosing with DEN significantly increased the number of PGST-(+) hepatocytes compared to the uninitiated groups. Groups fed F proliferatum-containing diets also had a significantly increased number of PGST-(+) AHF compared with those fed no F proliferatum. The volume percentage of liver occupied by PGST-(+) foci was significantly greater in the groups treated with DEN or F proliferatum. The number of PGST-(+) AHF/liver in the groups given DEN was also significantly greater than in the uninitiated groups. Fusarium proliferatum exposure also significantly increased the number of PGST-(+) AHF/liver. Feeding F proliferatum containing 20 mg FB1/kg promoted the development of DEN-initiated AHF in rats. Placental glutathione S-transferase was a more useful marker than GGT in detecting AHF produced by small amounts of F proliferatum mycotoxins fed after initiating dosing with DEN.
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PMID:Fusarium proliferatum-fermented corn stimulates development of placental glutathione S-transferase-positive altered hepatic foci in female rats. 770 94

The present study investigated the relationship between the concentration of the reduced form of glutathione (GSH) and GSH-dependent enzyme activities in the gastric mucosa during acute liver injury caused by carbon tetrachloride (CCl4) in rats. Transient decreases in glutathione S-transferase (GST) activity and in glutathione peroxidase (GSH-Px) activity was observed (p < 0.01). GSH concentration also decreased (p < 0.01) but then transiently increased (p < 0.05). Gamma-glutamyltransferase (GGT) activities in rats killed 6, 12, and 24 hr after exposure to CCl4 were all higher than in the control group (p < 0.01). There was a significant correlation between GSH concentration and GST activity (p < 0.05) and between GSH concentration and GSH-Px activity (p < 0.01). However, there was no correlation between GSH concentration and GGT activity. The gastric mucosa, as judged by light microscopy, was slightly more damaged in the rats exposed to CCl4 than in the control group. From the observed abnormalities of GSH and GSH-dependent enzymes in the gastric mucosa of the rats exposed to CCl4, changes in GSH content and GSH-related enzymes in gastric mucosa may be important in gastric protection during acute liver injury.
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PMID:Effects of liver damage induced by carbon tetrachloride on glutathione and glutathione-dependent enzymes in rat gastric mucosa. 809 31

In this study we investigated the effects of curcumin, derived from plant Curcuma longa, on oxidative toxicity, and the possible molecular mechanism of antitumour of curcumin in liver cancer rats. Results showed that blood levels of Gamma-glutamyltransferase, aspartate aminotransferase, alanine aminotransferase, glutathione S-transferase, and liver level of MD were significantly decreased after curcumin feeding. Levels of the liver malondialdehyde MDA, nitric oxide and antioxidant enzymes were significantly increased. Moreover, RT-PCR and Western blot analysis results showed that curcumin treatment significantly decreased liver vascular endothelial growth factor (VEGF), CyclinD1 and CDK4 mRNA expression levels and CyclinD1 and CDK4 proteins levels in liver cancer rats. These findings were confirmed by histopathology. It is concluded that curcumin can protect the liver from the damage caused by N-nitrosodiethylamine. Moreover, curcumin has the potential to be used in a therapy for liver cancer. The present data provide evidence to support the presence of free radicals and VEGF, CyclinD1 and CDK4 mRNA in rat tumour cells. Studies are in progress in order to further characterize the role of VEGF, CyclinD1 and CDK4 mRNA in liver cancer cells and in hepatic therapeutics.
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PMID:In vivo study on the effects of curcumin on the expression profiles of anti-tumour genes (VEGF, CyclinD1 and CDK4) in liver of rats injected with DEN. 2411 97