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:2.5.1.18 (glutathione S-transferase)
22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of intratracheal administration of fly ash, its benzene-extracted residue and the benzene extract has been studied on the activities of hepatic mixed-function oxidases in the rat. Fly ash and its fractions significantly increased the levels of cytochrome P-450, cytochrome b5, cytochrome b5 reductase, NADPH-cytochrome c reductase, aminopyrine N-demethylase, aniline hydroxylase, and glutathione S-transferase in a dose-dependent manner. Phenobarbital or 3-methylcholanthrene treatment along with the administration of fly ash or its fractions showed an additive effect on the activities of the mixed-function oxidases. The observed effects were due to chemical component, i.e., organic and inorganic fractions of fly ash, and not due to its particulate nature. This was shown by the administration of glass beads which did not cause any alteration in the activities of hepatic mixed-function oxidases.
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PMID:Induction of hepatic drug metabolizing enzymes by coal fly ash in rats. 312

After oral administration of rifampicin and 25-desacetylrifampicin, which is a major metabolite of rifampicin in man but not in rat, to male Wister rats for 7 days, hepatic microsomal cytochrome P450, cytochrome b5, and activities of aniline hydroxylase, aminopyrine demethylase, bilirubin-conjugating enzymes and supernatant glutathione S-transferase were measured. Rifampicin induced bilirubin UDP-glucuronyltransferase, bilirubin UDP-glucosyltransferase, bilirubin UDP-xylosyltransferase and glutathione S-transferase activities, but did not induce mixed function oxidase activities. No inductive effect of desacetylrifampicin on any enzymes was observed. Serum bilirubin increased till the third day, and decreased after 7 days of rifampicin treatment. Plasma clearances of indocyanine green and sulfobromophthalein showed a marked delay after 1 day and 7 days of rifampicin treatment. Induction of bilirubin-conjugating enzymes and glutathione S-transferase by rifampicin in rats was different from that in humans, in which selective induction of mixed function oxidase is reported to occur. This species difference does not seem to be derived from the species difference of rifampicin metabolism, because no effect of desacetylrifampicin was observed. These results suggested that in rats rifampicin directly inhibits the hepatic excretion of bilirubin, whereas it enhances bilirubin conjugation due to enzyme induction.
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PMID:Induction of rat liver bilirubin-conjugating enzymes and glutathione S-transferase by rifampicin. 316 72

Propiconazole, a foliar fungicide used for agricultural purposes was studied for its effects on the hepatic xenobiotic biotransformation in the rat. Rats were given an intraperitoneal injection of 0.1, 1, 10 or 100 mg/kg in corn oil for seven consecutive days. Induction was seen for cytochrome P-450, ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase, aldrin epoxidase, aminopyrine N-demethylase and microsomal expoxide hydrolase activities. Aniline p-hydroxylase and cytosolic glutathione S-transferase activities were unchanged. All responses occurred at only 100 mg/kg, except for that of aminopyrine N-demethylase which also occurred at the 10 mg/kg dose. SDS polyacrylamide gel electrophoresis showed increased staining of a protein band of molecular weight 54,000 corresponding to cytochrome P-450b and/or P-450d. Collectively these results suggest that cytochromes P-450b and P-450d have been induced after exposure of rats to propiconazole.
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PMID:The effects of propiconazole on hepatic xenobiotic biotransformation in the rat. 319 Jul 55

Vitamin A deficiency causes a significant decrease in superoxide dismutase, glutathione peroxidase and GSH levels. Simultaneously, it causes a marked increase in Phase I microsomal oxidation (cytochrome P-450, aniline hydroxylase, PNA-O-demethylase) as well as in enzymatic and non-enzymatic lipid peroxidation in lung. Among Phase II enzymes, cytosolic chlorodinitrobenzene glutathione-S-transferase (CDNB-GST) activity showed a significant increase whereas microsomal UDP-glucuronyl transferase and cytosolic p-nitrobenzoyl chloride- and dichloro nitrobenzyl chloride-S-transferase activities showed variable decrease reflecting an imbalance in the Phase I and Phase II enzyme systems. CDNB-GST and non-Se-GSH-Px, registered a parallel rise with pulmonary cytochrome P-450, aniline hydroxylase and O-demethylase, as an adaptive response to elevated Phase I enzyme activity.
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PMID:Effect of vitamin A deficiency on pulmonary defense systems of guinea pig lung. 324 89

Chlordimeform, 4-chloro-o-toluidine and o-toluidine have all been found to have carcinogenic properties. Due to an empirical link between such properties and alteration of some biotransformation enzymes, the abilities of these three chemicals to affect cytochrome P-450 mediated biotransformation, epoxide hydrolase and glutathione S-transferase have been examined. Chlordimeform had no effect on the cytochrome P-450 content, aniline p-hydroxylase or glutathione S-transferase activities, but induced ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase and epoxide hydrolase activities and decreased aldrin epoxidase and aminopyrine N-demethylase activities. The metabolite 4-chloro-o-toluidine increased cytochrome P-450, ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase, glutathione S-transferase and epoxide hydrolase activities. o-Toluidine induced cytochrome P-450, ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase, and aldrin epoxidase activities. Ethoxy-resorufin-O-deethylase activity was induced approximately eight times by chlordimeform and 18 times by 4-chloro-o-toluidine and o-toluidine. Induction was seen at 50 mg/kg with chlordimeform and at 10 mg/kg with the other treatments. Chlordimeform increased the 7 alpha and 16 alpha androstenedione hydroxylase pathways. 4-Chloro-o-toluidine increased the 7 alpha, 16 beta and 16 alpha hydroxylase pathways, while o-toluidine increased the 7 alpha, 6 beta, 16 beta and 16 alpha hydroxylase pathways. All three chemicals marginally decreased the testosterone pathways. SDS-PAGE of rat microsomes revealed an increase in a protein band of MW c54,000 for the chlordimeform and 4-chloro-o-toluidine treated groups. Taken together with the increase in ethoxyresorufin-O-deethylase activity these observations are consistent with the induction of hepatic isozyme P-450d. Thus each chemical has been shown to induce various pathways of biotransformation with increases in the P-450c and P-450d specific substrate ethoxyresorufin-O-deethylase being a consistent finding.
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PMID:Induction of xenobiotic biotransformation by the insecticide chlordimeform, a metabolite 4-chloro-o-toluidine and a structurally related chemical o-toluidine. 339 Feb 15

Hepatic microsomes from rats starved 48 hours and refed diets containing zero, 3 or 20% corn oil metabolized benzo(a)pyrene, aniline and N-nitrosodimethylamine in proportion to the quantity of corn oil in the diet. No diet-related changes in apparent Km for these reactions were evident. The content of microsomal cytochrome P-450 was also clearly dependent upon the content of corn oil in the refed diets. When metabolism of these three substrates is expressed as product formed per unit of cytochrome P-450, the activities are least in microsomes from rats fed the 20% corn oil diet, suggesting that P-450 species responsible for metabolizing substrates other than these are enhanced preferentially. Cytosolic glutathione S-transferase activities are also increased with increasing corn oil in the diet. The administration of 3-MC increased cytochrome P-448 content of microsomes from all rats, regardless of diet, however highest content was present in microsomes from rats fed the 20% corn oil diet. Induction of benzo(a)pyrene hydroxylase was not influenced by dietary corn oil and, as anticipated, 3-MC caused significant repression of DMN N-demethylase in microsomes from rats fed the 20% corn oil diet. In like manner, 3-MC induced glutathione S-transferase only in cytosol from rats fed the fat-free diet.
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PMID:Role of dietary corn oil in the function of hepatic drug and carcinogen metabolizing enzymes of starved-refed rats: response to the mixed function oxidase inducer, 3-methylcholanthrene. 355 14

Keeping male rats within a month on a ration deficient in vitamin A led to a distinct decrease in content of cytochrome P-450, in activities of carboxylase, epoxide hydrolase, aniline hydrolase and to a slight inhibition of UDP-glucuronosyl transferase in live tissue. At the same time, activity of glutathione transferase and content of reduced glutathione in liver tissue were increased. After administration of the epoxide-containing T-2 mycotoxin into rats within 10 days at a dose of 0.54 mg/kg activity of the enzymes catalyzing metabolism of xenobiotics was inhibited in the animals maintained on the complete half-synthetic ration, except of epoxide hydrolase and glutathione transferase, activity of which was elevated. The administration of T-2 toxin under conditions of deficiency in vitamin A caused especially distinct inhibition of the enzymes involved in the 1 phase of xenobiotic metabolism but it was accompanied by only slight increase in T-2 toxicosis. The enzymes participating in conjugation of xenobiotics as well as epoxide hydrolase appear to play major roles in detoxication of T-2 mycotoxin.
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PMID:[Activity of enzymes of xenobiotic metabolism in the liver of rats with vitamin A deficiency and mycotoxicosis T-2]. 370 7

Oral administration of Prudhoe Bay crude or Hibernia crude to nestling herring gulls increased the hepatic cytochrome P-450 content 4-fold. Concomitantly, there was an increase in various mixed-function oxidase and phase II enzyme activities. 7-Ethoxyresorufin O-deethylase was elevated 19-fold, benzo(a)pyrene 3-hydroxylase 6-fold, aniline hydroxylase 3-fold, and aminopyrine N-demethylase and uridine diphosphate glucuronyl transferase 2-fold. There was no change in reduced glutathione S-transferase activity. Renal mixed-function oxidase activities were also elevated. Herring gull livers contained very low levels of DT-diaphorase activity which was inducible 3- to 5-fold by oil administration.
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PMID:Effects of ingestion of hibernia and Prudhoe Bay crude oils on hepatic and renal mixed function oxidase in nestling herring gulls (Larus argentatus). 396 42

The authors studied the effect of a long-term intragastric administration to CBA X C57Bl/6 male mice of T-2 toxin in doses of 0.067 mg/kg bw a day (1/100 of the LD50) or 0.33 and 0.45 mg/kg a day (1/20 and 1/15 of the LD50) on the liver content of protein, cytochrome P-450 SH-glutathione and on the activity of 10 lysosomal and microsomal enzymes and glutathione transferase. A dose-dependent increase in the activity of lysosomal hydrolases and glutathione transferase localized in cytosol was revealed together with a fall in the activity of microsomal aniline hydroxylase, carboxyl esterase and epoxide hydrolase. Emphasis is laid on a dose-dependent reduction in the liver of nonsedimented activity of lysosomal enzymes. In T-2 mycotoxicosis, the most sensitive and the most stable parameter was the activity of lysosomal enzymes in blood serum. That activity also declined during the recovery period, namely 3 months after discontinuance of toxin administration. Both groups of mice showed a progressive decrease in the blood leukocyte count and lysozyme content, whereas in the spleen, there was a decrease in the number of antibody-forming cells. It is concluded that biochemical, hematological and hematological characteristics should be taken into consideration in evaluating the chronic action of T-2 toxin.
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PMID:[Biochemical, hematological and immunological criteria for assessing chronic T-2 mycotoxicosis in mice]. 406 Jun 87

Oral doses of the sedative/hypnotic estazolam (500 mg kg-1 day-1) to rats for 21 days caused statistically significant increases in liver weight, ascorbate excretion, cytochrome P-450 concentrations, and in aniline hydroxylase, ethylmorphine N-demethylase and glutathione S-transferase activities, as did approximately equivalent doses of flurazepam hydrochloride. Histologically, the centrilobular hepatocytes were enlarged. Some of these parameters were also increased after doses of estazolam of 100 mg kg-1 day-1, but not after 5 mg kg-1 day-1, which is about 50-fold greater than a clinical dose. Estazolam was a much less potent enzyme inducer than phenobarbitone under the conditions of these studies.
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PMID:Effect of the triazolobenzodiazepine estazolam on hepatic drug-metabolizing enzyme activity in rats. 612 39


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