Expression of glutathione S-transferases Ya, Yb1, Yb2, Yc1 and Yc2 and microsomal epoxide hydrolase genes by thiazole, benzotbiazole and benzothiadiazole

Kim, Sang Geon; Cho, Min Kyung

doi:10.1016/s0006-2952(96)00505-9

Biochemical Pharmacology

1996

DOI: 10.1016/s0006-2952(96)00505-9

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Expression of glutathione S-transferases Ya, Yb1, Yb2, Yc1 and Yc2 and microsomal epoxide hydrolase genes by thiazole, benzotbiazole and benzothiadiazole

Sang Geon Kim

Min Kyung Cho

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Cited by 33 publications

References 28 publications

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Effects of enzyme inducers or inhibitors on the pharmacokinetics of intravenous parathion in rats

Hurh¹,

Lee²,

Lee³

et al. 2000

Biopharm. Drug Dispos.

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In order to find what form of hepatic cytochrome P450 (CYP) is involved in the metabolism of parathion to form paraoxon, rats were pretreated with the enzyme inhibitors, such as SKF 525-A and ketoconazole or enzyme inducers, such as dexamethasone, isoniazid, phenobarbital, and 3-methylcholanthrene. Parathion, 3 mg/kg, was infused in 1 min via the jugular vein. In rats pretreated with SKF 525-A or ketoconazole, nonspecific CYP inhibitors, the area under the plasma concentration-time curve from time zero to time infinity (AUC) and total body clearance (Cl) of parathion were significantly greater and slower, respectively, than those in respective control rats, suggesting that parathion was metabolized by CYPs. In rats pretreated with dexamethasone (CYP3A23 inducer), the AUC was significantly smaller (41.5 compared with 52.5 microg min/mL), Cl was significantly faster (72.2 compared with 57.1 mL/min/kg), and the amounts and/or tissue-to-plasma ratios of parathion was significantly (or tended to be) smaller than those in control rats. However, the pharmacokinetic parameters of parathion were not significantly different after pretreatment with other enzyme inducers compared with respective control rats. The above data suggested that parathion was metabolized to paraoxon by dexamethasone-inducible CYP3A23, the induction of which was confirmed by Western blot analysis. This was supported by in vitro intrinsic clearance (Cl(int)) of parathion to form paraoxon in hepatic microsomal fraction; the Cl(int) in rats pretreated with dexamethasone was significantly faster (0.0900 compared with 0.0290 mL/min/mg protein) than that in control rats.

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Effects of enzyme inducers or inhibitors on the pharmacokinetics of intravenous parathion in rats

Hurh¹,

Lee²,

Lee³

et al. 2000

Biopharm. Drug Dispos.

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show abstract

Expression of cytochrome p‐450s and glutathione s‐transferases in the rat liver during water deprivation: effects of glucose supplementation

Kim¹,

Kim²,

Kim³

et al. 2001

J of Applied Toxicology

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Pharmacokinetic profiles of therapeutic agents change in dehydrated animals. The present study was designed to determine the expression of xenobiotic-metabolizing enzymes in the rat liver and the effect of glucose supplementation during water deprivation. Deprivation of water intake, which reduced food intake, resulted in no significant change in the cytochrome P-450 1A2, 2B1/2, 2C11 and 3A1/2 expression. Cytochrome P-450 2E1, however, was three-fold induced with an increase in the mRNA. Rehydration of 48-h water-deprived rats for the next 24 h with free access to foods restored the P-450 2E1 level to that of the control, although rehydration with 20% food supply failed to normalize the P-450 2E1 expression. Water deprivation caused a reduction in the plasma insulin level, which was prevented by rehydration with a sufficient food supply. The plasma insulin level was inversely related to the P-450 2E1 expression. Glucose feeding instead of foods during dehydration prevented P-450 2E1 induction in the absence of recovering the plasma insulin level. Western blot analysis revealed that the hepatic rGSTA2 level was 30% decreased in dehydrated rats, whereas the rGSTA3, M1 and M2 expression was not affected. Suppression of rGSTA2 accompanied a reduction in the mRNA. Glucose feeding further reduced rGSTA2 expression. The data indicated that expression of major P-450s and glutathione S-transferases, except P-450 2E1, was not greatly affected by water deprivation and that the P-450 2E1 induction and a decrease in plasma insulin resulted from the reduction in food intake but not from dehydration per se. Glucose supplementation restored P-450 2E1 expression but further suppressed rGSTA2 expression during water deprivation.

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Effects of E. Coli lipopolysaccharide on the pharmacokinetics of ipriflavone and its metabolites, M1 and M5, after intravenous and oral administration of ipriflavone to rats: Decreased metabolism of ipriflavone due to decreased expression of hepatic CYP1A2 and 2C11

Chung

Kang

Bae

et al. 2008

Journal of Pharmaceutical Sciences

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Expression of glutathione S-transferases Ya, Yb1, Yb2, Yc1 and Yc2 and microsomal epoxide hydrolase genes by thiazole, benzotbiazole and benzothiadiazole

Cited by 33 publications

References 28 publications

Effects of enzyme inducers or inhibitors on the pharmacokinetics of intravenous parathion in rats

Effects of enzyme inducers or inhibitors on the pharmacokinetics of intravenous parathion in rats

Expression of cytochrome p‐450s and glutathione s‐transferases in the rat liver during water deprivation: effects of glucose supplementation

Effects of E. Coli lipopolysaccharide on the pharmacokinetics of ipriflavone and its metabolites, M1 and M5, after intravenous and oral administration of ipriflavone to rats: Decreased metabolism of ipriflavone due to decreased expression of hepatic CYP1A2 and 2C11

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