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|Title:||Effect of phenobarbitone on cytochrome P450 activity and chlorpyrifos and 3,5,6-trichloropyridinol levels in liver and serum in rat|
|Authors:||Verma, Radhey S|
Cytochrome P450 induction
|Abstract:||Chlorpyrifos [O,O'-diethyl-O-(3,5,6-trichloro-2-pyridyl) phos-phorothionate, CPF] undergoes oxidative desulfuration or dearylation by hepatic microsomal cytochrome P450 (CYP)-mediated monooxygenase reaction to CPF oxon or desethyl CPF, which are further metabolized to 3,5,6-trichloropyridinol (TCP). The present study showed that CPF exposure caused induction of hepatic CYP levels in rats. Phenobarbitone (PB) treatment elevated CYP activity by about 2.2-folds in controls, while CPF exposure to PB-treated rats did not cause further elevation in CYP levels. The levels of CPF in liver tissue and serum of rats given 50 and 100 mg CPF/kg body wt for 3 weeks were 17.15 ng and 29.39 ng/g and 33.71 ng and 56.34 ng/ml, respectively. The levels of TCP in these rats were 123.58 ng and 215.26 ng/g in liver tissue and 391.73 ng and 599.32 ng/ml in serum respectively. On PB-treatment, CPF levels were decreased by 46% and 38% in liver and 23% and 20% in serum of rats receiving 50 mg and 100 mg CPF/kg body wt for 3 days, while TCP levels were increased by 6% and 22% in liver and 22% and 44% serum, respectively. Results of this study clearly show that CYP2B, the PB-inducible form can biotransform CPF faster into TCP.|
|Appears in Collections:||IJBB Vol.42(4) [August 2005]|
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