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- W2296961014 abstract "Dithiocarbamate drugs such as disulfiram are extensively metabolized in the body to carbon disulfide (CS2), which can produce a variety of toxic effects. When metabolized by phenobarbital-induced cytochrome P450s (CYPs), CS2 produces hepatic necrosis in rats. In this study we investigated whether CYPs induced by chlordane (CLD), a paradigm of chlorinated hydrocarbon pesticides, potentiate hepatotoxicity of CS2. Male Sprague-Dawley rats (n=3) were treated with CLD (25 mg/kg, ip) daily for 4 days and 24 h after the final injection, the rats were injected with CS2 (380 mg/kg, ip) in oil while controls received vehicle alone. The rats were then sacrificed at 3, 6 and 24 h. At 3 h post-treatment, total hepatic GSH decreased modestly but lipid peroxidation increased markedly while all CLD-inducible CYPs (1A1, 2B1, 2E1 and 3A2) were inhibited by CS2 significantly and variably. At 24 h there was a significant increase in GSH, lipid peroxidation, and ALT activity. Activity of the CYPs was also increased but still remained significantly depressed, especially that of CYP2B1. Livers taken at 3 and 6 h showed subtle to distinct apoptotic changes and at 24 h a severe lesion of hydropic degeneration of the centrilobular cells with apoptosis was observed. These results indicate that the metabolism of CS2 by CLD-induced CYPs and the generation of lipid peroxides may have contributed to the enhanced hepatocellular damage." @default.
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- W2296961014 date "2008-03-01" @default.
- W2296961014 modified "2023-09-26" @default.
- W2296961014 title "Potentiation of the hepatotoxicity of carbon disulfide by chlordane‐induced cytochrome P450 enzymes" @default.
- W2296961014 doi "https://doi.org/10.1096/fasebj.22.1_supplement.1137.5" @default.
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