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- W2003977145 abstract "Since administration of α-naphthylisothiocyanate (ANIT) to rats inhibits hepatic mixed-function oxidase (MFO) activity in vivo and in vitro, the nature of this inhibition was investigated; its role in the pathogenesis of ANIT-cholestasis was also examined. Male rats were treated (150 mg/kg, ip) with ANIT or β-naphthylisothiocyanate (BNIT), a noncholestatic isomer. ANIT was also given to hamsters (a resistant species) and to rabbits (a nonsusceptible species). The animals were killed at different intervals (2–72 hr); MFO activity was compared to plasma biochemical alterations (glutamic-pyruvic transaminase, bilirubin, 5′-nucleotidase) indicative of liver injury. In the rat, reductions in cytochrome P-450, aniline oxidase, and aminopyrine demethylase were evident before the development of hyperbilirubinemia. After 24 hr, cytochrome b5, total heme, and NADPH-cytochrome c reductase were also reduced, but glucuronyl transferase activity was increased. BNIT caused no elevation in plasma bilirubin or 5′-nucleotidase activity but decreased MFO activity in rats. Reductions in cytochrome P-450 and microsomal metabolism were also observed in hamsters and rabbits treated with ANIT, although only a moderate hyperbilirubinemia was observed in hamsters and none in rabbits. Both ANIT and BNIT caused reductions in cytochrome P-450 when incubated in vitro with microsomes. Loss of cytochrome P-450 due to increased degradation is suggested. We conclude that the metabolic lesion induced by ANIT is primary and does not result from the accumulation of bile acids within the hepatocyte. It appears, however, that this lesion has no causal relationship to the subsequent development of ANIT-induced cholestasis." @default.
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- W2003977145 title "Impairment of hepatic mixed-function oxidase activity by α- and β-naphthylisothiocyanate: Relationship to hepatotoxicity" @default.
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- W2003977145 doi "https://doi.org/10.1016/0041-008x(79)90428-9" @default.
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