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- W1966652042 abstract "This study was undertaken to determine if interactions of toxicologic importance might occur during simultaneous exposure of mice to acetaminophen and fenitrothion. Acetaminophen administration induced dose-dependent hepatic morphologic changes which were accompanied by leakage of sorbitol dehydrogenase (SDH) into plasma 18 hr after dosing. Glutathione (GSH) depletion was maximal 2 hr after acetaminophen even at doses below those required for hepatic necrosis. Pretreatments with fenitrothion (50 or 500 mg/kg, ip) decreased hepatic GSH concentration and inhibited microsomal aniline hydroxylase and paranitroanisole O-demethylase activities. Similar treatments in mice subsequently challenged with acetaminophen (400 or 600 mg/kg, po) prevented the elevations in plasma SDH activity and lethality. Massive necrosis and 70% lethality were observed after 800 mg acetaminophen/kg and these effects were prevented by earlier pretreatment with 50 mg fenitrothion/kg. This pretreatment also decreased the degree of hepatic GSH depletion detected at 2 hr after 800 mg of acetaminophen. This finding would suggest that production of acetaminophen electrophile had been deceased by the pretreatment. Thus, with respect to interaction with acetaminophen, these results suggest that fenitrothion inhibition of mixed function oxidases predominated over fenitrothion depletion of GSH. Thus, even though GSH stores were lowered, less acetaminophen electrophile was generated and critical macromolecules were spared." @default.
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- W1966652042 date "1982-12-01" @default.
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- W1966652042 title "Protection against acetaminophen-induced hepatotoxicity by prior treatment with fenitrothion" @default.
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- W1966652042 doi "https://doi.org/10.1016/0041-008x(82)90305-2" @default.
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