作者: B. B. Brodie , W. D. Reid , A. K. Cho , G. Sipes , G. Krishna
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摘要: Abstract Treatment of rats with phenobarbital, which stimulates the activity drug-metabolizing enzymes in liver, potentiates hepatic necrosis elicited by bromobenzene and a number other chemically inert halogenated aromatic hydrocarbons. Radioautographic studies indicate that [14C]bromobenzene is covalently bound at sites necrosis. From these results, it inferred hepatotoxic effects hydrocarbons are mediated active metabolites formed hepatocytes. In accord this view, converted microsomes vitro to intermediates form covalent complexes glutathione (GSH).