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Hepatic bromobenzene epoxidation and binding: prevention by ascorbyl palmitate.

Bromobenzene undergoes metabolic activation via 2,3- and 3,4-epoxidation catalyzed by the hepatic cytochrome P-450 mixed-function oxidase system. Its reactive metabolites, especially bromobenzene 3,4-oxide, presumably lead to severe centrolobular necrosis. A study of relative rate of binding of 14C-bromobenzene metabolites to hepatic microsomal protein indicated a significant difference in the rate of binding of the bromobenzene 3,4-oxide compared to its positional isomer, bromobenzene 2,3-oxide. However, the rate of bromobenzene metabolism indicated no significant difference in the formation of products o-bromophenol and p-bromophenol. A search for protective agents revealed that 6,7-dimethyl-5,6,7,8-tetrahydropterine and ascorbyl palmitate were very effective in protecting against macromolecular adduct formation at a concentration of 1 mM-in fact, at least a twofold increase in protection compared to the known protective agents such as glutathione or cysteine. Furthermore, 6,7-dimethyl-5,6,7,8-tetrahydropterine and ascorbyl palmitate inhibited the metabolism of bromobenzene over 90% at a concentration of 2.5 mM.