Abstract
There was good correlation of lipid peroxidation and covalent binding of acetaminophen (AAP) to liver microsomal protein in mice, guinea pigs and rabbits, but not in rats. By increasing concentrations of EDTA which is an inhibitor of lipid peroxidation, the degree of microsomal lipid peroxidation decreased in mice, guinea pigs, rabbits and rats, and the amount of covalent binding of AAP metabolite to liver microsomal protein increased in mice, guinea pigs and rabbits, but no consistent results were observed in rats. GSH depletion caused by AAP metabolite was increased in accordance with increase in the concentration of EDTA in mice and rats. In rats, the metabolism of AAP increased with increasing concentrations of EDTA and, in contrast to liver microsomes, the radioactivity of enzyme-mediated 14C-AAP metabolite in liver microsomal lipid was not observed. These results indicated that the decrease in covalent binding for AAP metabolite to liver microsomal protein with increasing concentrations of EDTA was not due to the decrease in the amount of AAP metabolite and the binding of 14C-AAP metabolite to liver microsomal lipid layer.
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