3-methylcholanthrene blocks hepatic necrosis induced by administration of bromobenzene or carbon tetrachloride

In vivo and in vitro binding of carbon tetrachloride with nucleic acids and proteins in rat and mouse liver

“…It should be noted that without MCA treatment the binding in presence of mouse liver microsomes is scant and lower than that in the presence of the microsomal fraction from mouse liver. Differences in toxicity and binding of CCI, to macromolecules between rats and mice after treatment with MCA have been reported by Reid (1971).…”

The role of biotransformation in chemical-induced liver injury.

“…In contrast, the pretreatment of rats with 3methylcholanthrene decreases both the covalent binding of radiolabeled bromobenzene to liver protein and the severity of liver necrosis (30,33). Since the pretreatment does not alter the biological half-life of bromobenzene in rats (30) and actually increases the rate of bromobenzene metabolism by liver microsomes (30), the protective effect cannot be due to a decrease in the rate of bromobenzene elimination.…”

Enhanced Hepatic Microsomal Activity by Pretreatment of Rats with Acetone or Isopropanol

“…The lack of any change in cytochrome P-450 is not consistent with the type of induction produced after pretreatment with 3-MC (1 7). Pretreatment of rats with 3-MC reduces the rate of demethylation of DMN (18), decreases the covalent binding of l4Ccl4 to microsomal protein (Sipes, unpublished results) and blocks hepatic necrosis induced by CCll (19). On the other hand, pretreatment with acetone or isopropanol enhances the rate of N-demethylation of DMN, increases the covalent binding of l4ccI4 and potentiates the hepatotoxicity induced by CC14.…”