Comparison of benzo(a)pyrene metabolism and sister chromatid exchange induction in mice

Abstract

To determine the relationship of metabolic potential to an easily quantified, short-term in vivo end point of genetic damage, the ability of AHH inducible and uninducible mice to metabolize a procarcinogen, benzo(a)pyrene (BP), was compared with the in vivo induction by BP of sister chromatid exchanges (SCE). SCE induction was correlated with mutagenesis. Although BP did cause an increase in SCE in test animals, the extent of this increase did not differ between the inducible C57BL/6 mice and the uninducible DBA/2 mice. Prior exposure to an AHH[arylhydrocarbon hydroxylase](EC 1.14.14.2) inducer, 3-methylcholanthrene (3-MC), did not increase the number of BP-induced SCE in C57BL/6 mice. This lack of correlation between benzo(a)pyrene hydroxylase inducibility and SCE response reinforces the idea that other metabolic steps, such as detoxification or DNA repair, may influence the overall genetic impact of a drug.