Abstract
Genetic differences in aromatic hydrocarbon “responsiveness” exist among various mouse strains. New formation of cytochrome P1–450 and the induction of aryl hydrocarbon (benzo [a]pyrene) hydroxylase (as well as numerous other monooxygenase activities) appear to be associated ultimately with genes that cosegregate at a small number of genetic loci. By comparing “responsive” and “nonresponsive” siblings, we can evaluate the susceptibility of each individual to various mutagenic chemicals in vitro or carcinogenic agents in vivo.

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