Benzo[ a ]pyrene (BP) is a well-studied polycyclic aromatic hydrocarbon (P AH) .Many mechanisms have been suggested to explain its carcinogenic activity, yet many questions still remain. K-region dihydrodiols (diols) ofPAHs are common metabolites and some are genotoxic. We are testing the hypothesis that the genotoxicity ofK-region diols result from their metabolism to diol-quinones that support redox cycling which generates ROS that induces DNA damage. In the case ofBP, we have previously shown that the K-region diol ofBP, BP-4,5-diol, was further metabolized to the bis-diol, BP-4,5 :7 ,8-bis-diol. Here we present evidence that BP-4,5-diol induced morphological cell transformation (MCT) in C3H10TY2CL8 mouse embryo cells (10TY2 ::,ells). This diol also induced DNA damage in these cells, but did not form stable covalent DNA adducts. BP-4,5-diol and BP induced MCT in 10TY2 cells by producing significant numbers of Type II & III foci (2-11 uM). The dose response curves for BP-4,5-diol and BP were the same. Using the comet assay and experimental conditions and concentrations similar to those used in the MCT studies, both BP-4,5-diol and BP induced significant DNA damage without significant concurrent cytotoxicity. A positive control, BP- 7 ,8-quinone also induced significant DNA damage. DNA adduct patterns in 10TY2 cells were examined after P AH treatment using 32P- postlabeling and TLC elution systems designed to separate polar adducts. While BP treatment produced one major DNA adduct (BP-diol epoxide-dGuo ), no stable covalent DNA adducts were detected in BP-4,5-diol-treated cells. We propose that BP-4,5-diol is metabolized to BP-4,5 :7,8- bis-diol which is further converted to BP-4,5-diol- 7 ,8-quinone by dihydrodiol dehydrogenase. This diol-quinone produces ROS through redox cycling which induces DNA damage and MCT . These data suggest a new mechanism for the bioactivation of P AHs. This abstract does not reflect EP A policy.