To determine the contribution of the diol-epoxide to the genotoxicity of benz[j]aceanthrylene (BjAA), the mutagenic activity of BjAA and its bay-region metabolites were evaluated in the Ames assay. BjAA, the 9,10-oxide, and the 9,lO-dihydrodiol are indirect acting mutagens with specific activities of 12.9 rev/nmole, 5.6 rev/nmol, and 9.4 rev/nmole, respectively. The 9,10-dihydrodiol-7,8-oxide was direct acting having the same activity as the parent compound, BjAA. Metabolism studies using Aroclor 1254 induced rat liver S9 were conducted on the BjAA-9,10-dihydrodiol metabolite. Four metabolites were isolated. Three metabolites were identified as 1,2,9,10-tetrahydro-l,2,9,10-tetrahydroxy-BjAA, 7,8,9,10-tetrahydro-7,8,9,10-tetrahydroxy-BJAA and the 9,10-dihydroxy-BjAA. The fourth metabolite was tentatively identified as BJAA-9,10-dihydrodiol-2-one. Similarly, the metabolism of cyclopentafused benzo[e]pyrene (cpBeP) was also investigated to determine whether the previously observed mutagenic activity of this compound was due to metabolism at the bay-region or the etheno bridge. Only one major metabolite was observed, the 3,4-dihydrodiol cpBeP. Additional minor metabolites were isolated, but not enough material was available to identify them. Oxidation occurs at the cyclopentafused ring for both BjAA and cpBeP when incubated with rat liver 59. This structure is of importance when considering mutagenic activation of a compound, and is an exception to the bay-region theory proposed by Jerina and colleagues.