Strain A/J mice received intraperitoneal injections of benz(j)aceanthrylene(B(j)A) or benzo(a)pyrene (B(a)P). At 24, 48, and 72 h, lung tissues were removed for analysis of B(a)P- or B(j)A-derived DNA adduct formation during the first 3 d of exposure. One group of mice exposed to these hydrocarbons was kept for 8 mo to determine lung tumor multiplicity, the occurrence of mutations in codons 12 and 61 of the Ki-ras gene in the tumors that arose, the relationship between Ki-ras oncogene mutations in tumors, and the presence and quantity of genomic DNA adducts. Analysis of adduction patterns in DNA suggested that B(j)A was activated to form DNA-binding derivatives in A/J mouse lungs primarily at the cyclopenta ring even though B(j)A contains a bay region. As reported in the published literature, the mutation spectrum induced by 3-MCA in Ki-ras codon 12 of mouse cells is similar to that of B(a)P but not to that of its close relative B(j)A. In contrast to B(j)A, 3-MCA is activated mostly via a bay-region diol-epoxide since its cyclopenta ring is saturated and not easily epoxidated. Therefore, we propose that the GGT --> CGT mutations produced by B(j)A in Ki-ras codon 12 were mostly the result of cyclopenta-ring-derived adducts.