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N -Heterocyclic polynuclear aromatic hydrocarbons (NHA) areenvironmental pollutants formed during the combustion of organic materials.7H -Dibenzo[ c,g ]carbazole (DBC) is a potentcarcinogen in lung, liver and skin. We undertook these studies to determinewhether tissue specificity for DBC lung carcinogenicity inthe strain A/Jmouse is mirrored by formation of DBC-DNA adducts in lung tissue and whetherthese adducts are consistent with mutation patterns in theK- ras  gene. Strain A/J mice were given a single i.p.injectionof DBC at doses of 0, 5, 10, 20 or 40 mg/kg and levels of DNAadducts in the lung were monitored by  32 P-postlabeling on days1,3,5,7,14 and 21. The remaining animals were sacrificed 8 months after DBCtreatment and lung tumor multiplicity and K- ras  mutationpatterns in the tumors were determined. The lung tumor response to DBC was doserelated, with an average of 4.7 ± 1.2 tumors/mouse at 5mg/kg and 48.1 ± 5.5 tumors/mouse at 40 mg/kg. Asmany as seven DBC-DNA adducts were observed in the lung. DNA binding levels inthe lung were highest at 40 mg/kg, with maximum binding at 5-7 days. Atlower dose levels the maximum binding to DNA decreased and shifted to earliertime points. The DBC-DNA adduct in the lung with the highest level of binding atall dose levels was DBC-DNA adduct 3. The majority of DBC-induced mutations inthe K- ras  gene in the lung were A↑T(80%)transversions in the third base of codon 61, a mutation that has not beenpreviously observed in chemically induced lung tumors in strain A/Jmice.

carcinogenesis

Carcinogenicity, DNA adduct formation and K- ras                      activation by 7 H -dibenzo[ c, g ]carbazole in                     strain A/J mouse lung