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Products of Binding of 7,12-Dimethylbenz(a)anthracene to DNA in Mouse Skin¹

LBI-Basic Research Program, Chemical Carcinogenesis Program, NCI-Frederick Cancer Research Facility, Frederick, Maryland 21701

7,12-Dimethylbenz(a)anthracene (DMBA):deoxyribonucleoside-adducts, from enzymatic hydrolysis of DNA from mouse skin exposed to [³H]DMBA in vivo, were analyzed by reversephase high-pressure liquid chromatography. Double-labeling studies showed that the adducts were qualitatively identical to those formed in mouse embryo cell cultures. These have been tentatively identified as bay-region anti-dihydrodiol epoxide: deoxyguanosine- and :deoxyadenosine adducts and a bay-region syn-dihydrodiol epoxide:deoxyadenosine-adduct (where the terms syn and anti define dihydrodiol-epoxides wherein the benzylic hydroxyl group and epoxide oxygen are cis or trans to one another, respectively). The relative amounts of individual adducts did not vary substantially with time or with the sex of the mice. However, the syn-dihydrodiol-epoxide:deoxyadenosine-adduct did increase with dose and constituted as much as 40% of the total DNA binding at high doses of DMBA. This is in contrast to the much lower (2 to 3%) levels of binding to deoxyadenosine residues in mouse skin reported for the less potent tumor initiator benzo(a)pyrene. The greater reactivity of DMBA with deoxyadenosine residues in mouse skin may play a role in determining its greater tumor initiating potential.

¹ Research sponsored by the National Cancer Institute, Department of Health and Human Services, under Contract NO1-CO-23909 with Litton Bionetics, Inc.

² To whom requests for reprints should be addressed.

³ The work reported in this paper was undertaken during the tenure of a Research Training Fellowship awarded by the International Agency for Research on Cancer. J. T. Sawicki's permanent address is Department of Environmental Health Sciences, Medical Academy, Warsaw, Poland.

Received 5/27/83. Accepted 8/ 1/83.