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Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830 [T. J. S., G. L. G.]; Department of Pharmacology, University of Washington School of Medicine, Seattle, Washington 98195 [J. D., K. B. S.]; and Ben May Laboratory for Cancer Research, University of Chicago, Chicago, Illinois 50537 [R. G. H.]
The abilities of the racemic trans-3,4-, 5,6-, and 8,9-dihydrodiols of 7,12-dimethylbenz(a)anthracene to initiate skin tumors in mice were determined by using a two-stage system of tumorigenesis. The 7,12-dimethylbenz(a)anthracene trans-3,4-dihydrodiol was found to be much more active as a tumor initiator than the parent hydrocarbon. The 7,12-dimethylbenz(a)anthracene trans-5,6- and 8,9-dihydrodiols were essentially inactive as skin tumor initiators. Our results suggest that the 3,4-dihydrodiol of 7,12-dimethylbenz(a)anthracene is a proximal carcinogen and that the "bay region" diol-epoxide may be the ultimate carcinogenic form of DMBA.
1 Research sponsored by NIH Grants CA-20076 and CA-11968; American Cancer Society Grant BC-132C; and the Office of Health and Environmental Research, United States Department of Energy, under Contract W-7405-eng-26 with the Union Carbide Corporation.
2 To whom requests for reprints should be addressed, at Biology Division, Oak Ridge National Laboratory, P. O. Box Y, Oak Ridge, Tenn. 37830.
3 Present address: McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison, Wis. 53706.
Received 12/ 8/78. Accepted 2/23/79.
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