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The Effects of Antioxidants on Skin Tumor Initiation and Aryl Hydrocarbon Hydroxylase¹

Cancer and Toxicology Program, Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830 [T. J. S.], and East Tennessee Cancer Research Center, Knoxville, Tennessee 37919 [T. J. S., W. M. B.]

Butylated hydroxytoluene, butylated hydroxyanisole, and vitamins C and E are effective inhibitors of 7,12-dimethylbenz(a)anthracene tumor initiation in a two-stage system of tumorigenesis. These antioxidants did not significantly induce epidermal aryl hydrocarbon [benzo(a)pyrene]hydroxylase, nor did they have any effect when added directly to the in vitro aryl hydrocarbon [benzo(a)pyrene]hydroxylase assay. However, butylated hydroxytoluene and butylated hydroxyanisole, when applied topically to mice, inhibited the in vitro, epidermally mediated, covalent binding of radioactive benzo(a)pyrene and 7,12-dimethylbenz(a)anthracene to DNA. When butylated hydroxytoluene and butylated hydroxyanisole were added in vitro, they did not inhibit the epidermally mediated covalent binding of the hydrocarbons to DNA. The inhibition of polycyclic hydrocarbon tumorigenesis by antioxidants may be related to the ability of antioxidants to prevent the in vivo activation of hydrocarbons to carcinogenic epoxides and/or other electrophilic intermediates or may be related to their ability to increase detoxification of the reactive intermediate that requires intact cells to be operational. In any event, the results suggest that the antioxidants have an indirect effect on the epidermal metabolizing system which leads to a decrease in covalent binding to DNA.

¹ Supported by NIH Grant CA-17605 and by the Energy Research and Development Administration under contract with the Union Carbide Corporation. By acceptance of this article, the publisher or recipient acknowledges the right of the U. S. Government to retain a nonexclusive, royalty-free license in and to any copyright covering the article.

² To whom requests for reprints should be addressed, at Biology Division, Oak Ridge, National Laboratory, Post Office Box Y, Oak Ridge, Tenn. 37830.

Received 7/19/76. Accepted 2/24/77.

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