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Carcinogenesis, Vol. 22, No. 9, 1505-1510, September 2001
© 2001 Oxford University Press

CARCINOGENESIS

The ability of four catechol estrogens of 17ß-estradiol and estrone to induce DNA adducts in Syrian hamster embryo fibroblasts

Eiichi Yagi, J.Carl Barrett1,2 and Takeki Tsutsui

Department of Pharmacology, The Nippon Dental University, School of Dentistry at Tokyo, Tokyo 102-8159, Japan and
1 National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA and National Cancer Institute, Bethesda, MD 20892, USA

Catechol estrogens are considered critical intermediates in estrogen-induced carcinogenesis. We demonstrated previously that 17ß-estradiol (E2), estrone (E1) and four of their catechol estrogens, 2- and 4-hydroxyestradiols (2- and 4-OHE2), and 2- and 4-hydroxyestrones (2- and 4-OHE1) induce morphological transformation in Syrian hamster embryo (SHE) fibroblasts, and the transforming abilities vary as follows: 4-OHE1 > 2-OHE1 > 4-OHE2 > 2-OHE2 E2, E1. To examine the involvement of catechol estrogens in the initiation of hormonal carcinogenesis, we studied the ability of E2, E1 and their catechol estrogens to induce DNA adducts in SHE cells by using a 32P-post-labeling assay. DNA adducts were detected in cells treated with each of all the catechol estrogens at concentrations of 10 µg/ml for 1 h and more. 2- or 4-OHE2 formed a single DNA adduct, which was chromatographically distinct from each other. In contrast, 2- or 4-OHE1 produced one major and one minor adduct, and the two adducts formed by each catechol estrogen exhibited identical mobilities on the chromatograms. Neither E2 nor E1 at concentrations up to 30 µg/ml induced DNA adducts. The abilities of the estrogens to induce DNA adducts were ranked as follows: 4-OHE1 > 2-OHE1 > 4-OHE2 > 2-OHE2 > > E2, E1, which corresponds well to the transforming and carcinogenic abilities of the estrogens. In addition, the level of DNA adducts induced by the catechol estrogens was markedly decreased by co-treatment of cells with the antioxidant L-ascorbic acid. The results indicate the possible involvement of oxidative metabolites of catechol estrogens of E2 and E1 in the initiation of endogenous estrogen-induced carcinogenesis.


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