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Carcinogenesis, Vol. 23, No. 8, 1369-1372, August 2002
© 2002 Oxford University Press

CARCINOGENESIS

Catechol estrogen formation in liver microsomes from female ACI and Sprague–Dawley rats: comparison of 2- and 4-hydroxylation revisited

Sonia Mesia-Vela1, Rosa I. Sanchez1, Jonathan J. Li3, Sara Antonia Li3, Allan H. Conney2 and Frederick C. Kauffman1,4

1 Laboratory of Cellular and Biochemical Toxicology, Department of Pharmacology and Toxicology, and
2 Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, College of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854 and
3 Department of Pharmacology, Toxicology and Experimental Therapeutics, Hormonal Carcinogenesis Laboratory, Kansas Cancer Institute, The University of Kansas Medical Center, Kansas City, KS 66160-7158, USA

Estradiol (E2)-hydroxylation was studied in liver microsomes from ACI and Sprague–Dawley female rats, which differ markedly in their susceptibility to E2-induced formation of mammary tumors. NADPH-dependent oxidation of E2 by liver microsomes from ACI and Sprague–Dawley rats produced several metabolites of which 2-hydroxyestradiol (2-OH-E2), estrone (E1), and 2-hydroxyestrone (2-OH-E1) were predominant. Incubations with either low (9 nM) or high (50 µM) concentrations of radiolabeled E2 and with varying amounts of microsomal protein indicated the formation of only small amounts of 4-hydroxyestradiol (4-OH-E2). The ratio of 2-OH-E2 to 4-OH-E2 formed with the low concentration of E2 was about 10:1 regardless of the amount of microsomal protein used, and about 20:1 using a high concentration of E2. Thus, oxidation of E2 by liver microsomes from female ACI and Sprague–Dawley rats occurs primarily via 2-hydroxylation, and 4-hydroxylation is only a minor pathway. These results are in disagreement with a recent report indicating substantial 4-hydroxylation of E2 by liver microsomes from female ACI rats.


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