Journal Article

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

Sonia Mesia-Vela, Rosa I. Sanchez, Jonathan J. Li, Sara Antonia Li, Allan H. Conney and Frederick C. Kauffman

in Carcinogenesis

Volume 23, issue 8, pages 1369-1372
Published in print August 2002 | ISSN: 0143-3334
Published online August 2002 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/23.8.1369
Catechol estrogen formation in liver microsomes from female ACI and Sprague–Dawley rats: comparison of 2- and 4-hydroxylation revisited

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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.

Keywords: E2, estradiol; E1, estrone; 2-OH-E2, 2-hydroxyestradiol; 2-OH-E1, 2-hydroxyestrone; 4-OH-E2, 4-hydroxyestradiol

Journal Article.  3408 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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