Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (9)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Mesia-Vela, S.
Right arrow Articles by Kauffman, F. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mesia-Vela, S.
Right arrow Articles by Kauffman, F. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
S. Mesia-Vela, R. I. Sanchez, K. R. Reuhl, A. H. Conney, and F. C. Kauffman
Phenobarbital Treatment Inhibits the Formation of Estradiol-Dependent Mammary Tumors in the August-Copenhagen Irish Rat
J. Pharmacol. Exp. Ther., May 1, 2006; 317(2): 590 - 597.
[Abstract] [Full Text] [PDF]

Home page
 J EndocrinolHome page
V K Turan, R I Sanchez, J J Li, S A Li, K R Reuhl, P E Thomas, A H Conney, M A Gallo, F C Kauffman, and S Mesia-Vela
The effects of steroidal estrogens in ACI rat mammary carcinogenesis: 17{beta}-estradiol, 2-hydroxyestradiol, 4-hydroxyestradiol, 16{alpha}-hydroxyestradiol, and 4-hydroxyestrone
J. Endocrinol., October 1, 2004; 183(1): 91 - 99.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
R. R. Riley, S. Duensing, T. Brake, K. Munger, P. F. Lambert, and J. M. Arbeit
Dissection of Human Papillomavirus E6 and E7 Function in Transgenic Mouse Models of Cervical Carcinogenesis
Cancer Res., August 15, 2003; 63(16): 4862 - 4871.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.