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Biology of Reproduction 61, 91-100 (1999)
©Copyright 1999 Society for the Study of Reproduction, Inc.


Articles

Differential Activity of Diethylstilbestrol versus Estradiol As Neonatal Endocrine Disruptors in the Female Hamster (Mesocricetus auratus) Reproductive Tract1

William J. III Hendry2,a, Brian L. DeBrota, Xinglong Zheng3,a, William S. Branhamb, and Daniel M. Sheehanb

a Department of Biological Sciences, Wichita State University, Wichita, Kansas 67260-0026 b Division of Reproductive and Developmental Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, Arkansas 72079

The synthetic estrogen diethylstilbestrol (DES) is a potent neonatal endocrine disruptor in the hamster. To test the specificity of this phenomenon, newborn animals were treated with 100 µg of either DES or the natural estrogen, estradiol-17ß (E2). Of the two, neonatal DES exposure caused greater morphological disruption throughout the female reproductive tract in prepubertal animals and in adults that either retained their ovaries or were ovariectomized and then given the same levels of chronic E2 stimulation. In the uterus, a characteristic histopathological profile, including enhancement of both hyperplastic and apoptotic activity, was initiated prepubertally and exclusively in the endometrial epithelial cell compartment from the neonatally DES-treated animals and then was promoted by E2 stimulation during adulthood. Interestingly, apoptotic activity was not detected in an area of endometrial epithelium that progressed to the neoplastic state in a DES-exposed animal. Lastly, chronic estrogen induction of lactoferrin was also restricted to the DES-exposed endometrium. We conclude that 1) DES is more active than E2 as a perinatal endocrine disruptor in the hamster and 2) this experimental system should be generally useful as a means to screen compounds for such activity and then probe their mechanism of action.

1 This work was supported by the National Cancer Institute (CA60250), the Flossie West Memorial Trust Foundation, and the United States Food and Drug Administration.

2 Correspondence: William J. Hendry III, Department of Biological Sciences, Wichita State University, 1845 Fairmount, Wichita, KS 67260–0026. FAX: 316 978 3772; hendry{at}wsuhub.uc.twsu.edu

3 Current address: Howard Hughes Medical Institute, Division of Hematology and Oncology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8125, St. Louis, MO 63110–1093.




This article has been cited by other articles:


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Biol. Reprod.Home page
W. J. Hendry III, W. S. Branham, and D. M. Sheehan
Diethylstilbestrol Versus Estradiol as Neonatal Disruptors of the Hamster (Mesocricetus auratus) Cervix
Biol Reprod, May 1, 2004; 70(5): 1306 - 1316.
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Biol. Reprod.Home page
C. T. Teng, C. Beard, and W. Gladwell
Differential Expression and Estrogen Response of Lactoferrin Gene in the Female Reproductive Tract of Mouse, Rat, and Hamster
Biol Reprod, November 1, 2002; 67(5): 1439 - 1449.
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Exp. Biol. Med.Home page
W. J. Hendry III, D. M. Sheehan, S. A. Khan, and J. V. May
Developing a Laboratory Animal Model for Perinatal Endocrine Disruption: The Hamster Chronicles
Experimental Biology and Medicine, October 1, 2002; 227(9): 709 - 723.
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