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BOR - Papers in Press, published online ahead of print October 6, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.029769
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biolreprod.104.029769v1
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BIOLOGY OF REPRODUCTION 72, 423–435 (2005)
DOI: 10.1095/biolreprod.104.029769
© 2005 by the Society for the Study of Reproduction, Inc.

Effects of Neonatal Exposure to Diethylstilbestrol, Tamoxifen, and Toremifene on the BALB/c Mouse Mammary Gland1

Russell C. Hovey2, Mikiko Asai-Sato3, Anni Warri4, Barbara Terry-Koroma5, Nira Colyn, Erika Ginsburg, and Barbara K. Vonderhaar

Molecular and Cellular Endocrinology Section, Mammary Biology and Tumorigenesis Laboratory, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-1402

In this study, we compared the long-term effects of neonatal exposure to diethylstilbestrol (DES, 0.0125–50 µg), tamoxifen (TAM, 0.0125–50 µg), and toremifene (TOR, 53 µg) on mammary gland development and differentiation. Allometric growth of the mammary ducts was stimulated by neonatal DES exposure (12.5 µg) and impaired by exposure to TAM (25 µg). Neonatal treatment with high doses of DES resulted in mammary ducts that displayed extensive dilatation and precocious lactogenesis in postpubertal, nulliparous females. Initiation of this precocious differentiation coincided with the absence of corpora lutea, increased levels of serum prolactin (PRL), and the induction of Prl mRNA expression within the mammary glands. Neonatal exposure to 1.25 µg TAM increased alveolar development in postpubertal, nulliparous females similar to that recorded in females treated with low doses of DES. Lower doses of TAM did not affect alveolar development, whereas branching morphogenesis and alveolar development were impaired by higher doses. Increased alveolar development in females exposed to 1.25 µg TAM was associated with elevated serum progesterone (P) and increased alveolar development in response to exogenous P. Taken together, our findings demonstrate that neonatal exposure to both DES and TAM exerts long-lasting effects on the proliferation and differentiation of the mammary glands in female BALB/c, primarily as the result of endocrine disruption

1 R.C.H. and M.A.S. contributed equally to this work.

2 Correspondence: Russell C. Hovey, Lactation and Mammary Gland Biology Group, Department of Animal Science, University of Vermont, 121 Terrill Hall, 570 Main St., Burlington, VT 05405

3 Current address: Department of Obstetrics, Gynecology and Molecular Reproduction Science, Yokohama City University Graduate School of Medicine, Yokohama, Japan

4 Current address: University of Turku, Turku, Finland

5 Current address: Congressionally Directed Medical Research Programs, Fort Detrick, MD 21702-5024






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Copyright © 2005 by the Society for the Study of Reproduction.