| Xenoestrogens Alter Mammary Gland Differentiation and Cell Proliferation in the Rat
Nadine M. Brown and Coral A. Lamartiniere Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL 35294 USA Abstract
We investigated mammary gland differentiation and cell proliferation in rats after acute exposure to xenoestrogens. Pubertal female Sprague-Dawley rats (six/group) were treated for 1 week with diethylstilbestrol (DES) , genistein, o,pī-DDT, Aroclor 1221, Aroclor 1254, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) , or the vehicle, sesame oil. Animals were killed 18 hr after the last treatment. Analysis of mammary whole-mounts revealed that exposure to DES, genistein, and o,pī-DDT resulted in enhanced gland differentiation and increased epithelial cell proliferation as measured by proliferating cell nuclear antigen immunohistochemistry. TCDD treatment inhibited cell proliferation and gland development. Aroclor 1221 and Aroclor 1254 treatments had slight but not statistically significant effects on cell proliferation and mammary gland development. We conclude that DES, genistein, and o,pī-DDT given to pubertal rats act as morphogens ; i.e., they increase cell proliferation, which promotes maturation of the undifferentiated terminal end buds to more differentiated lobular terminal ductal structures. Key words: Aroclor, cell proliferation, diethylstilbestrol, dioxin, genistein, mammary gland, o, pī-DDT, xenoestrogens. Environ Health Perspect 103:708-713 (1995)
Address correspondence to C.A. Lamartiniere, Department of Pharmacology and Toxicology, Volker Hall G78G, University of Alabama at Birmingham, Birmingham, AL 35294 USA. The authors thank Julie Foley (National Institute of Environmental Health Sciences) for assisting us in the analysis of PCNA immunohistochemistry and Judson Moore for assisting in the preparation of mammary whole mounts. We thank Charles Hebert (Southern Research Institute) for reviewing the manuscript. This research was supported in part by NIH grants RO1-CAG1742-01 and RO1-ES07273-01. Received 17 January 1995 ; accepted 4 May 1995.
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