You are not currently logged in.
Access JSTOR through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Estrogenic Chemicals in Plastic and Oral Contraceptives Disrupt Development of the Fetal Mouse Prostate and Urethra
Barry G. Timms, Kembra L. Howdeshell, Lesley Barton, Sarahann Bradley, Catherine A. Richter, Frederick S. vom Saal and Howard A. Bern
Proceedings of the National Academy of Sciences of the United States of America
Vol. 102, No. 19 (May 10, 2005), pp. 7014-7019
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3375472
Page Count: 6
You can always find the topics here!Topics: Prostate, Bisphenols, Dosage, Chemicals, Fetus, Urethra, Epithelial cells, Oral contraceptives, Female animals, Cell growth
Were these topics helpful?See somethings inaccurate? Let us know!
Select the topics that are inaccurate.
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
Exposure of human fetuses to man-made estrogenic chemicals can occur through several sources. For example, fetal exposure to ethinylestradiol occurs because each year ≈3% of women taking oral contraceptives become pregnant. Exposure to the estrogenic chemical bisphenol A occurs through food and beverages because of significant leaching from polycarbonate plastic products and the lining of cans. We fed pregnant CD-1 mice ethinylestradiol (0.1 μg/kg per day) and bisphenol A (10 μg/kg per day), which are doses below the range of exposure by pregnant women. In male mouse fetuses, both ethinylestradiol and bisphenol A produced an increase in the number and size of dorsolateral prostate ducts and an overall increase in prostate duct volume. Histochemical staining of sections with antibodies to proliferating cell nuclear antigen and mouse keratin 5 indicated that these increases were due to a marked increase in proliferation of basal epithelial cells located in the primary ducts. The urethra was malformed in the colliculus region and was significantly constricted where it enters the bladder, which could contribute to urine flow disorders. These effects were identical to those caused by a similar dose (0.1 μg/kg per day) of the estrogenic drug diethylstilbestrol (DES), a known human developmental teratogen and carcinogen. In contrast, a 2,000-fold higher DES dose completely inhibited dorsolateral prostate duct formation, revealing opposite effects of high and low doses of estrogen. Acceleration in the rate of proliferation of prostate epithelium during fetal life by small amounts of estrogenic chemicals could permanently disrupt cellular control systems and predispose the prostate to disease in adulthood.
Proceedings of the National Academy of Sciences of the United States of America © 2005 National Academy of Sciences