Abstract: 342

ESTROUS CYCLICITY AND OVARIAN MORPHOLOGY OF RATS EXPOSED TO BISPHENOL A OR DIETHYSTILBESTROL DURING PRENATAL AND POSTNATAL DEVELOPMENT.

Seok Kwon^{1 *}, D. Stedman¹ , B. Elswick¹ , R.C. Cattley¹ , F. Welsch¹
Chemical Industry Institute of Toxicology, Research Triangle Park, NC ¹

Bisphenol A (BPA) is used in the manufacture of plastics. Concerns have been raised that compounds like BPA may alter reproductive functions because BPA binds to estrogen receptors in vitro. The hypothesis is that pre- or neonatal exposure to BPA permanently alters normal reproductive functions. We determined whether BPA affects estrous cyclicity and ovarian morphology in rat offspring. BPA was given to pregnant Sprague-Dawley rats by gavage at 0, 3.2, 32, or 320 mg/kg/day from gestation day 11 through postnatal day 21. Diethystilbestrol (DES) at 15 mg/kg/day was used as a reference chemical for estrogenic effects. At the age of 4 months, 185 female offspring was examined for estrous cyclicity. Daily vaginal lavage cell smears were obtained for approximately 1 month, and estrous cyclicity was monitored by evaluating changes in the vaginal cytology. Estrous cyclicity was altered in 29 of 36 DES-treated animals (26, prolonged diestrus; 3, prolonged estrus), with all 7 litters (100%) affected. In control animals, only 2 of 34 animals showed prolonged diestrus, with 2 of 8 litters affected. Only 3 of 34 animals in the highest BPA dose group showed prolonged diestrus, with 3 of 8 litters affected. Four of 42 and 6 of 39 animals showed prolonged diestrus in the 3.2 and 32 mg/kg/day BPA dose groups, respectively, with 3 of 8 litters affected. Ovaries from selected offspring (1-2/litter) were examined for presence of normal corpora lutea at 6 months of age. Although the DES-treated animals had the highest incidence of offspring with abnormal ovaries, this was not significantly different from BPA or control animals. These data indicate that BPA affects neither estrous cyclicity nor ovarian morphology under the present experimental conditions and do not support the hypothesis that pre- or neonatal exposure to BPA alters normal reproductive functions in rats.

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