Department of Biological Sciences George Washington University Washington, DC 20052
In our study, we showed that the increase in uterine weight and uterine epithelial cell height induced by subcutaneous administration of bisphenol A (BPA) to ovariectomized B6C3F1 mice was reversed by co-administration of the estrogen receptor antagonist, ICI 182,780 (ICI). The maximum response to BPA was less than that for estradiol (E2), and more ICI was needed to block these responses to BPA than to E2. Little is known about the potential differences in BPA and E2 binding sites on the estrogen receptor, intrinsic activity, or their interaction with the ICI binding site(s) that may account for the observed differences in the pharmacology of E2- and BPA-mediated responses. Nevertheless, our data suggest that the BPA-induced increase in uterine weight and uterine epithelial cell height are mediated by the estrogen receptor. Our study does not rule out additional mechanisms of BPA-mediated uterotrophic effects, especially on the stromal and myometrial layers of the uterus, and these are briefly examined in the Discussion section of our paper.