We investigated the interaction of bisphenol A (BPA, an estrogenic environmental contaminant used in the manufacture of plastics) with the estrogen receptor alpha (ER α ) transfected into the human HepG2 hepatoma cell line and expanded the study in vivo to examine the effect of BPA on the immature rat uterus. Bisphenol A was 26-fold less potent in activating ER-WT and was a partial agonist with the ER α compared to E 2 . The use of ER α mutants in which the AF1 or AF2 regions were inactivated has permitted the classification of ER ligands into mechanistically distinct groups. The pattern of activity of BPA with the ER α mutants differed from the activity observed with weak estrogens (estrone and estriol), partial ER α agonists (raloxifene or 4-OH-tamoxifen), or a pure antagonist (ICI 182, 780). Intact immature female Sprague–Dawley rats were exposed to BPA alone or with E 2 for 3 days. Unlike E 2 , BPA had no effect on uterine weight; however, like E 2 , both peroxidase activity and PR levels were elevated, though not to the level induced by E 2 . Following simultaneous administration, BPA antagonized the E 2 stimulatory effects on both peroxidase activity and PR levels but did not inhibit E 2 -induced increases of uterine weight. These results demonstrate that BPA is not merely a weak estrogen mimic but exhibits a distinct mechanism of action at the ER α .
Molecular and Cellular Endocrinology – Elsevier
Published: Jul 25, 1998
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