Potential estrogenic effects of bisphenol-A estimated by in vitro and in vivo combination assays.

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  • KIM Hyung Sik
    Reproductive & Developmental Toxicology Division, National Institute of Toxicological Research, Korea Food and Drug Administration
  • HAN Soon-Young
    Reproductive & Developmental Toxicology Division, National Institute of Toxicological Research, Korea Food and Drug Administration
  • YOO Sun Dong
    College of Pharmacy, Sungkyunkwan University
  • LEE Byung Mu
    College of Pharmacy, Sungkyunkwan University
  • PARK Kui Lea
    Reproductive & Developmental Toxicology Division, National Institute of Toxicological Research, Korea Food and Drug Administration

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The potential estrogenic activities of bisphenol-A were investigated in vitro (E-screen and estrogen receptor competitive binding bioassays) and in vivo (uterotrophic assay). Uterotrophic responses were evaluated using mature ovariectomized Sprague-Dawley female rats treated subcutaneously with bisphenol A (1, 5, 10, 50, and 100 mg/kg/day), E2 (0.3 μg/kg), and DES (0.3 μg/kg) for 3 consecutive days. In a MCF-7 cell proliferation assay, E2 and DES used as positive estrogens induced maximum proliferation of MCF-7 cells at 1.0 nM, whereas BPA slightly induced MCF-7 cell proliferation at a higher level of 0.1μM and maximum proliferation at 10μM. In a competitive binding assay, E2 and DES showed inhibition of 17 β-[3H]estradiol binding to the rat uterus ER with an IC50 of 1.0 nM and 0.5 nM, respectively. However, BPA had an IC50 of 5 μM, which was approximately 5,000 or 10,000-fold greater than the IC50 of E2 and DES. In uterotrophic assays, uterus (wet and blotted) and vagina weights were significantly increased at the dose of BPA 100 mg/kg/day in OVX Sprague-Dawley rats. These studies demonstrate that BPA exhibits weak estrogenic activity in all experimental systems, and thus its migration from epoxy resins or polycarbonate products should be controlled not to exceed a safety levels for humans.

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