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Bisphenol-A acts as a potent estrogen via non-classical estrogen triggered pathways

► Animal and cellular studies demonstrate low dose effects of BPA. ► BPA has been traditionally considered a weak estrogen. ► ERα−/− and ERβ−/− mouse model indicate ERs involvement in low dose-initiated BPA actions. ► BPA is equally potent to E2 via ERs when actions are triggered out of the nucleus....

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Published in:Molecular and cellular endocrinology 2012-05, Vol.355 (2), p.201-207
Main Authors: Alonso-Magdalena, Paloma, Ropero, Ana Belén, Soriano, Sergi, García-Arévalo, Marta, Ripoll, Cristina, Fuentes, Esther, Quesada, Iván, Nadal, Ángel
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Language:English
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Summary:► Animal and cellular studies demonstrate low dose effects of BPA. ► BPA has been traditionally considered a weak estrogen. ► ERα−/− and ERβ−/− mouse model indicate ERs involvement in low dose-initiated BPA actions. ► BPA is equally potent to E2 via ERs when actions are triggered out of the nucleus. Bisphenol-A (BPA) is an estrogenic monomer commonly used in the manufacture of numerous consumer products such as food and beverage containers. Widespread human exposure to significant doses of this compound has been reported. Traditionally, BPA has been considered a weak estrogen, based on its lower binding affinity to the nuclear estrogen receptors (ERs) compared to 17-β estradiol (E2) as well as its low transcriptional activity after ERs activation. However, in vivo animal studies have demonstrated that it can interfere with endocrine signaling pathways at low doses during fetal, neonatal or perinatal periods as well as in adulthood. In addition, mounting evidence suggests a variety of pathways through which BPA can elicit cellular responses at very low concentrations with the same or even higher efficiency than E2. Thus, the purpose of the present review is to analyze with substantiated scientific evidence the strong estrogenic activity of BPA when it acts through alternative mechanisms of action at least in certain cell types.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2011.12.012