Open AccessEstrogen receptor-dependent effects of bisphenol a
Author(s) -
Pamela Bulzomi,
Alessandro Bolli,
Marianna Marino
Publication year - 2011
Publication title -
journal of biological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.218
H-Index - 6
eISSN - 2284-0230
pISSN - 1826-8838
DOI - 10.4081/jbr.2011.4502
Subject(s) - estrogen receptor , bisphenol a , estrogen receptor alpha , apoptosis , xenoestrogen , cell growth , western blot , estrogen , receptor , endocrine disruptor , antagonist , cell cycle , cell , medicine , endocrinology , chemistry , biology , hormone , microbiology and biotechnology , biochemistry , cancer , endocrine system , breast cancer , organic chemistry , epoxy , gene
Bisphenol A (BPA), commonly used as building block of polycarbonate plastics, significantly affects human and animal health interfering with the action of natural hormones. Within BPA disrupting effects, a mitogenic activity and, consequently, an increased incidence of neoplastic transformations has been reported in exposed organisms. Among the several mechanisms proposed for the mitogenic BPA effects, its ability to bind to estrogen receptors (ERα and ERβ) deserves particular attention. Aim of this work is to investigate ERα- and ERβ-dependent mechanisms underlying BPA proliferative effect. Binding assay confirms that BPA binds to both ERs. Cell vitality assay and Western blot analysis of protein involved in cell proliferation demonstrate that BPA acts as a double side disruptor of estrogenic effects. In fact in the presence of ERα, BPA mimics E2, increasing cell proliferation. On the contrary, in the presence of ERβ, BPA acts as an E2 antagonist preventing the hormone-induced cancer cells apoptosis. These two divergent aspects could act synergistically in the exposed organisms leading to the disruption of the balance between proliferation and apoptosis typical of E2 effects