Low Doses of Bisphenol A Promote Human Seminoma Cell Proliferation by Activating PKA and PKG via a Membrane G-Protein–Coupled Estrogen Receptor
Author(s) -
Adil Bouskine,
Marielle Nebout,
Françoise Brücker-Davis,
Mohamed Benahmed,
Patrick Fénichel
Publication year - 2009
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.0800367
Subject(s) - estrogen receptor , cell growth , protein kinase a , chemistry , creb , diethylstilbestrol , medicine , endocrinology , endocrine disruptor , estrogen , biology , kinase , transcription factor , biochemistry , hormone , endocrine system , cancer , breast cancer , gene
Fetal exposure to environmental estrogens may contribute to hypofertility and/or to testicular germ cell cancer. However, many of these xenoestrogens have only a weak affinity for the classical estrogen receptors (ERs,) which is 1,000-fold less potent than the affinity of 17beta-estradiol (E(2)). Thus, several mechanisms have been suggested to explain how they could affect male germ cell proliferation at low environmental relevant concentrations.
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