PDF(Pubmed)
Abstract：
Estrogen excess in females has been linked to a diverse array of chronic and acute diseases. Emerging research shows that exposure to estrogen-like compounds such as bisphenol S leads to increases in 17β-estradiol levels, but the mechanism of action is unclear. The aim of this study was to reveal the underlying signaling pathway-mediated mechanisms, target site and target molecule of action of bisphenol S causing excessive estrogen synthesis. Human ovarian granulosa cells SVOG were exposed to bisphenol S at environmentally relevant concentrations (1 μg/L, 10 μg/L, and 100 μg/L) for 48 h. The results confirms that bisphenol S accumulates mainly on the cell membrane, binds to follicle stimulating hormone receptor (FSHR) located on the cell membrane, and subsequently activates the downstream cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signaling pathway, leading to enhanced conversion of testosterone to 17β-estradiol. This study deepens our knowledge of the mechanisms of environmental factors in pathogenesis of hyperestrogenism.
摘要：
女性雌激素过量与各种慢性和急性疾病有关。新兴的研究表明，暴露于雌激素样化合物如双酚S导致17β-雌二醇水平的增加，但作用机制尚不清楚。这项研究的目的是揭示潜在的信号通路介导的机制，双酚S作用的靶位点和靶分子导致雌激素过度合成。人卵巢颗粒细胞SVOG暴露于环境相关浓度的双酚S（1μg/L，10μg/L,和100μg/L）持续48h。结果证实双酚S主要在细胞膜上积累，与位于细胞膜上的卵泡刺激素受体（FSHR）结合，并随后激活下游环磷酸腺苷/蛋白激酶A（cAMP/PKA）信号通路，导致睾酮向17β-雌二醇的转化增强。这项研究加深了我们对环境因素在高雌激素血症发病机制中的认识。
