Bisphenol S causes excessive estrogen synthesis by activating FSHR and the downstream cAMP/PKA signaling pathway

  • Commun Biol. 2024 Jul 10;7(1):844. doi: 10.1038/s42003-024-06449-2.
Xiaorong Zhang  #  1  2 ,  Xinda Zhang  #  1 ,  Zhenzhong Zhang  1 ,  Yijiao Shi  1 ,  Jun Wang  1 ,  Shaoguo Ru  1 ,  Hua Tian  3
Affiliations
  • 1. College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China.
  • 2. Tai'an Agriculture and Rural Affairs Bureau, 271000, Tai'an, Shandong Province, China.
  • 3. College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China. [email protected].
  • # Contributed equally.
PMID: 38987655 DOI: 10.1038/s42003-024-06449-2
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.

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