Abstract
Bisphenol A (BPA) is a ubiquitous environmental pollutant, mainly from the production and use of plastics and the degradation of wastes related to industrial plastics. Evidence from laboratory animal and human studies supports the view that BPA has an endocrine disrupting effect on Leydig cell development and function. To better understand the adverse effects of BPA, we reviewed its role and mechanism by analyzing rodent data in vivo and in vitro and human epidemiological evidence. BPA has estrogen and anti-androgen effects, thereby destroying the development and function of Leydig cells and causing related reproductive diseases such as testicular dysgenesis syndrome, delayed puberty, and subfertility/infertility. Due to the limitation of BPA production, the increased use of BPA analogs has also attracted attention to these new chemicals. They may share actions and mechanisms similar to or different from BPA.
Highlights
Leydig cells (LCs) are a group of cells located in the interstitium of the testis [see review [1]]
Bisphenol A (BPA) weakly inhibited both human and rat HSD11B2 with IC50 values about 100 or over 100 μM [103]. These results indicate that BPA directly inhibits steroidogenic enzyme activities at the higher concentrations
BPA is a ubiquitous environmental pollutant, mainly from the manufacture and use of plastics and its degradation of waste related to industrial plastics
Summary
Leydig cells (LCs) are a group of cells located in the interstitium of the testis [see review [1]]. BPA was orally administered to adult male rats at 0.005, 0.5, 50, and 500 μg/kg/day for 45 days, and it significantly increased testicular ROS levels, suggesting that BPAinduced ROS might be involved in its inhibition of T synthesis in LCs [111].
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