BDE-209 disturbed proliferation and differentiation of spermatogonia during mitotic process through estrogen receptor α.

Abstract

Deca-bromodiphenyl ether (BDE-209) exposure caused spermatogenesis disorder resulting in poor sperm quality has become a public concern in recent years. Spermatogenesis refers to the process by which the division of spermatogonia stem cells (SSCs) produces haploid spermatozoa, including mitosis, meiosis, and spermiogenesis. However, the mechanism of mitosis including proliferation and differentiation of spermatogonia dysfunction induced by BDE-209 remains largely unclear. Here, our data showed that BDE-209 exposure caused a decline in sperm quality with seminiferous tubule structure disorder in rats. In addition, BDE-209 exposure damage spermatogonia proliferation and differentiation with decreasing level of PLZF and cKit in testis. Moreover, rats exposed to BDE-209 decreased the expression of ERα, whereas an elevated expression of Wnt3a and Wnt5a. Mechanistically, supplementation with propipyrazole triol (PPT, a selective ERα pathway agonist) rescued sperm quality and attenuated impairment of proliferation and differentiation of spermatogonia in BDE-209-induced rats. Therefore, ERα plays a crucial role in the proliferation and differentiation of spermatogonia during mitotic process. In conclusion, our study clarified the role of ERα in BDE-209-induced spermatogonia proliferation and differentiation in rats and provides a potential therapeutic application on poor sperm quality caused by BDE-209 exposure.