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Bisphenol A (BPA), an estrogenic chemical, has been shown to reduce sperm count; however, the underlyingmechanisms remain unknown. Herein, we show that oral administration of BPA (2 μg/kg) for consecutive 14 daysin adult rats (BPA rats) significantly reduced the sperm count and the number of germ cells compared to controls.The serum levels of testosterone and follicle-stimulating hormone (FSH), as well as the level of GnRH mRNA inBPA rats were lower than those of control rats. Testosterone treatment could partially rescue the reduction of germcells in BPA rats. Notably, the number of apoptotic germ cells was significantly increased in BPA rats, which wasinsensitive to testosterone. Furthermore, the levels of Fas, FasL and caspase-3 mRNA in the testicle of BPA ratswere increased in comparison with controls. These results indicate that exposure to a low dose of BPA impairsspermatogenesis through decreasing reproductive hormones and activating the Fas/FasL signaling pathway.
Here, the underlying mechanisms remain unknown. Herein, we show that oral administration of BPA (2 μg / kg) for consecutive 14 days in adult rats (BPA rats) significantly reduced the sperm count and the number of germ cells compared to controls. serum levels of testosterone and follicle-stimulating hormone (FSH), as well as the level of GnRH mRNA inBPA rats were lower than those of control rats. partially rescue the reduction of germ cells in BPA rats. Notably, the number of apoptotic germ cells was significantly increased in BPA rats, which was insensitive to testosterone. Furthermore, the levels of Fas, FasL and caspase-3 mRNA in the testicle of BPA ratswere increased These results indicate that exposure to a low dose of BPA impairsspermatogenesis through reducing reproductive hormones and activating the Fas / FasL signaling pathway.