Abstract
Bisphenol A (BPA), an estrogenic chemical, has been shown to reduce sperm count; however, 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. The serum levels of testosterone and follicle-stimulating hormone (FSH), as well as the level of GnRH mRNA in BPA rats were lower than those of control rats. Testosterone treatment could 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 rats were increased in comparison with controls. These results indicate that exposure to a low dose of BPA impairs spermatogenesis through decreasing reproductive hormones and activating the Fas/FasL signaling pathway.
Highlights
Bisphenol A (BPA) is an estrogenic compound that is widely used in the manufacture of polycarbonate plastics, which serve as containers for foods and beverages, as well as a constituent of dental sealants[1]
In comparison with the control rats, oral BPA significantly decreased the number of type A spermatogonia (P < 0.05), preleptotene spermatocytes (P < 0.05), mid-pachytene spermatocytes (P < 0.01) and step 7 spermatids (P < 0.01, Fig 1C)
The results showed that testosterone propionate (TP) partially rescued the reduction of germ count compared to vehicle-treated BPA rats (P < 0.05, Fig 2D)
Summary
Bisphenol A (BPA) is an estrogenic compound that is widely used in the manufacture of polycarbonate plastics, which serve as containers for foods and beverages, as well as a constituent of dental sealants[1]. In the saliva of patients who had been treated with a dental sealant, 2030 μg of BPA/mL was detected[3]. The current reference dose [50 μg/kg/day (U.S EPA 1993)] determined by the U.S Environmental Protection Agency (EPA) is 1/1000 of the level that exerts the lowest adverse effect (LOAEL; 50 mg/kg/day). No evidence indicates that oral ingestion of BPA at typical environmental exposure level causes adverse effects, blood BPA levels in a group of pregnant women and their fetuses ranged from 0.3-18.9 and 0.2-9.2 ng/mL, respectively[4]. As BPA has been measured in several human populations, the effects of environmental doses of BPA
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