The health effects of bisphenol A (BPA) have become a great concern in recent years. In this study, the reproductive toxicity of BPA was investigated. Male CD-1 mice were orally administrated with BPA (0, 100, 300 and 600 mg kg-1 body weight) for 56 consecutive days. Results showed that relative testis weight to total body weight was significantly lower in the high-dose group ( p < 0.01, p < 0.05). Microscopic examination under light and transmission electron microscopes showed disorders of spermatogenesis after BPA exposure, including rough basal lamina of seminiferous tubules and damage of tight junctions between Sertoli cells. Further study by terminal-deoxynucleoitidyl transferase-mediated nick end labelling assay showed a significant induction of apoptosis in the testis tissue of the BPA groups ( p < 0.01). Immunohistochemical study found that the expression of androgen-binding protein (ABP) was significantly decreased in BPA-treated mice ( p < 0.01). Our results indicated that impairment of the basal lamina of seminiferous tubules and tight junctions may contribute to BPA-induced cell injury. A decrease in the level of ABP could be the possible mechanism for the reproductive toxicity of BPA. These findings provided direct evidence and novel insight into the reproductive toxicity of BPA and may have implications for understanding the toxicity of other endocrine disruptors.
Keywords: Bisphenol A; DNA fragmentation; histopathology; terminal-deoxynucleoitidyl transferase–mediated nick end labelling; testis; ultra-structural pathology.