Role of Bisphenol-A Induced Oxidative Stress in Spermatogenesis of Wistar Albino Rats

Abstract

Bisphenol-A is a known endocrine disruptor and reproductive toxicant. It has been associated with epigenetic modification, autophagy, oxidative stress and apoptosis. Many studies have indicated interferences in spermatogenesis due to Bisphenol-A exposure. Since oxidative stress plays important role in regulation of various stages of spermatogenesis, therefore, excessive generation of Reactive Oxygen Species can also have effects on spermatogenesis that may reach beyond hormonal regulations. Three doses of Bisphenol-A (10, 50, and 100 mg/kg body weight) were investigated for its effect on testicular antioxidant status (Catalase, Glutathione, Glutathione S Transferase, , Glutathione Peroxidase and Glutathione disulphide). Stereological estimation of germ cells (spermatogonia, spermatocytes, spermatids) and Sertoli cells was carried out to spermatogenic interferences in the histological architecture. Cause and effect analysis was tested to elucidate association between oxidative stress and numeric spermatogenesis. This study indicated severe decline (30-70%) in the activities of major antioxidant enzymes in response to Bisphenol-A exposure. Higher doses (50 and 100 mg Bisphenol-A) induced maximum damage in histological architecture of testis. Seminiferous tubules indicated loss of germ cells and consequently sperms in the lumen. The histological evaluation went in accordance with stereological evaluation of germ cells. A pattern in disorientation of germ cells was intercepted through morphometric assessment that corresponded to activity of antioxidants. Bisphenol-A induced oxidative stress plays important role in regulation of spermatogenesis. There was a clear parallel between number of germ cell and Sertoli cell decline and loss of activity of major antioxidants. BPA induced oxidative stress had differential effect on germ cells, where spermatogonia and spermatids appeared to have low toleration than spermatocytes.