Immunohistochemical and Ultrastructural Evaluation of Spermatogenic Alteration by P53 under the Influence of Bisphenol-A

Abstract

The p53 gene is a tumor suppressor gene and, thus, plays an important role in cell cycle, cell senescence, DNA repair, and cell death. Since testicular tissues go through a continuous and complex process of spermatogenesis, p53 is likely to play a significant role in the regulation of germ cell proliferation and spermiogenesis. In the present study, the specific localization of p53 in testicular tissues was determined by comparing it with BPA induced toxicity. Four groups containing 10 albino rats each were designated as Group I: Control, Group II: 10 mg/kg BPA, Group III: 50 mg/kg BPA, and Group IV: 100 mg/kg BPA. Daily administration of BPA was carried out through oral gavage for 6 weeks by dissolving the assigned weight of BPA in olive oil. Testicular tissues were investigated for expression of p53 by immunohistochemistry, and testicular sperms were examined under a scanning electron microscope. Results showed that p53 was exclusively expressed in the spermatogonia of animals exposed to 10 mg/kg BPA. The highest expression of p53 was present in animals exposed to 50 mg/kg BPA; besides spermatogonia, spermatocytes and spermatids also indicated positive expression. However, relatively lower expression was evident in animals exposed to 100 mg/kg BPA, as most cellular architecture was already distorted significantly, and germ cells appeared to have fallen into the lumen of seminiferous tubules. The ultrastructure of testicular sperm indicated specific damage to the perforatorium, plasma membrane, and connecting pieces around the neck, and tail. Damages occurring in the head cap segment of the perforatorium indicated an alteration during spermiogenesis. In conclusion, it is highly likely that a BPA induced alteration in the expression of p53 may have affected spermiogenesis through spermatogenesis.