Abstract:
Biphenol A (BPA) is a common synthetic chemical used in manufacturing plastics, epoxy resins and polycarbonate materials. BPA has been reported to cause sperm abnormalities but the specific stage(s) of spermatogenesis most affected in mice has not been investigated. Therefore, this present study investigates the genotoxic effects of BPA on the stages of spermatogenesis in Swiss albino mice. Mice (n=30) were exposed orally to 0.3 mL of BPA at 1.0 mg/kg bw dose for 5 consecutive days. Their spermatozoa were assessed for sperm morphology based on BPA exposure at 35, 25, 18, 15, 5, and 1 day(s) corresponding to the 6 maturation stages of spermatogenesis: spermatogonia, primary spermatocytes, secondary spermatocytes, round spermatids, elongating spermatids, and spermatozoa respectively. Negative (0.3 mL olive oil) and positive (0.3 mL cyclophosphamide) controls were also considered. Mice were sacrificed by cervical dislocation, sperm cells excised, and stained with 1% Eosin Y for 45 minutes. Blood collected from the mice through cardiac puncture was used to assess the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST); and the total concentration of creatinine, urea and total protein. Results showed that there was significant (p<0.05) increase in abnormal sperm cells across the stages of spermatogenesis compared to the control. However, the highest frequency of sperm aberrations was induced in mice exposed to BPA while at the primary spermatocytes. The order of induced sperm abnormality at the different stages of exposure was: primary spermatocyte > elongating spermatids > spermatozoa > spermatogonia > round spermatids > secondary spermatocytes. The biochemical analysis showed significant (p<0.05) increase in serum urea, creatinine, ALT and AST activities with concomitant decrease in total protein content at the various stages of spermatogenesis. These data showed that BPA is most toxic to primary spermatocytes and alterations of biochemical parameters might be the mechanisms of induced
genotoxicity. Further studies are needed to confirm if this stage of spermatogenesis is also the most sensitive in human exposed to BPA so as to foster a stage specific treatment in BPA exposed males.
