Background.
Bisphenol A (BPA) is known to alter sperm morphology, but information is limited on the most susceptible stage(s) of spermatogenesis, especially in mice.
Objectives.
This study investigated the reproductive, biochemical, and hematological changes caused by exposure to BPA in male albino mice. The genotoxicity of BPA to the six stages of spermatogenesis in mice was determined.
Methods.
Mice were exposed orally to BPA at 0.5, 1.0, 2.0, and 5.0 mg/kg bw doses for 5 days and assessed for sperm morphology after 35 days. Based on the result, the second group of mice was exposed to BPA at 1.0 mg/kg bw dose for 5 days, their spermatozoa were assessed for sperm morphology based on BPA exposure at the 6 maturation stages of spermatogenesis: spermatozoa, elongating spermatids, round spermatids, secondary spermatocytes, primary spermatocytes, and spermatogonia. Biochemical and hematological analyses of the blood of exposed mice were also carried out.
Results.
The results showed that BPA induced concentration-dependent, significantly (p<0.05) increased sperm cell abnormalities at three of the four concentrations tested, with the exception of 0.5 mg/kg bw, in comparison with the negative control. The highest frequency of sperm aberrations was induced in spermatozoa exposed to BPA while at the primary spermatocytes. The order of induced sperm abnormality at the different stages of exposure was: primary spermatocytes > elongating spermatids > spermatozoa > spermatogonia > round spermatids > secondary spermatocytes. The results of the biochemical analysis showed significantly (p<0.05) increased serum urea, creatinine, and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities with a concomitant decrease in total protein content at the various stages of spermatogenesis. In addition, the results for hematological parameters showed several significant (p<0.05) modulations in mice exposed to BPA.
Conclusions.
These data showed that BPA is most toxic to primary spermatocytes and alterations of biochemical and hematological parameters might be the mechanisms of induced toxicity.
Ethics Approval.
The Research Ethics Committee, Federal University of Technology, Akure approved the study protocols.
Competing Interests.
The authors declare no competing financial interests