What is it about?
Epidemiological reports have indicated a correlation between the increasing bisphenol A (BPA) levels in the environment and the incidence of male infertility. In this study, the protective effects of melatonin on BPA induced oxidative stress and apoptosis were investigated in the rat testes and epididymal sperm. The concurrent administration of melatonin decreased oxidative stress by modulating the levels of glutathione, superoxide dismutase, and catalase as well as the malondialdehyde and hydrogen peroxide concentrations in the testes and sperm. Melatonin sustained Bcl-2 expression and controlled apoptosis. Furthermore, melatonin maintained the testosterone levels, ameliorated histopathological changes, increased the percentages of seminal haploid germ cells, and protected sperm chromatin condensation process, indicating appropriate spermatogenesis with production of functional sperm. In conclusion, melatonin protected against BPA-induced apoptosis by controlling Bcl-2 expression and ameliorating oxidative stress in the testes and sperm. In conclusion, melatonin is a promising pharmacological agent for preventing the potential reproductive toxicity of BPA following occupational or environmental exposures.
Featured Image
Why is it important?
Epidemiological reports have indicated a correlation between the increasing bisphenol A (BPA) levels in the environment and the incidence of male infertility. In this study, the protective effects of melatonin on BPA induced oxidative stress and apoptosis were investigated in the rat testes and epididymal sperm.
Perspectives
Read the Original
This page is a summary of: Melatonin controlled apoptosis and protected the testes and sperm quality against bisphenol A-induced oxidative toxicity, Toxicology and Industrial Health, July 2016, SAGE Publications,
DOI: 10.1177/0748233714561286.
You can read the full text:
Contributors
The following have contributed to this page