Bisphenol A and Male Murine Reproductive System: Finding a Link between Plasticizer and Compromised Health

The global burden of male infertility is rising at an alarming rate affecting the lives of millions in terms of physical, emotional, and societal perspectives. Among several existing endocrine-disrupting chemicals, bisphenol A (BPA) has been reported by many to inflict male reproductive toxicity in different experimental models, especially in mice. This review article critically discusses the overall reproductive toxicity of BPA with a special note to its ubiquitous existence, contamination route, effects on the reproductive system, and toxicity mechanisms in male mice. Disturbed redox status in germ cells and spermatozoa plays a pivotal role in BPA-induced male reproductive toxicity. In this context, the involvement of mitochondria and endoplasmic reticulum is also of grave importance. Induction of caspase-dependent apoptosis is the extreme consequence that leads to deterioration of cellular parameters. Besides the oxidative cellular and histoarchitectural damages, perturbed endocrine regulation, subsequent impaired hormonal and cellular genesis program, epigenetic alterations, and inflammation cumulatively reflect poor sperm quality leading to compromised reproduction. Moreover, several key issues have also been highlighted that, if addressed, will strengthen our understanding of BPA-mediated male reproductive toxicity.

Automated summary

The global burden of male infertility is rising rapidly, with BPA impacting male reproductive toxicity in mice through disturbed redox status and induction of caspase-dependent apoptosis. In addition to oxidative cellular and histoarchitectural damages, perturbed endocrine regulation, epigenetic alterations, and inflammation are also contributing factors.