Bisphenol A and reproductive health: a comprehensive overview of toxicological effect.

Abstract

Bisphenol A (BPA), a synthetic compound extensively used in the production of polycarbonate plastics and epoxy resins, is a pervasive environmental contaminant and a potent endocrine disruptor. By mimicking oestrogen and binding to oestrogen receptors, BPA interferes with normal hormonal signalling, leading to significant disruptions in reproductive systems. In males, BPA exposure has been linked to reduced sperm count, impaired spermatogenesis, and histopathological alterations in testicular tissue, including disrupted Leydig cell function. In females, it affects ovarian follicle development, disrupts reproductive cyclicity, and causes morphological abnormalities in ovarian tissues. These reproductive effects are exacerbated by BPA-induced oxidative stress, which damages cellular structures and exacerbates hormonal imbalances. The mechanisms underlying BPA's reproductive toxicity involve disruptions in gene expression, signalling pathways, and hormonal homeostasis, highlighting its far-reaching effects on both male and female fertility. This study explores the hormonal havoc caused by BPA exposure, emphasizing its multifaceted impact on reproductive health and the urgent need for mitigative strategies to address its toxicity.