Insights into bisphenol A exposure and male fertility: The role of vitamin D in modulating oxidative stress, inflammation, apoptosis, spermatogenesis, and the hypothalamic-pituitary-gonadal axis.

Bisphenol A (BPA) is a well-known endocrine disruptor commonly found in materials such as polycarbonate plastics, food packaging, toothpaste, and medical devices. This study aimed to investigate the potential protective effects of vitamin D against BPA-induced oxidative stress, inflammation, apoptosis, and disturbances in spermatogenesis, as well as the hypothalamic-pituitary-gonadal (HPG) axis. Hence, Wistar rats were treated with BPA (25 mg/kg) or with vitamin D (400 IU/day) for 30 days. The results indicated that vitamin D supplementation reduced testicular damage caused by BPA by decreasing oxidative stress markers, inflammation indices, and apoptosis. Additionally, vitamin D increased the activities of antioxidant enzymes SOD and CAT, as well as levels of GSH. Furthermore, the disturbances in spermatogenesis (PDGFRa levels) and HPG axis hormones improved following vitamin D supplementation in rats exposed to BPA. The treatment with vitamin D also helped restore the architecture of the seminiferous tubules, which were altered due to BPA-induced testicular toxicity. In summary, the findings of this study suggest that vitamin D treatment can provide significant protective effects against the male reproductive toxicity of BPA by restoring the balance between oxidants and antioxidants, regulating apoptosis and spermatogenesis, suppressing inflammatory cytokines, and activating the release of HPG axis hormones.