Bisphenol F induced alteration in testicular p53 and localization: Implications for cauda epididymal sperm characteristics and morphology

Bisphenol F (BPF), a structural analogue of Bisphenol A (BPA), is widely used in the production of plastics and epoxy resins. Emerging evidence suggests that BPF may disrupt endocrine function and impair fertility. This study investigates the effects of BPF on sperm characteristics, morphology, and germ cell viability, with a focus on its potential mechanisms of action in male reproductive toxicity. Wistar rats were randomly assigned to five groups (n=5/group): control (Group I), BPF-treated groups (100 (Group II), 500 (Group III), and 1000 (Group IVa) µg/kg/day for 45 days), and a recovery group (IVb) (1000 µg/kg/day for 45 days followed by a 45-day recovery). Post-treatment, sperm parameters were assessed, and immunohistochemical analysis of p53 expression in testicular tissue was performed. BPF exposure led to significant, dose-dependent declines in sperm count, motility, and viability, accompanied by increased morphological abnormalities, particularly in the sperm head region. Irregularities in the acrosomal system, plasma membrane, and perforatorium suggested oxidative stress during epididymal transit. A 5–8% reduction in sperm viability and a 2–15% increase in abnormalities were observed across dose groups. Elevated p53 expression in testicular tissues indicated germ cell apoptosis and impaired spermiogenesis. Recovery period showed significant resumption, indicative of temporary damage to testicular function. In conclusion, BPF exerts direct, dose-dependent toxicity on male reproductive function by promoting oxidative stress and upregulating p53-mediated germ cell elimination, ultimately contributing to teratozoospermia and reduced fertility potential. Keywords: Bisphenol F, Spermatogenesis, P53, Sperm morphology