Bismuth (Bi) exposure has been linked to various health effects, but its direct impact on male fertility remains largely unexplored. This study investigated the effects of bismuth oxide nanoparticles (Bi₂O₃ NPs) on male reproductive function in Naval Medical Research Institute (NMRI) mice. The mice were randomly allocated to seven groups: one control receiving physiological saline and six treatment groups receiving Bi₂O₃ NPs (25, 50, 100, 200, 400, and 800 mg/kg body weight/day) for 35 days. Treatment was administered via oral gavage. Following treatment, we evaluated body weight, blood serum biochemistry, Dazl gene expression, sperm quality, testicular histology, and cell counts (spermatogenic, Leydig, and Sertoli cells). Compared with the control, Bi₂O₃ NPs exposure resulted in significant reductions in testosterone levels, total antioxidant capacity, superoxide dismutase activity, Dazl gene expression, sperm motility, count, viability, normal morphology, and DNA integrity, and the level of malondialdehyde (MDA) increased. Additionally, testicular tissue and seminiferous tubule volume decreased, whereas interstitial tissue volume increased. Notably, sperm production was impaired, as evidenced by reduced numbers of spermatogonia, spermatocytes, spermatids, Sertoli cells, and Leydig cells. Body weight and seminiferous tubule basement membrane parameters remained largely unaffected. These findings suggest that Bi₂O₃ NPs induce oxidative stress, leading to lipid peroxidation and ultimately compromising male fertility. Our study highlights the potential detrimental effects of Bi₂O₃ NPs exposure on male reproductive health and warrants further investigation into their impact on human fertility at relevant concentrations.
