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Polystyrene Microplastics Disrupt Spermatogenesis through Oxidative Stress in Rat Testicular Tissue
Summary
Male Wistar rats orally administered polystyrene microplastics showed excessive oxidative stress in testicular tissue across all exposure groups, with spermatogenesis impairment and reduced fertility correlating with dose, demonstrating reproductive toxicity in a mammalian model.
Polystyrene-based microplastics (PS-MPs) induce excessive oxidative stress in testicular tissues. The present study evaluated the role of PS-MP induced oxidative stress on spermatogenesis and consequent fertility in male rats. Five groups of Wistar albino rats, each consisting of seven animals, were formed. Group I served as the sham-treated control, while Groups II-V received oral administrations of 5, 50, 500, and 5000 µg/kg body weight (b.w.) of PS-MPs, respectively, for 120 days. Fertility rates and testicular functions, specifically spermatogenic activity, were assessed using stereological and histological analyses. Oxidative stress in testicular tissues was evaluated to determine its potential impact on testicular function. Results showed a significant decline in testicular weight across all treated groups compared to controls, irrespective of the PS-MP dose. Notably, a maximum fertility reduction of 30% was observed in rats treated with 5000 µg/kg b.w. of PS-MPs after 120 days. Groups exposed to lower doses exhibited a 10–20% decrease in fertility compared to controls. Stereological analysis revealed substantial reductions (40-50%) in the volumes of spermatogonia and spermatids, while the number of spermatocytes remained largely unaffected. Histological examination indicated depleted luminal contents with fewer spermatozoa in higher-dose groups. Furthermore, more than a 50% decrease in glutathione (GSH) levels, accompanied by significant reductions in the enzymatic activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), was evident in testicular tissues of rats treated with 500 and 5000 µg/kg b.w. of PS-MPs. In conclusion, PS-MPs significantly impair spermatogenic performance, leading to reductions in germ cell populations and sperm production. This disruption in spermatogenesis contributes to decreased fertility rates and potential regression in testicular development. Further research on the long-term effects of microplastics is warranted to better understand their implications for reproductive health and population dynamics.