Polystyrene microplastics induced spermatogenesis disorder via disrupting mitochondrial function through the regulation of the Sirt1-Pgc1α signaling pathway in male mice.

Microplastics (MPs) have emerged as hazardous substances, eliciting widespread concern regarding their potential toxicity. Although our previous research has indicated that polystyrene MPs (PS-MPs) might cause male reproductive toxicity in mammals, their precise effects on sperm motility parameters and acrosomal development remain uncertain. Herein, the effects on sperm motility of PS-MPs at varied particle sizes (0.5 μm, 4 μm and 10 μm) and the underlying mechanisms were examined. The results revealed that PS-MPs caused a decrease in sperm motility, accompanied by abnormalities in the structure and function of the sperm acrosome. Meanwhile, PS-MPs triggered the elevation of intracellular reactive oxygen species levels and the abnormal expression of antioxidant enzymes (γH2AX, GPX4, Peroxiredoxin 5 and SDHB), indicating disruption of the sperm antioxidant system. Furthermore, we observed aberrant expression of key factors involved in mitochondrial fission/fusion (Drp1, Fis1, Mfn1, Mfn2) and biogenesis (Tfam, Nrf1, Pgc1α), potentially resulting in disrupted mitochondrial dynamics and biogenesis in mice testis and Sertoli cells exposed to PS-MPs. Additionally, PS-MPs induced mitochondrial dysfunction by regulating the Sirt1-Pgc1α signaling pathway. Our data provided novel insights into potential mechanisms underlying the spermatogenesis disorders triggered by PS-MPs.