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Polystyrene microplastics induced spermatogenesis disorder via disrupting mitochondrial function through the regulation of the Sirt1-Pgc1α signaling pathway in male mice
Summary
Researchers investigated how polystyrene microplastics of different sizes affect sperm development in male mice and found that exposure decreased sperm motility and caused structural abnormalities. The microplastics disrupted mitochondrial function in reproductive cells by interfering with a key energy regulation pathway. The study provides evidence that microplastic exposure may contribute to male reproductive health problems through mitochondrial damage.
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.
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