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Disturbance of mitochondrial dynamics led to spermatogenesis disorder in mice exposed to polystyrene micro- and nanoplastics
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Polystyrene micro- and nanoplastics caused spermatogenesis disorders in mice by disrupting mitochondrial dynamics, triggering excessive mitochondrial fission that activated both apoptosis and pyroptosis pathways in testicular tissue. Nanoplastics caused mitochondrial DNA to leak into the cytoplasm, activating the cGAS-STING inflammatory pathway — a mechanism confirmed by rescue experiments with a mitochondrial fission inhibitor.
The widespread presence of polystyrene micro- and nanoplastics (PS-MPs/NPs) in the environment poses a threat to the health of the population. Animal studies have shown PS-MPs/NPs had male reproductive toxicity, while its mechanisms are unclear. To investigate that, male Balb/c mice were randomized into 3 groups: the control, 1 μm PS-MPs and 70 nm PS-NPs group, and they were given PS-MPs/NPs by intratracheal instillation for 28 days. Results revealed that PS-MPs/NPs up-regulated the expression of mitochondrial fission related factors (p-DRP1/DRP1, FIS1) and down-regulated the level of mitochondrial fusion related factors (MFN1/2, OPA1), causing over mitochondrial fission, which activating mitochondrial apoptotic pathway (BAX, Cleaved-Caspase9, Cleaved-Caspase3), resulting in cell apoptosis. Moreover, the damaged structure of mitochondria and over mitochondrial fission caused mitochondrial DNA (mtDNA) to translocate from mitochondria to cytoplasm, which activated DNA sensing pathway (cGAS-STING) and induced cell pyroptosis in testis by raising the expression of inflammation factors (NLRP3, ASC, Caspase1 p20, IL-1β). In vitro, by using the mitochondrial fission inhibitor Mdivi-1, it is found that PS-NPs-induced cell apoptosis and pyroptosis were associated with over mitochondrial fission. Taken together, we conclude that PS-MPs/NPs cause spermatogenesis disorder possibly through damaging mitochondrial structure and dynamic homeostasis, which on the one hand results in mitochondria-mediated apoptosis, and on the other hand leads to mtDNA mislocalization, activating cGAS-STING pathway and inflammation, ultimately resulting in pyroptosis. This study may provide a new reference to the potential mechanisms of male reproductive toxicity caused by PS-MPs/NPs.
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