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Microplastics and Nanoplastics and Their Effects on Reproductive Health: Potential Risks and Mechanisms

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This review summarizes existing animal and cell studies on how tiny plastic particles (microplastics and nanoplastics) may harm fertility, damaging eggs, sperm, and embryo development by triggering cell stress and hormone disruption. While the exact risk to humans isn't confirmed yet, the findings highlight why reducing plastic exposure may matter for reproductive health.

Microplastics and nanoplastics (MNPs) are persistent pollutants that widely exist in a variety of environmental media and can enter organisms through a variety of exposure pathways. An increasing number of experimental studies suggest that MNPs may have an effect on reproductive processes. This review will integrate recent research and explore the mechanisms of MNPs and their related chemicals in the reproductive system, including male and female germ cells, embryos, mitochondrial function, and apoptosis-related pathways. The aim is to gain a clearer understanding of the reproductive toxicity mechanisms of MNPs and to provide ideas and references for future research. Animal experiments and cell models are mainly used to summarize the toxic effects and mechanisms of MNPs on the reproductive system of both sexes, as well as the abnormal embryonic development caused by maternal exposure and developmental exposure. In terms of mechanism, MNPs can lead to oxidative stress, mitochondrial dysfunction, inflammatory signaling, endocrine disorders, and activation of apoptosis-related pathways. In addition, the degree and performance of reproductive effects are also affected by factors such as particle size, shape, polymer type, and multiple physicochemical properties of the material itself. Overall, the current evidence supports that MNP-related reproductive toxicity is characterized by model dependence and multimechanism involvement, rather than being dominated by a single mechanism. Future studies should strengthen the standardization of particle characterization and long-term exposure studies at environmentally relevant doses, clearly distinguish between association evidence and intervention mechanism evidence, and further improve the source control and exposure reduction strategies.

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