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Microplastics and Reproductive Dysfunction in Animals
Summary
This review of existing research shows that tiny plastic particles called microplastics can build up in animal reproductive organs and cause serious fertility problems, including damaged sperm and eggs, hormone disruption, and birth defects. While these studies focused on animals, the findings are concerning for humans since we're also exposed to microplastics through food, water, and air. More research is needed to understand the long-term risks to human fertility and reproduction.
Microplastics (MPs) are pervasive environmental contaminants increasingly detected across aquatic and terrestrial ecosystems. Growing experimental evidence indicates that MPs and nano plastics can translocate beyond the gastrointestinal tract and accumulate in reproductive tissues of animals. This review synthesizes current findings on microplastic-induced reproductive dysfunction, focusing on exposure pathways, mechanistic insights, and organ-level outcomes. Accumulated data from mammalian and aquatic models demonstrate that MPs induce oxidative stress, endocrine disruption, inflammation, and apoptosis, leading to impaired spermatogenesis, follicular depletion, altered hormone profiles, and reduced gamete quality. Developmental consequences include decreased fertilization success, embryonic abnormalities, and potential transgenerational effects. Although many studies rely on controlled laboratory exposures, the convergence of mechanistic and phenotypic evidence across species underscores the potential ecological and agricultural implications of chronic microplastic exposure. Standardized methodologies and environmentally relevant models are essential to clarify long-term reproductive risks in animals.