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Micro/nanoplastic-induced alterations in cellular fate and full-cycle spermatogenesis: A mechanistic review and perspective on intergenerational risks

Environmental Pollution 2026
Dehong Liu, Tao Guo, Yanxin Guan, Jingyi Zhang, Meijing Wang, Degui Chang, Xujun Yu

Summary

This review pulls together animal and lab research suggesting that tiny plastic particles (microplastics and nanoplastics) can slip past the body's protective barriers in the testes and disrupt sperm production at multiple stages, damaging cell energy production and triggering harmful inflammation. Some studies even hint that this damage could potentially be passed down to future generations, though this research is still in early, preclinical stages and hasn't yet been confirmed in humans. Given how widespread plastic pollution is in our food, water, and air, this is an important area to watch as scientists work to understand what it might mean for human fertility.

Micro/nanoplastics (MNPs), ranging from 25 nm to 10 μm, have emerged as ubiquitous environmental pollutants, with an increasing body of research exploring their potential risks to male reproductive health. This review provides a synthesis of the observed impacts of MNPs on spermatogenesis, focusing on cellular fate, homeostatic disruption, and potential intergenerational consequences. Evidence from experimental models, utilizing dosages from 50 μg/kg/day to 75 mg/kg/day, suggests that MNPs may breach the blood-testis barrier and are associated with stage-specific impairments throughout the spermatogenic process-from spermatogonial proliferation to final sperm maturation.Proposed toxicological mechanisms identified in these studies include mitochondrial dysfunction, metabolic reprogramming, and the activation of various cell death pathways. Furthermore, experimental data indicate that MNPs may perturb the reproductive microenvironment by affecting Sertoli and Leydig cell functions and contributing to systemic inflammation. Notably, preclinical observations suggest that MNP-associated reproductive damage may have the capacity for intergenerational transmission. These insights provide a preliminary scientific framework for assessing MNP-related male reproductive risks and highlight the need for further research into targeted intervention strategies, as well as the continued validation of these findings in human clinical contexts.

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