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The Threat of Micro-/Nanoplastics to Male Fertility: A Review of the Data and the Importance of Future Research
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This review synthesizes findings from 21 studies examining how micro- and nanoplastics and their associated endocrine-disrupting chemicals affect male reproductive health at the cellular level. Researchers found evidence of multiple toxicity mechanisms including damage to the blood-testis barrier, disruption of hormone signaling, oxidative stress, and structural damage to testicular tissues. The study notes that while these findings from cell and animal studies are concerning, translating the results to human health requires further research with realistic exposure conditions.
Micro-/nanoplastics (MNPs) and their associated endocrine-disrupting chemicals (EDCs) have emerged as pervasive environmental pollutants, with growing concern for their impact on male reproductive health. In this review, we synthesize the findings from twenty-one peer-reviewed studies published between January 2019 and March 2025, selected through a structured literature search conducted in accordance with the SANRA guidelines. Emphasis was placed on studies examining the cellular effects of MNPs and EDCs on Germ, Leydig, and Sertoli cells. The literature indicates multiple mechanisms of testicular toxicity, including degradation of the blood testis barrier, disruption of signaling pathways critical for spermatogenesis and hormone synthesis, induction of oxidative stress and inflammation, and structural and genetic damage to testicular tissues. These data, primarily derived from in vitro and animal models, not only highlight significant biological disruptions but also underscore the limitations in extrapolating results to human physiology. Differences in exposure routes, dosages, and species-specific responses present challenges to direct translation to humans. This review concludes that further human-centric research that mimics real-life exposure and impacts is essential to assess chronic, low-dose exposures and bridge the gap between experimental data and real-world reproductive outcomes, ultimately informing public health strategies and guiding future investigations into the reproductive risks posed by MNPs and EDCs.
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Microplastics and nanoplastics accumulate in testicular tissue and disrupt spermatogenesis through oxidative stress, inflammation, endocrine disruption, and structural damage to reproductive cells, consistently impairing sperm quality in experimental models. With global plastic production accelerating alongside documented declines in semen quality, this review highlights microplastic exposure as a plausible environmental contributor to male infertility warranting urgent human study.
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This systematic review found that micro- and nanoplastics accumulate in the testes and epididymis in rodent models, disrupting the blood-testis barrier, increasing germ cell death, reducing sperm motility, and causing hormone imbalance through oxidative stress and inflammation. Smaller nanoplastics penetrate tissues more readily for molecular disruption, while larger microplastics cause greater structural damage.
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Researchers review growing evidence that microplastics and nanoplastics, now detected in human semen and testicular tissue, disrupt spermatogenesis and testosterone production through oxidative stress, endocrine-disrupting additives, and blood-testis barrier damage, while also linking these mechanisms to elevated prostate cancer risk.
Microplastics and male reproductive system: A comprehensive review based on cellular and molecular effects
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This comprehensive review examines how microplastics affect the male reproductive system at cellular and molecular levels, drawing on studies from multiple scientific databases. Researchers found that microplastics can damage testicular structure and function, impair spermatogenesis, and disrupt sperm parameters through mechanisms including oxidative stress, inflammation, and activation of cell death pathways. The review highlights that microplastics reduce ATP production and trigger signaling cascades that may contribute to male fertility problems.
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