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Microplastics crossing the blood–testis barrier: A call to action for urological research

Current Urology 2025 Score: 48 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Benjamin Koff, Jamie Kim, Benjamin Koff, Jamie Kim, R. S. White, Tal Cohen, Tal Cohen

Summary

This letter to the editor highlighted growing evidence that microplastics and nanoplastics can cross the blood-testis barrier and accumulate in male reproductive tissues, calling for urological research to investigate potential impacts on sperm quality and male fertility. The authors argue this represents an urgent but understudied clinical concern.

To the Editor, Microplastics and nanoplastics, plastic particles smaller than 5 mm, are now pervasive in the environment and are increasingly detected in human tissues, raising growing concerns about their potential health impacts.[1] They can cross critical biological barriers such as the blood–brain barrier and blood–placenta barrier, accumulate in protected organs such as the brain and placenta, and exert effects ranging from oxidative stress and systemic inflammation to endocrine disruption, DNA damage, and interference with reproductive function.[2] Despite these findings, the effects of microplastics and nanoplastics on human health remain underexplored, highlighting the urgent need for further research and discussion, especially in fields that focus on the organs most susceptible to their accumulation. While focus has been centered on microplastic penetration of the blood–brain barrier and blood–placenta barrier, their potential impact on male reproductive health warrants urgent attention. Of particular concern is the blood–testis barrier (BTB), a highly selective barrier formed by tight junctions between Sertoli cells that protects developing germ cells from toxicants and immune attacks. Substances capable of breaching this barrier pose a unique threat to fertility by disrupting spermatogenesis and testicular immune privilege. This issue is particularly relevant for the fields of urology and reproductive health. Recent studies in murine models have shown that nanoplastics can disrupt the BTB, reduce sperm count, alter testosterone levels, and damage testicular tissue architecture.[3] Furthermore, particle size appears to influence these effects, with some sizes inducing more abnormal spermatogenic responses and others increasing testicular weight, while all tested sizes contributed to testicular inflammation (Fig. 1). Differently sized plastic particles caused differential expression of inflammatory markers.[4] Particles of 5 and 0.5 μm reduced the area occupied by Leydig cells, suggesting a decline in their number. Interestingly, larger microplastics appeared to induce more profound dysfunction, potentially due to reduced clearance from the testicular tissue.Figure 1.: Effects of microplastics and nanoplastics on testes. Created in BioRender. Koff, B. (2025) https://BioRender.com/roueyjc.In another study, rats administered nanoplastics accumulated these particles in their testicular tissue, and oxidative stress and inflammation increased in these rats compared with controls.[5] Microplastics not only cross the BTB but also impair its structural integrity by interfering with key tight junction proteins. Nanoplastics have been shown to disrupt the production of occludin and claudin-11, two proteins that play important roles in the cell junctions that constitute the BTB.[6] With the global decline in sperm counts and rising levels of microplastics in the environment, we urge the urology and reproductive health research community to take proactive steps to address this rapidly emerging issue.[7] Understanding the downstream effects of microplastic accumulation in the testes, including the mechanisms by which it affects the BTB and spermatogenesis, may prove crucial for the future of reproductive health. Addressing this challenge requires concerted efforts spanning environmental science, urology, reproductive medicine, and toxicology to understand and mitigate the reproductive risks associated with microplastic exposure. Acknowledgments None. Statement of ethics Not applicable. Conflict of interest statement The authors declare that they have no conflicts of interest. Funding source None. Author contributions BK: Investigation, methodology development, original draft writing, and manuscript review and editing;JK: Investigation, methodology development, and project administration;RW: Oversaw project administration and contributed to manuscript review and editing;TC: Manuscript review and editing. All authors have read and approved the final manuscript. Data availability Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.

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