ArticleJournal of nanobiotechnology2025
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Bioinspired zinc-doped carbon dots protect against polystyrene microplastic-induced spermatogenic dysfunction through Nrf2 activation and cuproptosis suppression.Materials today. Bio · 2026Article
- Glycine alleviates ovarian granulosa cell ferroptosis induced by ERα-mediated internalization of polystyrene microplastics.Communications biology · 2026Article
- High-dose polystyrene nanoparticles trigger aberrant activation of the MAPK pathway in spinal cord and pain hypersensitivity.Journal of nanobiotechnology · 2026Article
- From environment to organs: individual and combined effects of MPs and PFAS on urinary system health.Frontiers in physiology · 2026Review
- Polystyrene Nanoplastics in Human Gastrointestinal Models-Cellular and Molecular Mechanisms of Toxicity.International journal of molecular sciences · 2025Review
- Plastic Pollution and Child Health: A Narrative Review of Micro- and Nanoplastics, Additives, and Developmental Risks.Journal of clinical medicine · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundThere is a growing body of research regarding the potential reproductive toxicity of microplastics and nanoplastics. However, the underlying mechanisms by which nanoplastics exposure adversely affects the testes remain poorly understood. Our study aims to clarify the relationship between ferritinophagy and mitochondrial dysfunction based on polystyrene nanoplastics (PS-NPs)-caused testicular damage in mice.
resultsThe current study demonstrates that 50 nm PS-NPs accumulate in mouse testes and lead to a decrease in sperm quality and disruption of spermatocyte. Furthermore, PS-NPs trigger ferroptosis in GC-2 cells, which can be mitigated by deferiprone and 3-methyladenine. Further investigation reveals that PS-NPs initially aggregate in lysosomes and subsequently transfer to the mitochondria. This process increases mitochondrial Fe
conclusionsOur results indicate that PS-NPs cause mouse testicular damage through ferroptosis. Mechanistically, we confirmed that PS-NPs trigger NCOA4-mediated ferritinophagy and CISD1 downregulation in spermatocyte, which aggravates the flow of ferrous iron from the cytoplasm to the mitochondria.
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Registered trials
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