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Microplastic and Car Tire Particles: A Genotoxicity Evaluation in European Perch Perca fluviatilis (Linnaeus, 1758)

Environments 2026
Patrizia Guidi, Joachim Sturve, Mara Palumbo, M. Gabriele, Margherita Bernardeschi, Bethanie Carney Almroth, Giada Frenzilli

Summary

Scientists exposed fish to microplastics and tiny bits of car tire debris (which wash into waterways from road runoff) for several months and found that the combination caused DNA damage and abnormal cell changes, especially when tire particles were added to the mix. Since people are exposed to these same materials through contaminated food and water, this research suggests car tire particles might pose a genetic health risk that hasn't gotten as much attention as plastics alone—and the two together may be worse than either one by itself.

Body Systems

The potential effects of microplastics (MPs) on humans and ecosystems are of great concern, and it has been reported that the ingestion of contaminated food is the main route of exposure. In the present study, Perca fluviatilis was selected as a vertebrate model to evaluate the possible cellular effects induced by five different plastic polymers and car tire debris (CT) after 4- and 7-month exposure periods. The Cytome assay was chosen to check chromatin alteration in perch’s peripheral blood. The results indicated an increase in micronuclei and cytotoxic effect in specimens co-exposed to MPs + CT for 7 months. Increases in dicentric chromosomes were observed in specimens exposed both to MPs alone and to the mixture of MPs + CT, indicating for the first time a genotoxic effect induced by CT debris in fish in terms of structural aberrations. Increases in micronucleated erythrocyte frequency assessed after 7 months only after the addition of CT debris to the mixture of MPs might suggest an aneugenic action of CT in fish. In the same groups, the higher values of frequency in 8-shaped erythrocytes also indicate possible cell cycle toxicity exerted by CT exposure. An association between total erythrocyte nuclear morphology abnormalities (ENA) and glutathione reductase activity was also found, indicating a potential involvement of oxidative processes in modulating the genotoxicity observed. The present experimental model is a useful tool to study cellular mechanisms related to both MP- and CT-induced chromatin structure alterations indicating possible interference with human health as well.

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