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Assessment of the Toxicity of Polystyrene Microplastic in the Colon and Liver of Adult NMRI Mice

Iranian Journal of Veterinary Medicine 2025
Somaye Zangene, Hassan Morovvati, Hojat Anbara, Nicola Bernabò

Summary

Researchers orally administered polystyrene microplastics to adult male mice at four doses for four weeks and examined histological changes in the colon and liver. Both organs showed dose-dependent tissue damage including inflammation and oxidative stress markers, with the colon showing earlier onset injury due to direct contact with ingested particles.

Background: In recent years, microplastics (MPs), emerging environmental contaminants measuring less than 5 mm in diameter, have garnered significant attention. Objectives: This study aims to evaluate the impact of MPs on colon samples, which are directly exposed to MPs that enter the digestive tract through food, and on the liver, which is responsible for processing chemicals from the digestive tract in mice. Methods: During this experiment, 36 adult male mice were randomly divided into four groups of nine animals each. Three groups received polystyrene MPs (PS-MPs) at doses of 0.001, 0.01, and 1 (gavage) for 42 days; a control group was also considered. Tissue samples were collected for histomorphological, histomorphometric, inflammatory factor, and gene expression analyses 24 h after the last treatment. Results: The results showed that receiving PS-MPs negatively affected on the histomorphology and histomorphometry of the colon and liver. Also, PS-MPs caused a significant increase (P<0.05) in inflammatory factors, such as tumor necrosis factor α (TNF-α) and prostaglandin E2 (PGE2), compared to the control group. In addition, a significant increase (P<0.05) in β-catenin and hypoxia-inducible factor 1-alpha (HIF-1α) messenger ribonucleic acid (mRNA) expression was observed in the groups treated with PS-MPs compared to the control group. Conclusion: PS-MPs negatively affect histomorphology and histomorphometry and increase the concentration of TNF-α and PGE2 and the expression of HIF-1α and β-catenin genes in the colon.

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