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Subchronic, low-frequency polystyrene microplastic or nanoplastic exposure elicits molecular perturbations but minimal clinical phenotypes in the mouse gut-brain axis

Environmental Pollution 2026 Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Sheng-Han Lee, Sheng-Han Lee, Sheng-Han Lee, Sheng-Han Lee, Han Chang, Yuan-Horng Yan, Chu-Chun Chien, Tsun-Jen Cheng

Summary

Scientists fed mice tiny plastic particles (microplastics and nanoplastics) twice a week for 12 weeks and found they caused chemical changes in the brain and gut, including lower serotonin levels and increased inflammation. However, the mice didn't show obvious behavior changes or visible tissue damage, suggesting these plastics may cause hidden health effects that aren't immediately noticeable. This matters because humans are increasingly exposed to these tiny plastics from food packaging and the environment, and we may need better ways to assess their long-term health risks.

The global public concerns about micro- and nanoplastics (MNPs) are on the rise, whereas the mechanisms underlying MNP-mediated toxicity have not been fully elucidated. In particular, toxic responses in the gut-brain axis of mice varied across studies due to the high variability in experimental exposure designs. Thus, we employed a mouse model (n= 46) with a standardized exposure regimen of 0.3 mg per treatment, administered twice weekly for 12 consecutive weeks, to systematically evaluate MP (5 μm) and NP (0.5 μm) induced toxicity in both the gut and the brain. In the mouse brain, 5 μm MP exposure significantly depleted serotonin levels, whereas both MNP sizes induced a compensatory elevation in SOD activity and substantial dysregulation of pro-inflammatory cytokines. Notably, these biochemical alterations occurred without a distinct corresponding shift in behavioural or histopathological profiles. Our results also highlighted that exposure frequency may be a key determinant of MNP-induced toxicity, suggesting a potential need for risk assessment of MNP in humans.

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