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

Mar 14, 2026Environmental pollution (Barking, Essex : 1987)

Short-term exposure to small plastic particles causes molecular changes but little obvious effect in the mouse gut-brain system

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Abstract

Exposure to 5 μm microplastics in mice resulted in significant depletion of serotonin levels in the brain.

Both microplastics (MP) and nanoplastics (NP) resulted in elevated antioxidant enzyme activity.
Significant dysregulation of pro-inflammatory cytokines was observed following exposure to both particle sizes.
No clear behavioral or tissue damage changes were detected despite biochemical alterations.
Exposure frequency may play a critical role in determining the toxicity of micro- and nanoplastics.

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

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