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Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
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Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Health hazards associated with microplastics (MPs) remain largely unknown, and the effects of aged MPs, one of their persistent forms, are poorly characterized. Male ICR mice were intratracheally instilled with 0.01 and 1 mg/day pristine and ultraviolet (UV)-aged polystyrene microplastics (PS and APS) with an average diameter of 4 - 5 μm daily for 1 week. UV irradiation caused the PS to have a rough surface, become fragmented, and increase their carbonyl groups. Both PS and APS caused structural damage to the mouse gut, liver, spleen, and testis. Inflammatory infiltration in liver, swollen and congested gut, and loose spleen globules, as well as the loose interstitium of the seminiferous tubules in testis were found in 1 mg/day APS group. Increases in serum alanine aminotransferase and immunoglobulin A levels in 1 mg/day APS group (p < 0.05) demonstrated that APS exposure could induce greater liver and spleen functional damage than PS. Meanwhile, triglyceride and total cholesterol levels in liver were enhanced in 1 mg/day APS group (p < 0.05). Superoxide dismutase and glutathione contents in 0.01 and 1 mg/day APS groups significantly decreased (p < 0.05), which suggesting that PS and APS could interfere with the antioxidant capacity in mice. Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) levels in the PS and APS groups showed significant increases in the liver and testis (p < 0.05), and a significant decrease in the spleen (p < 0.05), which were analyzed to get a first survey for Nrf2/HO-1-mediated tissue-specific defense mechanisms. In conclusion, acute exposure to PS and APS induced potential metabolic disorders, and APS could produce more serious immune damage and reproductive toxicity. These findings provide new insights in health risk assessment of aged MPs.
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