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Microplastic-induced NAFLD: Hepatoprotective effects of nanosized selenium

Ecotoxicology and Environmental Safety 2024 18 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Qi Shen, Qi Shen, Yun Jie Liu, Yun Jie Liu, Tian Qiu, San Loon k, San Loon k, Donghai Zhou Donghai Zhou Donghai Zhou

Summary

This study found that polystyrene microplastics caused nonalcoholic fatty liver disease in mice by disrupting fat metabolism and triggering oxidative stress, but selenium nanoparticles derived from a yak-sourced bacterium significantly prevented this damage. The microplastics suppressed two key protective pathways in the liver, while the selenium nanoparticles activated those same pathways to counteract the harm. These findings suggest that microplastic exposure may contribute to liver disease in humans and point to selenium-based supplements as a potential protective strategy.

Polymers
Body Systems
Models

Polystyrene microplastics (MPs) are persistent environmental pollutants commonly encountered in daily human life. Numerous studies have demonstrated their ability to induce liver damage, including oxidative stress, inflammation, and lipid accumulation. However, limited information exists regarding preventive measures against this issue. In our study, we investigated the potential preventive role of selenium nanoparticles (YC-3-SeNPs) derived from Yak-derived Bacillus cereus, a novel nanobiomaterial known for its antioxidant properties and lipid metabolism regulation. Using transcriptomic and metabolomic analyses, we identified key genes and metabolites associated with oxidative stress and lipid metabolism imbalance induced by MPs. Upregulated genes (Scd1, Fasn, Irs2, and Lpin) and elevated levels of arachidonic and palmitic acid accumulation were observed in MP-exposed mice, but not in those exposed to SeNPs. Further experiments confirmed that SeNPs significantly attenuated liver lipid accumulation and degeneration caused by MPs. Histological results and pathway screening validated our findings, revealing that MPs suppressed the Pparα pathway and Nrf2 pathway, whereas SeNPs activated both pathways. These findings suggest that MPs may contribute to the development of nonalcoholic fatty liver disease (NAFLD), while SeNPs hold promise as a future nanobio-product for its prevention.

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