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.

Di-(2-ethylhexyl) phthalate (DEHP) is a common plasticizer which is mainly used as a kind of plastic additive to increase the flexibility of plastic products. Given the widespread use of plastic products, DEHP, as a ubiquitous artificial pollutant, are widely present in the environment. In addition, DEHP could cause biological damage in various organs through oxidative stress. Nano-Selenium, a novel form of selenium, has a wide variety of biomedical applications as an antioxidant, anticancer and anti-inflammatory agent. Nevertheless, researches on the toxicity of DEHP in chicken hepatocyte lines is insufficient. In particular, researches on the interaction between DEHP and nano-selenium is insufficient in chicken cell. Therefore, the innovation of this study is to explore the theoretical mechanism of DEHP toxicity in hepatocytes and the antagonistic effect of nano-selenium on a series of damage in chicken hepatocytes caused by DEHP. Our results showed that, after DEHP exposure, oxidative stress levels in hepatocytes increased, and the mRNA and protein levels of apoptosis-related genes p53, Capsase9, Caspase3 and Bax increased significantly except Bcl-2. The protein levels of apoptosis markers cleaved-Caspase9 and cleaved-Caspase3 also increased significantly. Moreover, the result of TUNEL assay also showed that the level of apoptotic cells increased after DEHP exposure. Meanwhile, the mRNA and protein levels of PI3K, AKT and p-AKT decreased. Therefore, DEHP is able to enhance the degree of oxidative damage and apoptosis of chicken liver cells. Nevertheless, the addition of nano-selenium can reverse the above changes. Experimental results revealed that nano-selenium antagonizes the toxic effects of DEHP via the PI3K/AKT pathway.