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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Detection Methods Food & Water Human Health Effects Nanoplastics Policy & Risk Remediation Sign in to save

Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice

Environmental Toxicology 2021 71 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 55 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ling Li Hui Wang, Hui Wang, Minjie Xu, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Minjie Xu, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Chao He, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Qinglian Hu, Qinglian Hu, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Hui Wang, Ling Li Hui Wang, Hui Wang, Hui Wang, Hui Wang, Ling Li

Summary

Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.

Polymers
Body Systems
Models

Polystyrene nanoparticles (PS-NPs) as an issue of global environmental concern, have been shown to induce hepatic toxicity via triggering oxidative injury and inflammation. Non-alcoholic fatty liver disease (NAFLD) is initiated when excessive lipid is accumulated in the liver and will proceed to liver fibrosis with repeatedly chronic liver injury. In this study, we examined whether intravenous injection of PS-NPs could enhance the hepatic toxicity and potentiate the development of liver fibrosis in experimental high fat diet (HFD)-induced mice. The results demonstrated that PS-NPs could aggravate chronic hepatitis by interfere with liver lipid metabolism in HFD induced mice. Further, hepatic tissue in PS-NPs treated HFD mice displayed substantially lowered superoxide dismutase (SOD) activity, which confirming the oxidative stress induced by PS-NPs. PS-NPs exposure also resulted in the up-regulation of inflammation response in liver, as evidenced by the enhanced infiltration of Kupffer cells (KCs) and elevated expression of pro-inflammatory related indicators. Meanwhile, Masson trichrome staining revealed that PS-NPs could aggravate steatohepatitis with higher collagen fiber in HFD fed mice. Our data suggests that PS-NPs can induce oxidative stress and inflammation in HDF-induced experimental mice and further aggravate liver fibrosis, which highlight the potential health risks of PS-NPs.

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