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Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
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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.
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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Researchers found that polystyrene microplastics detected in blood were the polymer most consistently linked to elevated liver fibrosis markers in type 2 diabetic patients, and confirmed in diabetic mice that PS-MPs worsen hepatic steatosis and fibrosis by activating the NLRP3 inflammasome and TGF-β1/Smad signaling pathways.
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Researchers studied the effects of polystyrene microplastics on the livers of mice fed a high-fat diet and found that the particles triggered significant inflammatory responses and disrupted lipid metabolism. The microplastics worsened fat accumulation in the liver and activated inflammatory signaling pathways. The findings suggest that microplastic exposure combined with a high-fat diet may amplify liver damage and metabolic disturbances.
Polystyrene Nanoplastics Exacerbate HFD-induced MASLD by Reducing Cathepsin Activity and Triggering Large Vacuole Formation via Impaired Lysosomal Acidification
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Researchers found that polystyrene nanoplastics, when combined with a high-fat diet in mice, significantly worsened fatty liver disease symptoms compared to either factor alone. The nanoplastics impaired the function of lysosomes, the cell's recycling centers, by preventing proper acidification and reducing enzyme activity. The study suggests that nanoplastic exposure could amplify diet-related liver problems by interfering with how cells process and break down fats.
Chronic environmental exposure to polystyrene microplastics increases the risk of nonalcoholic fatty liver disease
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A mouse study found that long-term exposure to polystyrene microplastics increased the risk of developing non-alcoholic fatty liver disease. The microplastics accumulated in the liver and disrupted fat metabolism, causing inflammation and liver damage, which is concerning because most previous studies only looked at short-term exposure effects.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
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In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
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