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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.
Environmental nanoplastics (NPs) have harmful effects on health. This study investigated the effects of polystyrene (PS) NPs on steatosis and fatty liver disease. PS-NP oral administration, in conjunction with a high-fat diet (HFD), synergistically exacerbated the symptoms of steatosis in mice, leading to increased alanine transaminase, aspartate aminotransferase, and cholesterol levels; no effects were observed with PS-NPs on a normal chow diet. Transcriptome analysis unveiled that PS-NPs interfered with actin organization, cell-cell adhesion, PPAR signaling, and lipid metabolism. In HepaRG cells, PS-NPs rapidly entered by inducing actin rearrangement, resulting in the formation of numerous small cytoplasmic vesicles. This treatment led to an augmented number of acidic organelles, leading to development and buildup of large vacuoles, indicative of enlarged pre-lysosomal and lysosomal compartments. PS-NP exposure hampered p62 degradation, leading to LC3B accumulation and decreased cathepsin B and D activity. Additionally, PS-NP exposure resulted in accumulation of lipid droplets and elevated expression of lipogenesis-, transport-, and storage-related genes. These findings suggest that excessive endocytosis driven by PS-NPs worsens MASLD in HFD through accumulation of lysosomes and large vacuoles with reduced cathepsin activity.
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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 nanoplastics induce lipophagy via the AMPK/ULK1 pathway and block lipophagic flux leading to lipid accumulation in hepatocytes
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Polystyrene nanoplastics caused fat to accumulate in human liver cells by disrupting the normal fat-breakdown process called lipophagy. The nanoplastics triggered the cells to start digesting fat droplets but then blocked the final cleanup step by damaging the cell's recycling centers (lysosomes), leaving excess fat trapped inside. This newly identified mechanism helps explain how nanoplastic exposure could contribute to fatty liver disease.
Low-dose polystyrene microplastics exposure increases susceptibility to obesity-induced MASLD via disrupting intestinal barrier integrity and gut microbiota homeostasis
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A mouse study found that even low doses of polystyrene microplastics made fatty liver disease significantly worse when combined with a high-fat diet, creating a "double hit" effect. The microplastics damaged the gut lining, disrupted beneficial gut bacteria, and triggered inflammation that spread to the liver, and these harmful effects were difficult to reverse even after two weeks of stopping exposure.
Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
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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 trigger ferroptosis-dependent liver injury caused by ACSL4 overaccumulation.
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In liver cells and mice, exposure to polystyrene nanoplastics caused liver damage linked to a cell death process called ferroptosis. The plastics disrupted lysosomes, cell structures involved in breaking down materials, leading to buildup of a protein called ACSL4 that drove this damage.
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