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Exposure to submicroplastics promotes the progression of nonalcoholic fatty liver disease in ApoE-deficient mice
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Researchers found that exposing mice to submicron-sized polystyrene plastics in their drinking water for 12 weeks accelerated the progression of nonalcoholic fatty liver disease. The tiny plastic particles accumulated in the liver, worsened fat buildup, increased inflammation, and disrupted cholesterol metabolism. This study suggests that people who already have risk factors for liver disease may be especially vulnerable to health effects from microplastic exposure.
Microplastics (MPs) pose emerging threats to human health, with growing concerns about liver toxicity and other harmful effects from plastic particles. While aquatic species exhibit hepatic vulnerability to micro/nanoplastics, the role of submicroplastics (100 nm-1 μm) in mammalian non-alcoholic fatty liver disease (NAFLD) progression remains unclear. We investigated the effects of a 12-week exposure to 0.5 μm polystyrene MPs (submicroplastics) in drinking water, administering this to ApoE-deficient mice fed either a chow diet (CD) or a Western diet (WD). Submicroplastics accumulated predominantly in the liver and were excreted in the feces. Histologically, submicroplastics significantly increased NAFLD activity scores, hepatic steatosis (Oil Red O-positive area), and fibrosis (Masson-positive area), with maximal severity in the WD+MPs group. Also, the MPs exposure group had increases in positive areas for F4/80 and inflammatory markers TNF-α, IL-1β and IL-6 expression under both diets. Concurrently, submicroplastics inhibited antioxidant defenses by lowering levels of superoxide dismutase and glutathione, while also increasing the lipid peroxidation marker malondialdehyde. WD-fed mice exhibited pronounced MPs-induced lipid dysregulation, including elevated hepatic triglycerides, total cholesterol, and free fatty acids (FAs). Mechanistically, submicroplastics upregulated FA synthesis regulators (ACC, FASN, SREBP1) while downregulating FA oxidation mediators (CPT1A, ACOX1, PPARα) in the livers under a WD. Our findings demonstrate that chronic submicroplastics-exposure exacerbates the progression of NAFLD in ApoE-deficient mice by disturbing lipid metabolism, enhancing oxidative stress, and amplifying inflammatory responses. This study provides experimental evidence linking environmental plastic pollution to accelerated metabolic liver disease, thereby highlighting the urgent need for plastic exposure control strategies.
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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.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
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Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
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.
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.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
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In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
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