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Suboptimal Thermal Storage Facilitates Aging of Bottle-Sourced Polyethylene Terephthalate Microplastics Fueling Hepatic Steatosis through Gut-Liver Axis Disruption
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Scientists found that plastic water bottles stored in hot conditions (like in a car or warehouse) release aged microplastics that can cause fatty liver disease in fish. These heat-damaged plastic particles disrupt gut bacteria and damage the intestinal lining, leading to inflammation that spreads to the liver. This suggests people should avoid drinking from plastic bottles that have been stored in hot places, as the aged microplastics may pose greater health risks than fresh plastic particles.
Long-distance transportation and improper storage unavoidably lead to the leaching, retention, and aging of bottle-sourced poly(ethylene terephthalate) (PET) microplastics (MPs) in bottled water, posing an exposure risk to public health. Using a zebrafish model, we discovered that chronic exposure (80 days) to thermally aged bottle-derived PET MPs (retained for 7 days at 60 °C) at realistic concentrations (10 and 100 μg/L) caused substantial hepatic histopathological damage and steatosis, whereas pristine PET MPs stored at 25 °C did not. Integrative analyses suggested that thermal aging induced PET fragmentation, surface roughening, and enhancement of bioadhesion, intensifying gut MP retention (maximally 6.524 μg/g tissues), barrier integrity damage, and microbiota dysbiosis. Biochemical analyses, transcriptomics, and blocking experiments validated that intestinal homeostasis disruption stimulated lipopolysaccharide oversecretion and induced intestinal inflammation through activating the LPS/TLR4/NF-kB pathway, which further contributed to systemic and hepatic inflammations, insulin resistance, and de novo lipogenesis, culminating in steatosis. Intervention with Lactobacillus rhamnosus and sodium butyrate reduced MP-driven hepatic steatosis by restoring gut microbiota and barrier functions. Our findings clarified the mechanisms by which thermally aged PET exacerbated progression to steatosis through the gut-liver axis and proposed the intestine-targeted mitigation strategies against hepatic disorders, advocating concerns on long-term exposure risks of bottle-derived MPs under improper storage conditions.
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Chronic PET‐Microplastic Exposure: Disruption of Gut–Liver Homeostasis and Risk of Hepatic Steatosis
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Researchers exposed mice to PET microplastics ground from plastic bottles over 29 weeks and found that the particles caused obesity, liver enlargement, fatty liver disease, and early-stage scarring of liver tissue. The microplastics also disrupted gut bacteria and bile acid metabolism, pointing to damage along the gut-liver connection. The findings raise concerns about the long-term health effects of chronic exposure to the type of microplastics commonly found in food and beverages.
Comparative Analysis of Metabolic Dysfunctions Associated with Pristine and Aged Polyethylene Microplastic Exposure via the Liver-Gut Axis in Mice
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Mice fed both new and weathered polyethylene microplastics developed disrupted fat metabolism, liver oxidative stress, and shifts in gut bacteria, with weathered (aged) particles causing more severe effects. This study suggests that the microplastics people encounter in the real world, which have been degraded by sunlight and time, may be more harmful than the pristine particles typically used in lab studies.
Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice
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Researchers found that mice exposed to PET microplastics (the type commonly found in plastic bottles) over 17 weeks developed liver damage, including fat buildup, oxidative stress, and cell death. The study revealed that the damage was driven by changes in gut bacteria that altered lipid metabolism, and when researchers depleted the gut bacteria, the liver damage was reduced. This suggests the gut microbiome plays a key role in how microplastics cause harm to internal organs.
Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study
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Researchers tested UV-aged polypropylene microplastics from everyday plastic cup lids on mice and lab-grown liver tissue, finding that more heavily aged particles caused greater liver damage. The aged microplastics disrupted energy production in liver cells and caused a harmful buildup of antioxidant molecules, suggesting that the weathered microplastics people encounter in daily life may be more toxic than pristine ones.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
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Researchers fed mice low doses of pristine and aged polyethylene microplastics for several weeks and analyzed changes in blood metabolites, liver proteins, and gut bacteria. Both forms caused lipid metabolism disruptions and reduced beneficial gut bacteria, with aged microplastics showing greater toxicity linked to changes in fatty acid processing enzymes.
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