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Unraveling Persistent Health Impacts in Mice Following Cessation of Microplastic Exposure: Insights beyond the Surface
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In a study of mice exposed to microplastics at environmentally realistic levels for 21 weeks, researchers found that harmful effects on fat metabolism and gut bacteria persisted even after 4 weeks with no further exposure. Higher doses and smaller particles caused the most lasting damage, and the body's key metabolic regulator (AMPK pathway) remained suppressed. This is one of the first studies to show that the health effects of microplastic exposure may not simply reverse once exposure stops.
The ability of organisms to recover from microplastic (MP) exposure is critical for forming global strategies for MP regulation, risk mitigation, and health protection. However, the recovery dynamics following chronic exposure to environmentally relevant concentrations (ERCs) of MPs remains poorly understood. Here, we present a comprehensive investigation into postexposure recovery following long-term ingestion of polystyrene MPs (40-100 μm) in mice. Animals were fed MPs at either an ERC (approximately 512-2060 particles/day) or a high-dose level (ten times ERC) for 21 weeks, followed by a 4 week recovery period without exposure. Despite cessation of exposure, disruptions in lipid metabolism and gut microbiota persisted in dose- and size-dependent manners, with high-dose groups showing markedly limited recovery. Mechanistic in vitro studies using Caco-2 cells further revealed that MPs impair lipid metabolic homeostasis via sustained suppression of the AMP-activated protein kinase (AMPK) signaling pathway. Together, our findings provide crucial in vivo evidence via a mammalian model that chronic exposure to ERCs of MPs can lead to long-lasting metabolic and microbiome disturbances postexposure. These results underscore the urgency of reassessing the long-term health risks of MPs and developing strategies that address both exposure and postexposure recovery.
More Papers Like This
UnravelingPersistent Health Impacts in Mice FollowingCessation of Microplastic Exposure: Insights beyond the Surface
AI summary Read the abstract
Mice were fed polystyrene microplastics (40-100 µm) at environmentally relevant or 10x doses for 21 weeks, then monitored for four weeks after exposure ceased. Despite stopping exposure, lipid metabolism disruption and gut microbiota dysbiosis persisted at high doses, indicating that microplastic-induced health impacts may not fully reverse after cessation.
Continuous oral exposure to micro- and nanoplastics induced gut microbiota dysbiosis, intestinal barrier and immune dysfunction in adult mice
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Researchers fed mice micro- and nanoplastics at environmentally relevant levels and found significant gut damage, including disrupted gut bacteria, weakened intestinal barriers, and reduced immune function. The ratio of beneficial to harmful gut bacteria shifted, and immune cells in the gut decreased. Importantly, the duration of exposure and the size of plastic particles mattered more than the amount consumed, suggesting even low-level long-term exposure could harm gut health.
Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure
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Researchers fed mice polystyrene microplastics of two sizes and tracked where the particles accumulated in the body, finding them in the liver, kidneys, and gut with distribution patterns depending on particle size. Biochemical analysis revealed that microplastic exposure disrupted energy and fat metabolism, caused oxidative stress, and altered markers of neurotoxicity in the blood. The study provides evidence that microplastics can accumulate in mammalian tissues and may pose widespread health risks.
In Vivo Tissue Distribution of Microplastics and Systemic Metabolomic Alterations After Gastrointestinal Exposure
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Researchers fed mice a mixture of common microplastics and then tracked where the particles ended up in the body and how they affected metabolism. They found that ingested microplastics crossed the gut barrier and accumulated in the liver, kidneys, and other tissues, causing measurable changes in metabolic pathways. The study provides evidence that microplastic exposure through the digestive system can lead to widespread tissue distribution and systemic metabolic disruption in mammals.
Long-Term Exposure to Environmentally Relevant Doses of Large Polystyrene Microplastics Disturbs Lipid Homeostasis via Bowel Function Interference
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Researchers exposed mice to environmentally relevant doses of large polystyrene microplastics in their diet for 21 weeks and found significant disruptions to fat metabolism and gut bacterial communities. The microplastics interfered with bowel function, which in turn altered how the body processes and stores lipids. The study provides evidence that even low-level, long-term microplastic exposure through food may affect metabolic health in mammals.
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