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The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis
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A rat study using metabolomics analysis found that long-term exposure to high concentrations of polystyrene microplastics led to abnormal fat metabolism and cardiovascular damage. The harm appeared to be driven by oxidative stress and inflammation, suggesting that chronic microplastic exposure could contribute to heart and blood vessel disease.
These results suggest that long-term exposure to high concentrations of PS-MPs may lead to abnormal lipid metabolism and cardiovascular system damage. The mechanism may be related to oxidative stress and inflammatory response. Exogenous antioxidants and changes in own metabolites may have a protective effect on the injury. Therefore, understanding the toxicological mechanism of PS-MPs not only helps to elucidate its pathogenesis, but also provides new ideas for the treatment of chronic diseases.
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Reproductive and metabolic toxic effects of polystyrene microplastics in adult female Wistar rats: a mechanistic study
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Researchers gave female rats polystyrene microplastics orally for 45 days and found disruptions to both metabolic and reproductive hormone levels, including increased cholesterol, insulin resistance, and altered sex hormones. The microplastics also caused liver fibrosis and elevated inflammatory markers. The study suggests that chronic microplastic exposure may contribute to metabolic and endocrine disruption in mammals.
Untargeted lipidomics uncover hepatic lipid signatures induced by long-term exposure to polystyrene microplastics in vivo
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Researchers exposed rats to polystyrene microplastics over 6 and 12 months and used advanced lipid profiling to assess liver damage. They found that long-term exposure caused liver inflammation, fatty liver changes, and significant alterations in eight key lipid metabolites involved in fat processing. The study provides evidence that chronic microplastic exposure can disrupt liver lipid metabolism, raising concerns about long-term health effects.
Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice
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Researchers fed mice polystyrene microplastic beads and found that ingestion promoted fat accumulation and markers of cardiometabolic disease, including changes in cholesterol levels and inflammatory markers. The microplastics appeared to disrupt metabolic processes related to fat storage and energy regulation. The study suggests that dietary microplastic exposure may contribute to obesity and cardiovascular risk factors, adding a new dimension to concerns about microplastics in the food supply.
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
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Mice exposed to polystyrene nanoplastics for 12 weeks gained weight without eating more and showed increased cholesterol levels and fat accumulation in their livers. Gene and metabolite analysis revealed that the nanoplastics disrupted fat metabolism pathways in the liver, essentially reprogramming how the body processes and stores fat. These findings suggest that nanoplastic exposure could be a hidden factor contributing to obesity and fatty liver disease in humans.
In Vivo Tissue Distribution of Polystyrene or Mixed Polymer Microspheres and Metabolomic Analysis after Oral Exposure in Mice.
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Mice orally exposed to polystyrene or mixed polymer microspheres showed plastic particle distribution across multiple tissues including the liver, kidney, and spleen, with metabolomic analysis revealing distinct alterations in lipid, amino acid, and energy metabolism pathways.
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