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61,005 resultsShowing papers similar to Dataset for the manuscript "Lipidomic analysis of single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human hepatoma cells"
ClearDataset for the manuscript "Lipidomic analysis of single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human hepatoma cells"
This dataset provides untargeted lipidomics data from human hepatoma cells exposed to polyethylene microplastics, polychlorinated biphenyl congeners, and their combinations. The data support research showing that microplastics and PCBs can individually and jointly alter lipid profiles in human liver cells, offering insights into how these contaminants may affect cellular lipid metabolism.
Lipidomic analysis of single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human hepatoma cells
Researchers used lipidomic analysis to study the single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human liver cancer cells. While microplastics alone did not cause significant cell death, the combined exposure with PCBs produced distinct changes in cellular lipid profiles that differed from individual exposures. The study suggests that microplastics may alter how cells respond to co-occurring chemical pollutants through a "Trojan Horse" transport mechanism.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study assessed the liver toxicity of polypropylene microplastics in mice using combined lipidomics and transcriptomics, identifying disrupted lipid metabolism, altered cholesterol handling, and fibrotic tissue remodeling as key pathological outcomes.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers used combined lipidomic and transcriptomic analysis to demonstrate that polypropylene microplastics accumulated in mouse liver and disrupted key metabolic pathways including lipid biosynthesis, cholesterol metabolism, and energy homeostasis.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers examined polypropylene microplastic retention in mouse liver using lipidomics and transcriptomics, finding that chronic exposure disrupted lipid metabolism, cholesterol turnover, and antioxidant defense, with high-dose treatment causing regional liver fibrosis.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Proteomic and lipidomic profiling of mouse livers after polypropylene microplastic exposure revealed crosstalk between hepatic lipid fluctuations, nutrient metabolism disorders, and energy pathway disarrangements, providing mechanistic insight into microplastic-induced liver toxicity.
Combined effect of polystyrene microplastics and bisphenol A on the human embryonic stem cells-derived liver organoids: The hepatotoxicity and lipid accumulation
Researchers used human stem cell-derived liver organoids to study the combined toxic effects of polystyrene microplastics and the plasticizer bisphenol A. The study found that co-exposure produced enhanced hepatotoxicity and lipid accumulation compared to individual exposures, with changes in markers related to oxidative stress, inflammation, and energy metabolism in the liver tissue model.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.
Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements
Researchers fed mice polypropylene microplastics chronically and used lipidomics and transcriptomics to show that microplastics accumulated in the liver and disrupted lipid metabolism, cholesterol homeostasis, and redox balance, with high doses causing fibrotic liver changes.
Lipidomics and transcriptomics insight into impacts of microplastics exposure on hepatic lipid metabolism in mice
Researchers used lipidomics and transcriptomics to examine how polystyrene microplastic exposure affects liver lipid metabolism in mice over eight weeks. The study found that while body weight and serum lipid levels were not significantly affected, microplastics caused impaired glucose metabolism and specific changes in hepatic lipid profiles, revealing subtle but measurable disruptions to liver function.
Metabolomic and sphingolipidomic profiling of human hepatoma cells exposed to widely used pharmaceuticals
This study used metabolomic and sphingolipidomic profiling of human hepatoma cells exposed to wine bottle-associated microplastics, identifying disrupted lipid metabolism pathways and stress responses that may be relevant to human health risk assessment.
Toxicity of microplastics and plastic additive co-exposure in liver Disse organoids from healthy donors and patient-derived induced pluripotent stem cells
Researchers biofabricated liver Disse-like organoids from both healthy donor cells and patient-derived induced pluripotent stem cells (hiPSCs) to investigate the combined toxicity of microplastics and plastic additives, which typically co-exist in the environment as complexes that enter human blood circulation. The organoid model revealed that microplastic and additive co-exposure increased risks of steatohepatitis-related pathological responses in hepatic tissue.
Combined exposure to polyvinyl chloride and polystyrene microplastics induces liver injury and perturbs gut microbial and serum metabolic homeostasis in mice
Mice exposed to a combination of PVC and polystyrene microplastics for 60 days developed liver damage, gut barrier breakdown, and disrupted gut bacteria. The co-exposure also raised cholesterol and triglyceride levels in both blood and liver, and altered hundreds of metabolites related to fat metabolism. Since people are typically exposed to multiple types of microplastics simultaneously, this study suggests the combined effects may be worse than exposure to a single type alone.
Transcriptome Sequencing and Metabolite Analysis Revealed the Single and Combined Effects of Microplastics and Di-(2-ethylhexyl) Phthalate on Mouse Liver
Mice exposed to microplastics, the plasticizer DEHP, or both together showed liver damage including oxidative stress, cell death, and disrupted metabolism. The combined exposure was worse than either pollutant alone, activating cancer-related genes and impairing the liver's ability to process fats and amino acids. Since DEHP is commonly found alongside microplastics in the environment, these findings suggest that real-world exposure to contaminated plastics could pose a greater liver health risk than previously estimated.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
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.
Untargeted lipidomics uncover hepatic lipid signatures induced by long-term exposure to polystyrene microplastics in vivo
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.
Impacts of polypropylene microplastics on lipid profiles of mouse liver uncovered by lipidomics analysis and Raman spectroscopy
Researchers found that polypropylene microplastics accumulated in mouse liver tissue and caused significant changes to lipid metabolism, even without obvious outward health symptoms. Advanced analysis revealed altered fat profiles and lipid droplet buildup in the liver. This study suggests that microplastic exposure could quietly disrupt liver fat processing, which is relevant to understanding long-term metabolic health effects in mammals.
Integrated transcriptomic and metabolomic analyses to decipher the regulatory mechanisms of polystyrene nanoplastic-induced metabolic disorders in hepatocytes
Using combined transcriptomic and metabolomic analysis, this study found that polystyrene nanoplastics disrupt lipid and amino acid metabolism in hepatocytes, identifying key regulatory genes and providing data relevant to assessing health risks from nanoplastic exposure.
Integrated multi-omics of gut-liver axis to dissect the mechanism underlying hepatotoxicity induced by sub-chronic tire wear particles exposure in mice
Researchers gavaged female mice with tire wear particles (a major microplastic source) at three doses and performed integrated gut-liver multi-omics analysis, finding that sub-chronic exposure disrupted lipid metabolism, promoted liver inflammation, and altered gut microbial communities in a dose-dependent manner.
Distinct toxicity of microplastics/TBBPA co-exposure to bioprinted liver organoids derived from hiPSCs of healthy and patient donors
Using 3D-bioprinted liver tissue models grown from human stem cells, researchers found that microplastics combined with the flame retardant TBBPA caused greater liver damage than either substance alone. The study suggests that microplastics may worsen the toxic effects of environmental chemicals on liver tissue, and that people with pre-existing liver conditions could be more vulnerable.
Co-exposure to polystyrene microplastics and perfluorooctanoic acid can exacerbate lipid metabolism disorders and liver damage in adult zebrafish
Researchers exposed zebrafish to polystyrene microplastics and the persistent pollutant PFOA separately and together for 28 days, finding that combined exposure caused greater intestinal barrier breakdown, liver damage, lipid metabolism disruption, and gut microbiome dysbiosis than either contaminant alone — raising concerns about nonalcoholic fatty liver disease risk from co-occurring plastic and chemical pollution.
Dysbiosis of gut microbiota in C57BL/6-Lepem1hwl/Korl mice during microplastics-caused hepatic metabolism disruption
Researchers administered polypropylene microplastics orally to obese mice for 9 weeks and found disruption of hepatic lipid, glucose, and amino acid metabolism alongside structural changes in gut microbiota, with microplastic-treated mice showing decreased hepatic lipid accumulation and altered abundance of specific bacterial genera.
Combined hepatotoxicity of imidacloprid and microplastics in adult zebrafish: Endpoints at gene transcription
Researchers investigated the combined liver toxicity of the pesticide imidacloprid and polystyrene microplastics in adult zebrafish over 21 days. The combination caused greater changes in gene expression related to fat and sugar metabolism and inflammatory responses than either contaminant alone. The study suggests that even low concentrations of microplastics and pesticides together may produce more severe hepatotoxic effects than individual exposures.