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20 resultsShowing papers similar to The Effect of Plastic-Related Compounds on Transcriptome-Wide Gene Expression on CYP2C19-Overexpressing HepG2 Cells
ClearImpact of plastic-related compounds on the gene expression signature of HepG2 cells transfected with CYP3A4
Researchers investigated how plastic-related compounds affect gene expression in human liver cells engineered to express the CYP3A4 enzyme, which is critical for metabolizing foreign substances in the body. They found that exposure to plastics and their chemical additives altered the expression patterns of genes involved in xenobiotic metabolism. The study suggests that microplastics and associated compounds entering the human body could interfere with normal liver enzyme function, raising concerns about long-term metabolic effects.
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.
Data mining of molecular data resulting from environmental exposure to xenobiotics
Researchers characterized the multi-layer gene expression response of human airway and liver cells exposed to polystyrene microplastics across multiple doses and time points. They found thousands of differentially expressed genes along with extensive reprogramming of gene isoforms, affecting protein coding capacity and RNA stability. The study demonstrates that microplastic exposure triggers a structured, dose- and time-dependent remodeling of cellular gene expression programs in human tissue models.
The Expectation and Reality of the HepG2 Core Metabolic Profile
This meta-analysis of 56 metabolomic datasets identified 288 core metabolites in HepG2 liver cells, revealing significant gaps and inconsistencies in how metabolomic studies report and standardize their findings. While focused on cell biology methodology rather than microplastics, HepG2 cells are commonly used in toxicology studies to assess the effects of microplastic exposure on liver function.
Environmentally relevant UV-light weathering of polystyrene micro- and nanoplastics promotes hepatotoxicity in a human cell line
Researchers found that UV-weathered polystyrene micro- and nanoplastics at environmentally relevant concentrations induced hepatotoxicity in human liver cells and caused significant changes in gene expression related to liver disease pathways.
PET microplastics alter the transcriptome profile and oxidative stress markers in the liver of immature piglets: an in vivo study
Researchers fed immature piglets PET microplastics for four weeks and examined the effects on their livers. They found that microplastic exposure altered gene expression patterns related to metabolism and immune response, and increased markers of oxidative stress in the liver. The study suggests that even relatively short-term microplastic ingestion may disrupt liver function at the molecular level.
Chronic exposure to polyvinyl chloride microplastics induces liver injury and gut microbiota dysbiosis based on the integration of liver transcriptome profiles and full-length 16S rRNA sequencing data
Researchers exposed mice to polyvinyl chloride microplastics for 60 days and found significant liver damage accompanied by changes in gut bacteria composition. Gene expression analysis revealed that the liver injury involved inflammatory and metabolic pathways, while the gut microbiome shifted toward disease-associated bacterial profiles. The study suggests a connection between chronic microplastic exposure, gut health disruption, and liver toxicity.
An In Vitro Assay to Quantify Effects of Micro- and Nano-Plastics on Human Gene Transcription
Researchers developed an in vitro assay to quantify how micro- and nano-plastics affect human gene transcription, demonstrating that internalized plastic particles can alter gene expression patterns in human cells, providing a standardized tool for assessing plastic particle toxicity.
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.
Impact of environmental microplastic exposure on HepG2 cells: unraveling proliferation, mitochondrial dynamics and autophagy activation
Lab experiments on human liver cells found that exposure to common microplastics (polyethylene and PET) increased cell growth but also triggered oxidative stress, damaged mitochondria (the cell's energy centers), and activated autophagy -- a process where cells try to clean up internal damage. These findings suggest that microplastics may disrupt normal liver cell function in ways that could have long-term health consequences.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
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 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.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
Polystyrene microplastic exposure disturbs hepatic glycolipid metabolism at the physiological, biochemical, and transcriptomic levels in adult zebrafish
Researchers exposed adult zebrafish to polystyrene microplastics for 21 days and examined effects on liver metabolism at multiple biological levels. The study found that microplastic exposure caused significant decreases in body weight and disrupted glycolipid metabolism, with reduced levels of key metabolic enzymes and gene expression changes in the liver. Transcriptomic analysis confirmed widespread downregulation of genes related to fatty acid, amino acid, and carbon metabolism.
Multi-Omics Analysis Reveals the Toxicity of Polyvinyl Chloride Microplastics toward BEAS-2B Cells
Researchers used advanced gene and metabolite analysis to reveal how PVC microplastics damage human lung cells. Exposure altered the expression of 530 genes and nearly 4,000 metabolites, particularly disrupting fat metabolism pathways and activating inflammatory stress responses. These findings are important because airborne PVC microplastics are common in indoor and outdoor environments, and the study reveals specific biological pathways through which inhaled microplastics could contribute to lung disease.
Toxic effects of polyethylene microplastics on transcriptional changes, biochemical response, and oxidative stress in common carp (Cyprinus carpio)
Researchers exposed common carp to varying concentrations of polyethylene microplastics and assessed biochemical, oxidative, and gene expression changes. The study found that microplastic exposure caused significant oxidative stress, altered liver enzyme activity, and modified the expression of stress-related genes in a dose-dependent manner.
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.
Effects of polystyrene microbeads on cytotoxicity and transcriptomic profiles in human Caco‐2 cells
Polystyrene microbeads reduced viability of human intestinal Caco-2 cells in a dose-dependent manner and altered expression of 442 genes, including pathways related to metabolic processes and cellular stress. The transcriptomic findings reveal molecular mechanisms by which microplastics may harm human gut cells.