We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to Impact of plastic-related compounds on the gene expression signature of HepG2 cells transfected with CYP3A4
ClearThe Effect of Plastic-Related Compounds on Transcriptome-Wide Gene Expression on CYP2C19-Overexpressing HepG2 Cells
Researchers examined how plastic-related compounds affect gene expression in liver cells overexpressing the drug-metabolizing enzyme CYP2C19, revealing transcriptome-wide changes that suggest plasticizers and additives may disrupt hepatic metabolic pathways.
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.
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.
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.
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.
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.
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.
An evaluation of a hepatotoxicity risk induced by the microplastic polymethyl methacrylate (PMMA) using HepG2/THP-1 co-culture model
Researchers tested the liver toxicity of polymethyl methacrylate (PMMA) microplastics using a lab model combining human liver and immune cells. The microplastics triggered inflammation and oxidative stress at concentrations as low as 0.1 mg/mL, activating pathways linked to cell death and chronic disease. Since the liver is a primary organ where microplastics accumulate after entering the body, these findings suggest that long-term microplastic exposure could contribute to liver damage and inflammation-driven diseases.
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.
Epigenetics of Microplastics
This student-authored paper reviews how microplastics and nanoplastics (MNPs) can alter gene expression and enzyme activity in animals, with particular concern for effects on the liver, brain, and male reproductive system. MNPs act as carriers for toxic chemicals like BPA, phthalates, and heavy metals, which can trigger inflammation, oxidative stress, and potentially cancer when ingested by humans. The paper highlights that human exposure is already occurring through contaminated soil, water, and food, making understanding these epigenetic risks an urgent public health priority.
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.
An assessment of the toxicity of polypropylene microplastics in human derived cells
Researchers assessed the toxicity of polypropylene microplastics on human-derived cell lines and found that the particles triggered inflammatory responses and oxidative stress at concentrations relevant to environmental exposure. The microplastics also affected cell viability and caused measurable changes in immune-related gene expression. The study raises concerns about potential health effects from chronic human exposure to one of the most commonly produced plastic types.
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.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
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.
Integration of transcriptomics and metabolomics reveal cytotoxic mechanisms of Polyethylene terephthalate microplastics in BEAS-2B cells
Researchers exposed human lung cells to PET microplastics and used combined gene and metabolite analysis to uncover the mechanisms of toxicity. They found that the microplastics disrupted lipid metabolism and activated cell death pathways, reducing cell viability over time. The study suggests that inhaled PET microplastics could pose risks to respiratory health by triggering harmful molecular changes in lung tissue.
Emerging threat of environmental microplastics: A comprehensive analysis of hepatic metabolic dysregulation and hepatocellular damage (Review)
This review summarizes existing research on how microplastics damage the liver, which is a key organ for filtering toxins from the body. Studies show that microplastics can cause liver tissue damage, trigger cell death, and disrupt fat metabolism, with smaller particles and longer exposure causing worse effects. The findings highlight the liver as a particularly vulnerable organ because it accumulates microplastics that enter the body through food and water.
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.
Polystyrene microplastics induce biochemical and metabolism changes in human placental explants
Researchers investigated the effects of polystyrene microplastics on human placental cells, finding that exposure altered biochemical pathways and metabolic activity. The results suggest that microplastics reaching the placenta can disrupt cellular functions important for fetal development.
Microplastic-induced hepatic adverse effects evaluated in advanced quadruple cell human primary models following three weeks of repeated exposure
Scientists tested the effects of microplastics on a sophisticated model of human liver cells over three weeks of repeated exposure, finding that certain microplastic types triggered inflammation and altered liver function. The advanced cell model, which combines four types of human liver cells, provides more realistic results than simpler lab tests. These findings add to growing evidence that microplastics accumulating in the liver could contribute to chronic inflammation and liver damage in humans.
Altered gene expression in Chironomus riparius (insecta) in response to tire rubber and polystyrene microplastics
Researchers investigated changes in gene expression in the aquatic insect Chironomus riparius after exposure to polystyrene and tire rubber microplastics. The study found that both types of microplastics altered the expression of genes involved in stress response and detoxification, suggesting that microplastic pollution can cause molecular-level effects in freshwater organisms even at sublethal concentrations.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
Researchers exposed mice to tiny polystyrene particles for 16 weeks and found the plastics accumulated in their livers, disrupting fat metabolism and energy production. The microplastics altered lipid profiles and interfered with key enzymes involved in cellular energy cycles. The study suggests that long-term microplastic exposure may contribute to liver damage through metabolic disruption.
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.