We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Metabolic disturbance and transcriptomic changes induced by methyl triclosan in human hepatocyte L02 cells
Summary
Exposure of human hepatocyte L02 cells to methyl triclosan demonstrated that oxidative stress and metabolic dysregulation are involved in its cytotoxicity, as shown by transcriptomic changes and metabolic disturbance. These findings suggest methyl triclosan poses a hepatotoxic risk at concentrations that may be encountered through environmental exposure.
These results demonstrated that oxidative stress and metabolism dysregulation might be involved in the cytotoxicity of MTCS in L02 cells.
Sign in to start a discussion.
More Papers Like This
Single-cell transcriptomic dissection of the cellular and molecular events underlying the triclosan-induced liver fibrosis in mice
Researchers used single-cell analysis to map exactly which liver cell types are damaged by triclosan — a common antimicrobial found in personal care products — and found it activates star-shaped cells called hepatic stellate cells, leading to liver scarring (fibrosis). This is the first detailed cellular atlas of triclosan's toxic effects on the liver.
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.
The 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.
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.
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.