We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Combined effect of arsenic and polystyrene-nanoplastics at environmentally relevant concentrations in mice liver: Activation of apoptosis, pyroptosis and excessive autophagy
AI summary Read the abstract
Researchers investigated the combined toxic effects of arsenic and polystyrene nanoplastics on mouse liver at environmentally relevant concentrations. The study found that co-exposure activated multiple cell death pathways including apoptosis, pyroptosis, and excessive autophagy in liver tissue, suggesting that the interaction between nanoplastics and heavy metals may amplify liver damage.
The ecological risks caused by the coexistence of pollutants such as arsenic (As) and polystyrene-nanoplastics (PSNPs) in the environment have become a non-negligible problem. However, the effects of As and PSNPs co-exposure on mammals and the underlying toxicity mechanisms have remained unclear. Therefore, the present study established mouse models of As and/or PSNPS exposure to systematically analyze the underlying role of autophagy, apoptosis and pyroptosis in hepatotoxicity induced by co-exposure of As and PSNPs. Our findings demonstrated for the first time that mice co-exposure to As and PSNPs displayed significant pathological changes in the liver, while exposure to As or PSNPs alone did not produce significant toxic effects. More importantly, As and PSNPs co-exposure activated excessive autophagy through altered expression levels of PI3K, mTOR, Beclin-1, ATG5, LC3 and P62. Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc). Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions. Overall, our findings provide deeper insight into the roles of apoptosis, pyroptosis and excessive autophagy in the aggravation of liver injury, which could contribute to a better understanding of the interactions between As and PSNPS exposure and the molecular mechanisms of hepatotoxicity.
More Papers Like This
The effect of polystyrene nanoplastics on arsenic-induced apoptosis in HepG2 cells
AI summary Read the abstract
Researchers studied the combined effects of polystyrene nanoplastics and arsenic on human liver cells in the laboratory. They found that nanoplastics, particularly those around 50 nanometers in size, significantly enhanced arsenic-induced cell death by disrupting mitochondrial function. The study identifies key genes involved in this interaction, suggesting that microplastic exposure may worsen the toxic effects of heavy metals on liver cells.
Polystyrene Microplastics Exacerbate Arsenic-Induced Ferroptosis and Lipid Metabolism Dysregulation in Chicken Hepatocytes through SIRT7-SIRT1 Axis-Associated Transcriptomic Alterations
AI summary Read the abstract
New research using liver cells found that microplastics and arsenic together cause more cell damage than either one alone, the plastic appears to help arsenic build up in cells and disrupts proteins that normally protect against damaging cell death and fat buildup. While this study was done in chicken cells rather than humans, it adds to growing concerns that everyday exposure to multiple pollutants at once, like microplastics combined with heavy metals in our food and water, could be more harmful to our liver health than scientists previously realized when studying these toxins separately.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
AI summary Read the abstract
Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Combined toxicity of co-exposure to polystyrene nanoplastics and arsenic on the gut-liver axis in mice.
AI summary Read the abstract
Mice exposed to both nanoplastics and arsenic together, common pollutants that can show up in food and water, suffered worse gut and liver damage than expected, including a weakened gut barrier, disrupted gut bacteria, and increased inflammation. This suggests that real-world exposure to multiple pollutants at once may pose greater health risks than studying each one alone would predict.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
AI summary Read the abstract
Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.