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The effect of polystyrene nanoplastics on arsenic-induced apoptosis in HepG2 cells
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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.
Microplastics are detrimental to the environment. However, the combined effects of microplastics and arsenic (As) remain unclear. In this study, we investigated the combined effects of polystyrene (PS) microplastics and As on HepG2 cells. The results showed that PS microplastics 20, 50, 200, and 500 nm in size were taken up by HepG2 cells, causing a decrease in cellular mitochondrial membrane potential. The results of lactate dehydrogenase release and flow cytometry showed that PS microplastics, especially those of 50 nm, enhanced As-induced apoptosis. In addition, transcriptome analysis revealed that TP53, AKT1, CASP3, ACTB, BCL2L1, CASP8, XIAP, MCL1, NFKBIA, and CASP7 were the top 10 hub genes for PS that enhanced the role of As in HepG2 cell apoptosis. Our results suggest that nano-PS enhances As-induced apoptosis. Furthermore, this study is important for a better understanding of the role of microplastics in As-induced hepatotoxicity.
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Combined effect of arsenic and polystyrene-nanoplastics at environmentally relevant concentrations in mice liver: Activation of apoptosis, pyroptosis and excessive autophagy
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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.
Polystyrene Microplastics Exacerbate Arsenic-Induced Ferroptosis and Lipid Metabolism Dysregulation in Chicken Hepatocytes through SIRT7-SIRT1 Axis-Associated Transcriptomic Alterations
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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.
Nanoplastics aggravate the toxicity of arsenic to AGS cells by disrupting ABC transporter and cytoskeleton
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Researchers investigated how polystyrene nanoplastics of various sizes affect the toxicity of arsenic in human gastric cells. They found that while nanoplastics alone at noncytotoxic concentrations did not harm cells, they significantly enhanced arsenic accumulation and toxicity by disrupting cell membrane integrity, damaging the cytoskeleton, and inhibiting ABC transporter activity. The study highlights that nanoplastics can aggravate the harmful effects of co-occurring environmental contaminants even at concentrations previously considered safe.
ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells
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This study found that polystyrene nanoplastics damage human liver cells by triggering harmful interactions between reactive oxygen species (ROS) and a protein called DRP1 that controls mitochondria. The nanoplastics caused mitochondria to break apart, leading to cell injury and death. This research helps explain how microplastic exposure could contribute to liver damage in humans at the cellular level.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
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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.
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