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Co-exposure to cadmium and microplastics promotes liver fibrosis through the hemichannels -ATP-P2X7 pathway
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Researchers found that combined exposure to cadmium and microplastics caused worse liver scarring (fibrosis) in mice than either pollutant alone. The combination triggered a specific inflammatory pathway involving ATP signaling that activated the cells responsible for liver scarring. This is concerning because people are often exposed to both microplastics and heavy metals like cadmium simultaneously through food and water, and the combined effect may be more damaging to the liver than expected.
Microplastics (MPs) and cadmium (Cd) are important environmental pollutants, that damage the liver. However, the effect and mechanism of combined Cd and MPs exposure on liver fibrosis are still largely unknown. In this study investigated, Cd + MPs exposure increased superoxide anion production and promoted extracellular ATP release compared with exposure to Cd or MPs individually. Cd + MPs increased inflammatory cell infiltration, activated the P2X7-NLRP3 signaling pathway, and promoted inflammatory factor release. Cd + MPs aggravated Cd- or MPs-induced liver fibrosis and induced liver inflammation. In AML12/HSC-T6 cell in vitro poisoning model, exposure of AML12 cells to Cd + MPs increased the opening of connexin hemichannels and promoted extracellular ATP release. Treatment of HSC-T6 cells with the supernatant of AML12 cells exposed to Cd + MPs significantly promoted HSC-T6 cell activation. Treatment of HSC-T6 cells with different concentrations of ATP produced similar results. TAT-Gap19TFA, an inhibitor of connexin hemichannels, significantly inhibited the ATP release and activation of Cd + MPs-treated HSC-T6 cells. Finally, the expression of the ATP receptor P2X7 was silenced in HSC-T6 cells, which significantly inhibited their activation. In conclusion, exposure to Cd + MPs promoted liver fibrosis through the ATP-P2X7 pathway and synergistically affected liver inflammation and fibrosis.
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Co-exposure to cadmium and microplastics promotes liver fibrosis through the hemichannels -ATP-P2X7 pathway
AI summary Read the abstract
Researchers investigated co-exposure to cadmium and polystyrene microplastics in a mouse liver fibrosis model, finding that combined exposure promoted liver fibrosis progression through activation of the hemichannel-ATP-P2X7 purinergic signaling pathway, with microplastics acting as a carrier that enhanced cadmium bioavailability and toxicity.
Molecular regulatory networks of microplastics and cadmium mediated hepatotoxicity from NAFLD to tumorigenesis via integrated approaches
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This study mapped out how microplastics and the toxic metal cadmium work together to damage the liver, tracing a progression from fatty liver disease to cirrhosis and eventually liver cancer. Cadmium activates genes linked to cell growth and tumor formation, while microplastics trigger cell death pathways related to inflammation. When combined, the two pollutants accelerate liver damage more than either one alone, raising concerns about real-world exposure where people encounter both simultaneously.
Co-exposure of polyvinyl chloride microplastics with cadmium promotes nonalcoholic fatty liver disease in female ducks through oxidative stress and glycolipid accumulation
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Researchers found that female ducks exposed to both PVC microplastics and cadmium together developed nonalcoholic fatty liver disease, with the combination being worse than either pollutant alone. The co-exposure caused oxidative stress and abnormal fat and sugar buildup in the liver. This study is relevant to human health because people are also exposed to microplastics and heavy metals simultaneously, and the combined effects may be more damaging than exposure to either one individually.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
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This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
Microplastics Exacerbate Cadmium-Induced Hepatotoxicity via the IRE1α/TXNIP/NLRP3 Axis-Driven Endoplasmic Reticulum Stress and Pyroptosis
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New research in animals found that microplastics can make liver damage from cadmium (a toxic heavy metal found in some foods, cigarette smoke, and industrial pollution) significantly worse, by triggering a chain of cellular stress that causes liver cells to die through an inflammatory process. This matters because most safety research looks at pollutants one at a time, but in real life we're exposed to microplastics and heavy metals together — and this study suggests their combined effects on the liver could be more harmful than either pollutant alone.
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