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Co-exposure to cadmium and microplastics promotes liver fibrosis through the hemichannels -ATP-P2X7 pathway
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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.
Abstract Background The widespread use of plastic products and the imperfection of plastic recycling systems have led to a continuous increase in microplastics (PS) in the environment. Microplastics have an adsorption effect and can act as carriers for other pollutants in the environment. Cadmium (Cd) is a heavy metal that interacts with microplastics. However, the potential toxicity of co-exposure of cadmium and microplastics to the body is not clear. This study focuses on the effects of co-exposure to cadmium and microplastics on liver fibrosis and its mechanism. Results In this study investigated, Cd+PS exposure increased superoxide anion production and promoted extracellular ATP release compared with exposure to Cd or PS alone. Cd+PS increased inflammatory cell infiltration, activated the P2X7-NLRP3 signaling pathway, and promoted inflammatory factor release. Cd+PS aggravated Cd- or PS-induced liver fibrosis and induced liver inflammation. In AML12/HSC-T6 cell in vitro poisoning model, exposure of AML12 cells to Cd+PS 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+PS 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+PS-treated HSC-T6 cells. Finally, the expression of the ATP receptor P2X7 was silenced in HSC-T6 cells, which significantly inhibited their activation. Conclusion Cadmium and microplastics have a synergistic toxic effect on the liver, destroy the microenvironment in the liver, and promote the development of liver fibrosis through the hemichannel-ATP-P2X7 signaling pathway. Our study reveals the impact of co-exposure to cadmium and microplastics on chronic liver diseases, providing a theoretical basis for disease prevention and treatment.
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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.
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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.
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Researchers examined liver damage in mice exposed to polystyrene microplastics and cadmium, both alone and in combination, and found that triple exposure to 100-nanometer particles, 1-micrometer particles, and cadmium caused the most severe liver dysfunction. The study suggests that nanoscale microplastics significantly enhance cadmium-induced liver injury through disrupted autophagy via the PI3K/AKT/mTOR signaling pathway.
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Researchers exposed mice to polystyrene microplastics alone and combined with cadmium over eight weeks to study liver damage. Both exposures caused liver injury through oxidative stress and programmed cell death, but the combination of microplastics and cadmium produced more severe effects. The study suggests that microplastics may worsen the toxic impact of heavy metals on the liver when both are present together.
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Researchers found that co-exposure to polystyrene microplastics and bisphenol A caused liver fibrosis in mice by disrupting a key signaling pathway that controls cell adhesion. The combined exposure produced more severe liver damage than either substance alone, with excessive buildup of scar tissue in the liver. The study suggests that the widespread co-occurrence of microplastics and BPA in food packaging could pose synergistic risks to liver health.
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