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Co-exposure to polystyrene nanoplastics and F-53B induces vascular endothelial cell pyroptosis through the NF-κB/NLRP3 pathway
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Researchers found that combined exposure to nanoplastics and a common industrial chemical (F-53B, a PFOS replacement) caused significant blood vessel damage in mice. The combination thickened artery walls, reduced blood vessel elasticity, and triggered cell death in the vessel lining through an inflammatory pathway. This suggests that nanoplastics may worsen the cardiovascular harm caused by other environmental pollutants people are commonly exposed to.
6:2 Chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA; trade name F-53B) is an alternative to perfluorooctane sulfonate (PFOS) and is widely detected in various environmental media and biological samples. Polystyrene nanoplastics (PS-NPs) have become a significant pollutant in the global environment. However, the comprehensive effects of both on the vascular system of mammals are still unclear. This study aims to explore the impacts of F-53B and PS-NPs exposure on the vascular system. Experimental findings indicate that both individual and co-exposure to F-53B and PS-NPs could lead to arterial wall thickening, increase collagen deposition, and reduce elasticity in mice. Moreover, co-exposure results in loss of endothelial integrity, impairs the repair capabilities of endothelial cells by inhibiting their proliferation and migration, and increases the levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Mechanistic studies reveal that F-53B and PS-NPs exposure activate the NF-κB/NLRP3 signaling pathway, promoting endothelial cell pyroptosis and ultimately inducing vascular damage. In summary, this study provides novel insights into the synergistic impact of F-53B and PS-NPs on vascular injury, shedding light on the mechanism underlying the combined toxicity of PS-NPs and other pollutants.
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Polystyrene Microplastics Induce Injury to the Vascular Endothelial Through NLRP3 ‐Mediated Pyroptosis
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Researchers found that polystyrene microplastics caused blood vessel damage in rats by triggering a type of inflammatory cell death called pyroptosis through the NLRP3 pathway. The microplastics activated this destructive immune response in the cells lining blood vessels, leading to inflammation and tissue injury. This study provides a specific mechanism by which microplastic exposure could contribute to cardiovascular disease in humans.
Co-exposure to polystyrene nanoplastics and glyphosate exacerbates NETs-mediated pyroptosis by activating the NLRP3 inflammasome in mouse liver
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Researchers found that co-exposing mice to polystyrene nanoplastics and the herbicide glyphosate caused significantly worse liver damage than either pollutant alone. The combined exposure triggered a chain of inflammatory events including immune cell infiltration, formation of neutrophil traps, and cell death in liver tissue, all driven by activation of a key inflammatory pathway called NLRP3. The study suggests that nanoplastics may amplify the harmful effects of common agricultural chemicals when they enter the body together.
Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway
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Researchers found that polystyrene nanoplastics worsened intestinal inflammation and increased gut permeability in mice already exposed to bacterial endotoxin. The combined exposure triggered higher levels of oxidative stress and activated inflammatory pathways, leading to greater damage to the intestinal lining than either substance alone. The study suggests that nanoplastic exposure could make the gut more vulnerable to inflammation and barrier breakdown when other stressors are present.
Polystyrene nanoplastics induced toxicity in human endothelial cells via atherogenic and autophagy pathways.
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Researchers exposed human blood vessel cells and chicken embryos to polystyrene nanoplastics in lab tests. The particles entered the cells, altered interactions with immune cells, affected pathways linked to artery disease and cell cleanup processes, and caused heart tissue damage in the embryos after seven days.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
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Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
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