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Nanoplastics exacerbate the arsenic intestinal toxicity through oxidative stress, apoptosis and circadian rhythm disruption
Summary
Tiny plastic particles (nanoplastics) can team up with arsenic — a toxic metal sometimes found in food and water — to damage intestinal cells far more than either one does alone, according to lab and animal experiments. The smallest plastic particles caused the worst harm, triggering cell damage, inflammation, and disruptions to the body's internal clock in gut tissue. This matters because most safety testing looks at pollutants one at a time, so real-world exposure to combined contaminants like this could pose a bigger health risk than currently assumed.
Nanoplastics (NPs) can act as carriers to adsorb arsenic in the environment, and forming stable composite pollutants. These pollutants can enter the human intestinal tract through food chain. The co-exposure of NPs and As may lead to a synergistic toxic effect, thereby increasing the potential threat to intestinal health. Therefore, this study investigated the potential effects of As and different sizes (20, 50, 200 and 500 nm) polystyrene nanoparticles (PS NPs) when exposed alone or in combination on Caco-2 cells and the intestinal tract. The results indicate that at the concentration where neither PS NPs nor As exposure alone have a significant impact on cell viability. The co-exposure of PS NPs-As resulted in a significant synergistic toxic effect. Among then, 20 and 50 nm PS NPs-As can more significantly promote the release of LDH, and has a more prominent effect on the integrity of the Caco-2 cells membrane. The 50 nm PS NPs-As specifically enhanced the generation of ROS. The ELISA results confirmed that the synergistic effect promotes cell apoptosis by regulating the Bax / Bcl-2 ratio and activating the Caspase-3 protein. In addition, the in vivo experiments further demonstrated that the co-exposure of PS NPs-As caused more severe intestinal structural damagen and triggered enrichment pathway transformation. The specific manifestations include the enrichment of immune suppression, inflammatory apoptosis, PPAR signaling pathway, and NOD-like receptor pathway, as well as the aggravation of circadian rhythm disorders. This study elucidates that the co-exposure of different sized PS NPs-As can lead to synergistic toxicity. Among them, the small sized PS NPs-As exhibit a stronger ability to cause intestinal damage. This finding reveals that ignoring the combined effect of composite pollution in real environments may seriously underestimate the health risks of NPs.