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Cobalt nanoparticles attenuate microplastic-induced vascular endothelial injury via Nrf2 pathway activation
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Cell and zebrafish experiments showed that microplastics and cobalt nanoparticles — both environmental contaminants that can reach the bloodstream — each independently damage vascular endothelial cells and generate reactive oxygen species, but when combined, the damage was significantly less than from microplastics alone. The cobalt nanoparticles appeared to adsorb onto microplastics and partially counteract their toxicity through interactions with the Nrf2 antioxidant signaling pathway. These findings reveal that the health effects of microplastics in real-world environments depend heavily on what other particles they are combined with, complicating risk assessments based on single-contaminant studies.
The widespread utilization of plastic and cobalt alloy products in industries and medicine has led to the increased presence of their degradation byproducts, microplastics (MPs), and cobalt nanoparticles (Co NPs), in the environment and organisms. While these particles can circulate throughout the body via the circulatory system, their specific adverse effects and mechanisms on the vascular system remain unclear. Employing scanning electron microscope (SEM) analysis and other methodologies, we demonstrate the potential adsorption and aggregation phenomena between MPs and Co NPs. In vitro experiments illustrate that ingestion of either MPs or Co NPs compromises vascular endothelial cell function and induces the generation of reactive oxygen species (ROS). Notably, this effect is markedly attenuated when a combination of MPs and Co NPs is administered compared to MPs alone. Additionally, zebrafish experiments validate our in vitro findings. Mechanistic studies have demonstrated that both MPs and Co NPs induce aberrant Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. Intriguingly, a weaker activation level is observed when these agents are administered in combination compared to when they are administered individually. Our study provides novel insights into the interaction between MPs and Co NPs and their detrimental effects on vascular endothelial cells.
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Potential synergistic effects of microplastics and zinc oxide nanoparticles: biochemical and physiological analysis on Astacus leptodactylus
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Researchers exposed crayfish to microplastics and zinc oxide nanoparticles, both alone and combined, and found that the combination caused greater harm than either pollutant on its own, including increased liver stress markers and reduced antioxidant defenses. These findings suggest that microplastics may make other common environmental pollutants more toxic when they occur together in waterways that supply food and drinking water.
Polystyrene microplastics enhance microcystin-LR-induced cardiovascular toxicity and oxidative stress in zebrafish embryos
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Zebrafish embryos exposed to both microplastics and microcystin-LR (a toxin produced by algal blooms) developed significantly worse heart and blood vessel damage than those exposed to the toxin alone. The microplastics amplified oxidative stress and cell death, suggesting that in polluted waterways where both contaminants coexist, the combined health risks may be greater than either one individually.
Integration of physiology, microbiota and metabolomics reveals toxic response of zebrafish gut to co-exposure to polystyrene nanoplastics and arsenic
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Researchers exposed zebrafish to arsenic combined with polystyrene nanoplastics and found that the nanoplastics significantly increased arsenic accumulation in the gut, by up to 77% at the higher dose. The combined exposure caused more oxidative damage and greater disruption to gut bacteria and metabolism than arsenic alone. This study shows that nanoplastics can make other environmental pollutants more dangerous by helping them accumulate in the digestive system.
Nanoplastics Decrease the Toxicity of a Complex PAH Mixture but Impair Mitochondrial Energy Production in Developing Zebrafish
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Researchers studied the combined toxicity of polystyrene nanoplastics and a real-world mixture of polycyclic aromatic hydrocarbons on developing zebrafish. While the nanoplastics alone did not cause visible developmental defects, they impaired mitochondrial energy production and unexpectedly reduced the toxicity of the PAH mixture. The findings suggest that nanoplastics can interact with co-occurring pollutants in complex ways, sometimes moderating their effects while causing their own subtle cellular damage.
Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice
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Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
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