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Polystyrene-microplastics and Emamectin Benzoate co-exposure induced lipid remodeling by suppressing PPARα signals to drive ACSL4-dependent ferroptosis and carp splenic injury
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Researchers found that carp fish exposed to both polystyrene microplastics and the pesticide Emamectin Benzoate suffered severe spleen damage through a specific cell death process called ferroptosis. The combined exposure was worse than either pollutant alone, disrupting fat metabolism and causing iron-dependent damage to spleen cells. Since microplastics and pesticides often coexist in waterways, this study highlights how their combined effects on fish immune organs could be more dangerous than either pollutant by itself.
Microplastics (MPs) and Emamectin Benzoate (EMB) were identified as hazardous environmental pollutants, frequently coexisting in aquatic ecosystems, posing potential risk in the immune system of human and animal. However, the hazards of concurrent exposed to MPs and EMB on the carp spleen, and the specific mechanisms remain unclear. Here, we employed MPs and EMB-exposed carp models, and cultured splenocytes in vitro, to demonstrate that PPARα signals suppression underlay MPs and EMB-induced carp spleen injury, based on transcriptomics and lipomics analysis. This suppression exacerbated the buildup of polyunsaturated fatty acid (PUFA), and promoted ACSL4 expression, resulting in increased lipid peroxidation. Further studies found that the accumulation of lipid peroxides predominantly occurred in the mitochondria, which evoked mitochondrial homeostasis imbalance and compromised mitochondrial function, thereby initiating ferroptosis. Additionally, enhancing PPARα signaling, inhibiting ACSL4, or scavenging mitochondrial ROS was favor of mitigating accumulation of lipid peroxides, reducing mitochondrial damage and inhibiting ferroptosis. Notably, MPs and EMB co-exposure caused more severe damage than single exposure. These findings uncovered a potential mechanism, involving PPARα signaling inhibition by MPs and EMB co-exposure, which evoked lipid remodeling and increased ACSL4, to drive ferroptosis and carp splenic injury. This study highlighted the potential hazards to the aquaculture environments where co-exposure of MPs and EMB and provided reference for environmental toxicology research and the sustainable development of the aquaculture industry.
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Combined exposure of emamectin benzoate and microplastics induces tight junction disorder, immune disorder and inflammation in carp midgut via lysosome/ROS/ferroptosis pathway
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This study found that when carp were exposed to both the pesticide emamectin benzoate and microplastics together, the damage to their gut lining, immune system, and inflammation levels was significantly worse than exposure to either pollutant alone. The findings suggest that microplastics may amplify the harmful effects of pesticides in aquatic food sources, which could have implications for human health through seafood consumption.
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When zebrafish were exposed to both polystyrene microplastics and the pesticide cypermethrin together, the combination caused significantly more liver damage than either pollutant alone. The mixture disrupted fat metabolism in the liver and altered gut bacteria in ways not seen with individual exposures. This matters because microplastics and pesticides frequently co-exist in waterways, and their combined effects on fish health could affect the safety of fish as food.
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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.
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Researchers found that combined exposure of grass carp liver cells to polystyrene nanoplastics and the flame retardant DBDPE triggered stronger oxidative stress, iron overload-mediated cell death (ferroptosis), and inflammatory cytokine release than either pollutant alone, with the ferroptosis inhibitor ferrostatin-1 partially reversing the damage.
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When zebrafish were exposed to both polystyrene nanoplastics and silver nanoparticles together, the liver damage was significantly worse than from silver alone because the nanoplastics helped more silver accumulate in the body. The combined exposure triggered a specific type of cell death called ferroptosis in liver tissue, suggesting that nanoplastics can make other environmental pollutants more toxic.
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