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AIM2-PANoptosome-driven PANoptosis in hepatic lipid dysregulation induced by β-HCH and nanoplastics co-exposure
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Researchers found that combined exposure to the banned pesticide β-HCH and nanoplastics triggers simultaneous apoptosis, pyroptosis, and necroptosis (a multi-pathway cell death program called PANoptosis) in zebrafish liver through activation of the AIM2 inflammasome complex, resulting in lipid metabolism disruption.
Environmental pollutants pose an increasing threat to human health and ecosystems, with persistent organic pollutants (POPs) and nanoplastics (NPs) drawing significant attention due to their resistance to degradation, high mobility, and bioaccumulation. β-Hexachlorocyclohexane (β-HCH), a typical POP, poses a serious threat to organisms due to its long-term environmental persistence, despite being banned. In this study, we investigated the molecular mechanisms underlying hepatic lipid metabolism disorders induced by combined exposure to β-HCH and NPs using a zebrafish model and Hep G2 cell experiments. Histological staining, RT-qPCR, Western blotting, and immunofluorescence staining demonstrated that β-HCH and NPs co-exposure triggered multiple forms of programmed cell death (PCD), including apoptosis, pyroptosis, and necroptosis, through activation of the pyroptosis, apoptosis and necroptosis (PANoptosis) pathway mediated by the Absent in Melanoma 2 (AIM2)-PANoptosome complex, ultimately leading to lipid metabolism disturbances. RNA interference and gene overexpression experiments further revealed that down or overexpression of AIM2 significantly impacted PANoptosis, confirming the central regulatory role of AIM2 in this process. This study firstly elucidates the regulatory role of the AIM2-PANoptosome complex in the PANoptosis pathway under β-HCH and NPs co-exposure conditions. It provides valuable insights for developing intervention strategies targeting AIM2 for lipid metabolic diseases.
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Researchers exposed zebrafish to copper and PVC microplastics at environmentally relevant concentrations and found for the first time that the combination triggers CuPANoptosis — a novel cell death pathway integrating cuproptosis and PANoptosis — with PVC increasing gut copper load by 1.6–1.9-fold.
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Researchers investigated the combined toxic effects of arsenic and polystyrene nanoplastics on mouse liver at environmentally relevant concentrations. The study found that co-exposure activated multiple cell death pathways including apoptosis, pyroptosis, and excessive autophagy in liver tissue, suggesting that the interaction between nanoplastics and heavy metals may amplify liver 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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Scientists found that when fish (loaches) were exposed to both tiny plastic particles (nanoplastics) and a common pesticide called imidacloprid, their gut cells struggled to process fat normally, causing changes at the genetic and metabolic level. This matters because these same pollutants are widespread in our water and food supply, and this study suggests that combined exposure to plastics and pesticides could disrupt fat metabolism in ways that single-pollutant studies might miss—raising questions about similar risks for human health.
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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.
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