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Unraveling hepatotoxicity: mechanistic insights into food chain-transferred nanoplastics disrupting PPAR signaling and liver metabolism
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Researchers traced nanoplastics through a food chain into mouse livers and used transcriptomic, proteomic, and metabolomic analyses to show that food chain-transferred nanoplastics suppress the PPAR signaling pathway, disrupting fatty acid transport, retinoid and steroid metabolism, and redox balance—with molecular docking indicating a direct binding interaction between nanoplastics and the PPAR ligand-binding domain.
Against the backdrop of increasing global plastic consumption, nanoplastics (NPs) formed from the degradation of plastic waste have become widespread in ecological media. These particles can transfer through the food chain to higher trophic organisms, accumulating in organs and posing a health risk. As the primary metabolic organ for ingested NPs, the liver demands urgent investigation into the toxicity mechanisms induced by these particles. Here, we employed a multi-omics-integrated approach to investigate the impact of food chain-transferred nanoplastics (FCT-NPs) on hepatic metabolic and detoxification functions in mice. Our findings demonstrated substantial enrichment of FCT-NPs in liver, resulting in histopathological damage, impaired liver function, and metabolic homeostasis disruption. Transcriptomic, proteomic, and metabolomic analyses collectively identified the suppression of peroxisome proliferator-activated receptor (PPAR) signaling pathway as a central mechanism of FCT-NPs-induced hepatotoxicity. Molecular docking and dynamics simulations revealed a potential direct interaction site between NPs and the PPAR ligand-binding domain, suggesting a mechanistic basis for toxicity. Specifically, inhibition of the PPAR pathway downregulated key downstream processes, disrupting fatty acid transport and metabolism, retinoid and steroid metabolism, and redox balance. This study provides the first mechanistic evidence linking dietary FCT-NPs exposure to PPAR interaction and metabolic dysfunction, thereby advancing risk assessment for NPs-induced liver injury in both mammals and humans.
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Scientists tracked tiny plastic particles as they moved up the food chain—from plastic to worms to mice—and found the plastics built up throughout the body, affecting the heart and disrupting how the body processes fat and manages inflammation. The liver seemed to act as a control center, spreading these effects to other organs. This matters because it shows plastic pollution could pose real risks to our health through the food we eat, not just where the plastic ends up in the environment—though more research is needed to know what this means for long-term human health.
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Mice exposed to polystyrene nanoplastics for 12 weeks gained weight without eating more and showed increased cholesterol levels and fat accumulation in their livers. Gene and metabolite analysis revealed that the nanoplastics disrupted fat metabolism pathways in the liver, essentially reprogramming how the body processes and stores fat. These findings suggest that nanoplastic exposure could be a hidden factor contributing to obesity and fatty liver disease in humans.
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Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.
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Researchers developed a computational toxicology framework integrating multi-source data and network analysis to map associations between micro- and nanoplastics and hepatotoxicity, identifying key molecular pathways through which MNPs may damage the liver, offering a scalable alternative to traditional in vivo testing.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
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Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
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