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Gut microbiota and metabolic disruption induced by food chain-transferred nanoplastics: A mediating role of CYP26A1 in retinoic acid toxicity
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Researchers investigated how nanoplastics transferred through the food chain affect the gut-liver axis in mice. The study found that food chain-transferred polystyrene nanoplastics caused gut microbiota disruption, metabolic imbalance, and altered retinoic acid metabolism, with the enzyme CYP26A1 playing a key mediating role in the observed toxicity.
Polystyrene nanoplastics (PS-NPs) pollution has emerged as critical environmental and public health concerns due to their potential for bioaccumulation and systemic toxicity. While our previous work demonstrated the trophic transfer of micro- and nanoplastics from insect yellow mealworms (Tenebrio molitor) to mammals, the biological consequences remain poorly understood. This study aimed to investigate the impact of food chain-transferred PS-NPs (FCT-NPs) on the gut-liver axis in a mouse model. We demonstrate that FCT-NPs induce gut microbiota dysbiosis, disrupt metabolic homeostasis, and alter hepatic gene expression in mice. Crucially, we identify the upregulation of Cyp26a1 gene underlying FCT-NPs-induced hepatoxicity, which interferes with retinoic acid metabolism and leads to hypervitaminosis A. By elucidating the molecular link between gut microbial shifts and hepatic dysfunction, this study highlights gut-liver axis as a primary target of FCT-NPs and lays the foundational insights into their broader systemic ecological and physiological consequences.
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In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
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A subchronic mouse study found that low-dose polystyrene nanoplastics designed to mimic real-world particle characteristics impaired gut and liver health in a non-monotonic, diet-dependent manner, with Western-style diet amplifying the effects.
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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.
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.
Polystyrene nanoplastics exacerbate aflatoxin B1-induced hepatic injuries by modulating the gut−liver axis
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Mice exposed to both polystyrene nanoplastics and aflatoxin B1, a common food contaminant from mold, suffered worse liver damage than from either pollutant alone. The nanoplastics disrupted gut bacteria and weakened the intestinal barrier, allowing more toxins to reach the liver through the gut-liver axis. This study is concerning because it shows that microplastics can amplify the harmful effects of other food contaminants people are already exposed to.
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