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The mechanism of oxidative stress induced by nanoplastics in Caenorhabditis elegans: Integrated analysis of transcriptomics and metabolomics
Summary
Researchers exposed C. elegans nematodes to polystyrene nanoplastics across a concentration range and integrated transcriptomic and metabolomic data to identify disrupted fatty acid and glutathione metabolism as the central drivers of oxidative stress, with the gene gst-4 and specific metabolites serving as key molecular signatures.
Nanoplastics, as emerging contaminants, have attracted widespread global attention owing to their threats to ecosystems. The Caenorhabditis elegans nematode is regarded as a versatile model organism for disease mechanisms and toxicity mechanisms of various compounds studies. We investigated the toxicome of PS-NPs exposure in C. elegans (exposed to 0, 0.1, 1, 10, 50 and 100 mg/L) by combining transcriptomic and metabolomic analyses with measurements of survival rate, reproductive capacity and antioxidant capacity. The most pronounced oxidative stress responses were observed at 10 mg/L PS-NPs. Integrated omics analysis revealed disturbances in fatty acid metabolism, glutathione metabolism, drug metabolism-other enzymes, and glycine/serine/threonine metabolism upon exposure to 10 mg/L PS-NPs. These co-affected pathways are closely associated with the induction of oxidative stress. Essential genes gst-4 and ugt-33 as well as metabolite as (e)-2,6-dimethyl-2,5-heptadienoic acid are the key regulators of oxidative stress in C. elegans cells. This study used C. elegans as the main model to provide new insights for assessing the risks of PS-NPs exposure in the ecosystem.
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