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Assessment of nanopolystyrene toxicity under fungal infection condition in Caenorhabditis elegans
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Researchers found that exposure to nanopolystyrene at microgram-per-liter concentrations significantly worsens outcomes of fungal infection (Candida albicans) in C. elegans nematodes, suppressing the innate immune response and mitochondrial stress pathways, and increasing fungal colony formation — suggesting nanoplastics may compromise host defense against pathogens even at environmentally relevant concentrations.
Due to the potential of release and accumulation in the environment, nanoplastics have attracted an increasing attention. In this study, we investigated the effect of exposure to nanopolystyrene (30 nm) in nematode Caenorhabditis elegans after the fungal infection. After Candida albicans infection, exposure to nanopolystyrene (10 and 100 μg/L) for 24-h could cause the more severe toxicity on lifespan and locomotion behavior compared with fungal infection alone. The more severe activation of oxidative stress and suppression of SOD-3:GFP expression and mitochondrial unfolded protein response (mt UPR) were associated with this observed toxicity enhancement induced by nanopolystyrene exposure. Moreover, the more severe C. albicans colony formation and suppression of innate immune response as indicated by the alteration in expression of anti-microbial genes (abf-2, cnc-4, cnc-7, and fipr-22/23) further contributed to the formation of this toxicity enhancement induced by nanopolystyrene exposure. Our results demonstrated that short-term exposure to nanopolystyrene in the range of μg/L potentially enhances the adverse effects of fungal infection on organisms.
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Effect of chronic exposure to nanopolystyrene on nematode Caenorhabditis elegans
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Researchers chronically exposed C. elegans nematodes to nanopolystyrene across their adult lifespan and found that even low concentrations (≥1 µg/L) impaired locomotion and promoted oxidative stress, while also suppressing immune response genes, antioxidant defenses, and mitochondrial stress response pathways, with high concentrations shortening lifespan.
Exposure to polystyrene nanoparticles at predicted environmental concentrations enhances toxic effects of Acinetobacter johnsonii AC15 infection on Caenorhabditis elegans
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Researchers found that exposure to polystyrene nanoparticles at low, environmentally realistic concentrations made a bacterial infection significantly more harmful to the roundworm C. elegans. The nanoparticles increased bacterial accumulation in the worms' bodies and weakened their innate immune responses. The study suggests that nanoplastic pollution in the environment could amplify the toxicity of common microbial pathogens.
Neuronal damage induced by nanopolystyrene particles in nematodeCaenorhabditis elegans
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C. elegans nematodes were chronically exposed to nanopolystyrene particles and found to develop neuronal damage affecting both development and function of the nervous system after long-term exposure at environmentally relevant concentrations. The study provides early evidence that nanoplastics can cause neurological harm in an animal model, raising questions about potential neurotoxicity in other species.
Potential toxicity of nanopolystyrene on lifespan and aging process of nematode Caenorhabditis elegans
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Researchers chronically exposed C. elegans to nanopolystyrene across their aging lifespan and found that high concentrations shortened lifespan while lower concentrations still impaired locomotion and elevated intestinal reactive oxygen species in older animals, with nanoplastic exposure progressively suppressing immune genes, antioxidant defenses, and mitochondrial stress responses as worms aged.
Uptake of nanopolystyrene particles induces distinct metabolic profiles and toxic effects in Caenorhabditis elegans
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Researchers exposed the nematode C. elegans to 50 nm and 200 nm nanopolystyrene particles and used metabolomics to show that particles disrupt energy metabolism — reducing TCA cycle intermediates and altering glucose and lactate — while also decreasing locomotion, reproduction, and inducing oxidative stress.
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