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61,005 resultsShowing papers similar to The mechanism of oxidative stress induced by nanoplastics in Caenorhabditis elegans: Integrated analysis of transcriptomics and metabolomics
ClearUptake of nanopolystyrene particles induces distinct metabolic profiles and toxic effects in Caenorhabditis elegans
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.
Size-Dependent Disruption of Lipid Metabolism by Polystyrene Micro- and Nanoplastics in Caenorhabditis elegans Revealed Through Multi-Omics and Functional Genetic Validation
Researchers used the model organism C. elegans to study how polystyrene particles of different sizes affect lipid metabolism, finding that both 100-nanometer and 1-micrometer particles disrupted fat storage and lipid processing. Multi-omics analysis identified four core genes governing the size-dependent metabolic disruption, and elevated levels of specific lipid metabolites confirmed that microplastics can meaningfully interfere with lipid homeostasis.
Evaluation of nanoplastics toxicity in the soil nematode Caenorhabditis elegans by iTRAQ-based quantitative proteomics
Researchers used quantitative proteomics to evaluate nanoplastic toxicity in the nematode C. elegans, identifying disrupted proteins involved in oxidative stress, metabolism, and cellular defense pathways, providing molecular-level insight into how nanoplastics harm organisms.
Biochemical and physiological effects of multigenerational exposure to spheric polystyrene microplastics in Caenorhabditis elegans
Researchers found that multigenerational exposure of C. elegans to polystyrene microplastics at low concentrations triggered oxidative stress, increased detoxification enzyme activity, and caused accumulating physiological effects across five consecutive generations.
Potential toxicity of nanopolystyrene on lifespan and aging process of nematode Caenorhabditis elegans
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.
Effect of chronic exposure to nanopolystyrene on nematode Caenorhabditis elegans
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.
Integrated transcriptomic and metabolomic analyses to decipher the regulatory mechanisms of polystyrene nanoplastic-induced metabolic disorders in hepatocytes
Using combined transcriptomic and metabolomic analysis, this study found that polystyrene nanoplastics disrupt lipid and amino acid metabolism in hepatocytes, identifying key regulatory genes and providing data relevant to assessing health risks from nanoplastic exposure.
Toxicity induction of nanopolystyrene under microgravity stress condition in Caenorhabditis elegans.
This study used Caenorhabditis elegans to examine how nanopolystyrene exposure interacts with microgravity stress, finding that nanoplastic exposure amplified the toxicity of simulated weightlessness. The combined stress increased oxidative damage and triggered mitochondrial stress responses, suggesting that nanoplastics can worsen the effects of other environmental stressors.
Using acs-22 mutant Caenorhabditis elegans to detect the toxicity of nanopolystyrene particles
Researchers used C. elegans worms with a defective intestinal barrier to show that nanoplastics at environmentally predicted concentrations (1 µg/L) can translocate to internal organs and activate oxidative stress pathways when the gut barrier is compromised — suggesting susceptibility may increase under certain disease conditions.
Neuronal damage induced by nanopolystyrene particles in nematodeCaenorhabditis elegans
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.
Assessment of nanopolystyrene toxicity under fungal infection condition in Caenorhabditis elegans
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.
Different Toxic Effects of Polystyrene Microplastics and Nanoplastics on Caenorhabditis elegans
Researchers compared the toxicity of 2-μm polystyrene microplastics and 0.1-μm nanoplastics in C. elegans, finding both impaired growth, locomotion, reproduction, and lifespan at 1 mg/L and above, with microplastics causing greater locomotion and reproductive toxicity and nanoplastics inducing stronger oxidative stress.
Combinational effect of titanium dioxide nanoparticles and nanopolystyrene particles at environmentally relevant concentrations on nematode Caenorhabditis elegans
Researchers exposed the model nematode Caenorhabditis elegans to environmentally realistic concentrations of both titanium dioxide nanoparticles and nanopolystyrene simultaneously, finding that nanoplastics enhanced the toxicity of the metal oxide particles, worsening locomotion impairment and gut oxidative stress beyond what either pollutant caused alone.
Response of tyramine and glutamate related signals to nanoplastic exposure in Caenorhabditis elegans
Researchers exposed Caenorhabditis elegans to nanopolystyrene and characterized changes in tyramine and glutamate neurotransmitter pathways, finding that nanoplastic exposure disrupted both signaling systems and that mutations in these pathways altered the worm's sensitivity to nanoplastic toxicity.
Metabolism deficiency and oxidative stress induced by plastic particles in the rotifer Brachionus plicatilis: Common and distinct phenotypic and transcriptomic responses to nano- and microplastics
Researchers found that nanoplastics caused stronger reproductive and population growth inhibition in the marine rotifer Brachionus plicatilis than microplastics, with transcriptomic analysis revealing distinct size-dependent toxicity pathways involving metabolism deficiency and oxidative stress.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
Environmentally relevant concentrations of polystyrene nanoplastics induce Parkinson’s-like neurotoxicity in C. elegans via oxidative stress
Researchers exposed roundworms to environmentally realistic concentrations of polystyrene nanoplastics and observed movement problems and brain changes resembling Parkinson's disease. The nanoplastics selectively damaged dopamine-producing neurons and increased toxic protein clumping through oxidative stress, and when an antioxidant treatment was applied, it partially reversed the harmful effects.
The role of Sod-2 in different types of neuronal damage and behavioral changes induced by polystyrene nanoplastics in Caenorhabditis elegans
Researchers used the roundworm C. elegans to study how polystyrene nanoplastics damage the nervous system at concentrations found in agricultural soils. They found that the nanoplastics caused nerve damage in a specific order, first affecting dopamine neurons, then acetylcholine neurons, and finally GABA neurons, through a process involving oxidative stress and reduced antioxidant protein levels. The study identifies a specific cellular pathway through which nanoplastics cause neurotoxic effects, and shows that a mitochondrial antioxidant could help alleviate the damage.
Suborganismal responses of the aquatic midge Chironomus riparius to polyethylene microplastics
Researchers exposed Chironomus riparius larvae to polyethylene microplastics and used transcriptomics and metabolomics to characterize suborganismal responses, finding disruption of oxidative stress pathways, energy metabolism, and cuticle synthesis — effects not captured by standard life-history endpoints alone.
Polystyrene microplastics (PS-MPs) toxicity induced oxidative stress and intestinal injury in nematode Caenorhabditis elegans
Researchers exposed the nematode C. elegans to various concentrations of polystyrene microplastics and measured physiological, biochemical, and molecular responses. The study found that microplastics accumulated in the intestine and caused oxidative stress, intestinal injury, and adverse physiological effects at concentrations as low as 1 microgram per liter, suggesting that even low-level microplastic exposure can damage gut tissues.
The toxic differentiation of micro- and nanoplastics verified by gene-edited fluorescent Caenorhabditis elegans
Researchers used gene-edited fluorescent C. elegans to demonstrate that nanoplastic toxicity is size- and charge-dependent, with 100 nm positively charged polystyrene particles causing the greatest harm through intestinal accumulation and oxidative stress.
Comprehensive phenotyping and multi-omic profiling in the toxicity assessment of nanopolystyrene with different surface properties
Researchers applied comprehensive phenotyping and multi-omics profiling to assess how nanopolystyrene particles with different surface chemistries affect the soil nematode C. elegans, finding that all surface types impaired reproduction and locomotion while causing oxidative stress, but that uncharged particles triggered the most pronounced metabolic disruption — including altered autophagy and longevity pathways.
Nanoplastic exposure in soil compromises the energy budget of the soil nematode C. elegans and decreases reproductive fitness
Researchers found that soil exposure to polystyrene nanoplastics significantly reduced reproductive fitness in the nematode C. elegans by compromising energy budgets, decreasing ATP levels, and disrupting mitochondrial function in a concentration-dependent manner.
Identification of signaling cascade in the insulin signaling pathway in response to nanopolystyrene particles
Researchers used the nematode C. elegans to map the molecular signaling pathway that responds to nanopolystyrene particle exposure. They identified a cascade in the insulin signaling pathway where exposure to nanoplastics altered the expression of key genes controlling growth, metabolism, and stress response. The study suggests that this insulin signaling cascade may play a protective role against nanoplastic toxicity in living organisms.