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61,005 resultsShowing papers similar to Environmentally relevant concentrations of polystyrene nanoplastics induce Parkinson’s-like neurotoxicity in C. elegans via oxidative stress
ClearThe 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.
Nanoplastics exacerbate Parkinson's disease symptoms in C. elegans and human cells
Researchers discovered that tiny 25-nanometer plastic particles worsened symptoms similar to Parkinson's disease in both worm models and human cells, including nerve cell death, movement problems, and buildup of harmful protein clumps. The nanoplastics also damaged the intestinal barrier, causing a "leaky gut" condition, and broke apart mitochondria in muscle cells. These findings suggest nanoplastic exposure could be a risk factor for neurodegenerative diseases.
Neurodevelopmental Toxicity of Polystyrene Nanoplastics inCaenorhabditis elegansand the Regulating Effect of Presenilin
C. elegans exposed to 25, 50, and 100 nm polystyrene nanoplastics showed size-dependent neurodevelopmental toxicity — including reactive oxygen species generation, mitochondrial damage, and inhibited dopamine production — with smaller particles (25 nm) paradoxically showing weaker effects than the 50 nm size.
Environmentally persistent free radicals on photoaged nanopolystyrene induce neurotoxicity by affecting dopamine, glutamate, serotonin and GABA in Caenorhabditis elegans
Researchers found that when polystyrene nanoplastics age under sunlight, they generate environmentally persistent free radicals on their surface that make them significantly more toxic to the nervous system. Using the model organism C. elegans, they showed that aged nanoplastics disrupted movement and reduced levels of key neurotransmitters including dopamine, serotonin, and GABA. The study suggests that weathered nanoplastics in the environment may pose greater neurological risks than freshly produced particles.
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.
Polystyrene (nano)microplastics cause size-dependent neurotoxicity, oxidative damage and other adverse effects inCaenorhabditis elegans
Researchers found that polystyrene micro- and nanoplastics cause neurotoxicity and oxidative damage in the model organism C. elegans, with effects varying by particle size. Smaller nanoscale particles tended to cause more severe toxic responses than larger microplastic particles. The study highlights that the size of plastic particles is an important factor in determining how harmful they are to living organisms.
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.
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.
Brain single-nucleus transcriptomics highlights that polystyrene nanoplastics potentially induce Parkinson’s disease-like neurodegeneration by causing energy metabolism disorders in mice
In a mouse study, oral exposure to polystyrene nanoplastics caused brain changes resembling Parkinson's disease, including loss of dopamine-producing neurons and movement problems. Advanced single-cell brain analysis revealed that the nanoplastics disrupted energy production in brain cells, particularly in the brain regions most affected by Parkinson's disease. This research raises the alarming possibility that chronic nanoplastic exposure through food and water could contribute to neurodegenerative diseases.
Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology
Scientists found that polystyrene nanoplastics can travel from the gut to the brain along nerve pathways and worsen Parkinson's disease in mice. The nanoplastics accelerated the clumping of alpha-synuclein, a protein central to Parkinson's, which triggered brain inflammation, damaged mitochondria, and impaired the cellular cleanup system. Mice exposed to both nanoplastics and the disease protein showed progressive physical and motor decline resembling Parkinson's symptoms.
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.
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.
Photoaged polystyrene nanoplastics exposure results in reproductive toxicity due to oxidative damage in Caenorhabditis elegans
Researchers exposed the roundworm C. elegans to polystyrene nanoplastics that had been aged by sunlight, simulating real-world environmental conditions. The study found that these weathered nanoplastics caused more severe reproductive harm than pristine particles, primarily through increased oxidative stress, suggesting that aging makes plastic particles more toxic to living organisms.
Brain lipidomics identifies mitochondrial redox dysfunction and metabolic trade-offs associated with Parkinson’s disease-like pathology induced by Nanoplastics exposure
Using high-resolution lipidomics in Drosophila chronically exposed to polystyrene nanoplastics, researchers found dose-dependent remodeling of mitochondrial membrane lipids—particularly cardiolipins—along with increased fat storage molecules and signs of Parkinson's disease-like metabolic dysfunction.
Environmental Concentrations of Polystyrene Nanoplastics Induce Low‐Dose Tamoxifen Toxicity Through Oxidative Stress in Caenorhabditis elegans
Researchers used the model organism C. elegans to investigate how environmental concentrations of polystyrene nanoplastics interact with the cancer drug tamoxifen. Combined exposure significantly impaired locomotion, reproduction, and growth while inducing oxidative stress through the DAF-2/DAF-16 insulin signaling pathway. The study suggests that long-term exposure to environmental levels of nanoplastics could enhance the side effects of pharmaceutical drugs in living 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.
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.
Polystyrene nanoplastics trigger pyroptosis in dopaminergic neurons through TSC2/TFEB-mediated disruption of autophagosome-lysosome fusion in Parkinson’s disease
This study found that polystyrene nanoplastics accelerated the onset and progression of Parkinson's disease in lab models by disrupting the brain cells' waste-clearing system. The nanoplastics interfered with how brain cells break down damaged proteins, triggering a type of inflammatory cell death in the dopamine-producing neurons that are critical for movement control.
The mechanism of oxidative stress induced by nanoplastics in Caenorhabditis elegans: Integrated analysis of transcriptomics and metabolomics
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.
Uptake 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.
Nanoplastics induce neuroexcitatory symptoms in zebrafish (Danio rerio) larvae through a manner contrary to Parkinsonian's way in proteomics
Researchers found that polystyrene nanoplastics caused hyperactive behavior in zebrafish larvae by disrupting dopamine signaling and inhibiting a key brain enzyme. Interestingly, the mechanism was the opposite of what is seen in Parkinson's disease, with nanoplastics increasing rather than decreasing dopamine activity. The study provides evidence that nanoplastics can cross the blood-brain barrier and interfere with nervous system function in developing organisms.
The joint effects of nanoplastics and TBBPA on neurodevelopmental toxicity inCaenorhabditis elegans
Researchers used the model organism C. elegans to study the combined neurodevelopmental effects of polystyrene nanoplastics and the flame retardant TBBPA. The study found that combined exposure produced synergistic harmful effects including reduced survival, impaired movement, oxidative stress, and dopaminergic neuron loss, with specific genes related to neurodegenerative pathways playing key roles in the observed toxicity.
Neurotoxicity induced by aged microplastics from plastic bowls: Abnormal neurotransmission in Caenorhabditis elegans
Researchers found that microplastics released from aged plastic bowls caused nerve damage in the roundworm C. elegans at environmentally realistic concentrations. The aged microplastics disrupted neurotransmitter systems including dopamine and serotonin, leading to impaired movement. This study is concerning because it shows that everyday plastic items we use for food can release microplastics that have neurotoxic effects.
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.