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Environmentally relevant concentrations of polystyrene nanoplastics induce Parkinson’s-like neurotoxicity in C. elegans via oxidative stress
Summary
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.
This study reveals that environmentally relevant polystyrene nanoplastics (PS-NPs) induces Parkinson's disease (PD)-like pathology in Caenorhabditis elegans (C. elegans) through oxidative stress. Wild-type and transgenic strains were exposed to PS-NPs at concentrations of 0.1-100 μg/L to assess behavioral toxicity, neuronal damage, and molecular mechanisms. Locomotor deficits (reduction in body bends and head thrashes) and disrupted PD-associated behaviors (impairment of food-induced basal slowing response; increased swimming paralysis rate) were observed at all concentrations, while developmental parameters remained unaffected. Although some behavioral endpoints didn't exhibit a strictly monotonic dose-response, Jonckheere-Terpstra trend analyses confirmed significant overall trends for multiple key parameters, underscoring the pervasive impact of PS-NP exposure. Selective degeneration of dopaminergic neurons and exacerbated α-synuclein aggregation confirmed neuropathological specificity. Transcriptomic analysis linked these phenotypes to oxidative stress, showing elevated reactive oxygen species (ROS) and upregulation of antioxidant enzymes (SOD-3, GST-4), alongside paradoxical suppression of the redox regulator skn-1. Genetic validation using trx-1 mutants prevented PS-NP-induced paralysis, whereas trx-4 deficiencies exacerbated toxicity, highlighting their distinct roles in redox defense. Co-treatment with N-acetylcysteine (NAC) attenuated PS-NP-induced paralysis, lowering the rate from 51.33 % to 29.47 %, though rescue failure in trx-4 mutants indicated mechanistic complexity and the indispensable role of endogenous defense systems. Critically, neurotoxicity occurred even at 0.1 μg/L PS-NPs, a level relevant to environmental contamination. These findings establish PS-NPs as potent inducers of PD-like neurodegeneration via complex oxidative stress cascades, validated by genetic and antioxidant interventions at environmentally realistic exposure levels, and highlight the urgency of monitoring nanoplastic pollution and developing antioxidant-based interventions.
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