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Environmentally persistent free radicals on photoaged nanopolystyrene induce neurotoxicity by affecting dopamine, glutamate, serotonin and GABA in Caenorhabditis elegans
Summary
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.
Microplastics are widely detected in the environment and induce toxic effects in various organisms. However, the properties and toxicity associated with environmentally persistent free radicals (EPFRs) in photoaged nanopolystyrene (NPS) remain largely unknown. We investigated the generation of EPFRs on photoaged NPS and their neurotoxicity and underlying mechanism in Caenorhabditis elegans. The results suggested that photoaging induces the generation of EPFRs and reactive oxygen species (O, •OH, and O), which altered the physicochemical properties (morphology, crystallinity, and functional groups) of NPS. Acute exposure to 1 μg/L of NPS-60 (NPS with light irradiation time of 60 d) significantly decreased locomotion behaviors and neurotransmitter contents (e.g., glutamate, serotonin, dopamine, and γ-aminobutyric acid). Treatment with N-acetyl-L-cysteine (NAC) by radical quenching test significantly reduced EPFRs levels on the aged NPS, and the toxicity of NAC-quenching NPS was decreased in nematodes compared to those in photoaged NPS. EPFRs also caused dysfunction of neurotransmission-related gene expression in C. elegans. Thus, EPFRs generated on photoaged NPS contributed to neurotoxicity by affecting dopamine, glutamate, serotonin, and γ-aminobutyric acid neurotransmission. The study highlights the potential risks of photoaged NPS and the contributions of EPFRs to toxicity.