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Neurodevelopmental Toxicity of Polystyrene Nanoplastics inCaenorhabditis elegansand the Regulating Effect of Presenilin
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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.
As one of the most widely used materials, plastic polymer fragments can abrasively degrade into microplastic (MP) and smaller nanoplastic (NP) particles. The present study aimed to investigate the influence of particle size on neurodevelopmental toxicity induced by polystyrene nanoplastics (PS-NPs) in Caenorhabditis elegans and to explore the underlying potential mechanism. C. elegans were exposed to different concentrations of PS-NPs with various sizes (25, 50, and 100 nm) for 72 h. Our results showed that all of these PS-NPs could dose-dependently induce an increase in reactive oxygen species production and mitochondrial damage in C. elegans, resulting in inhibition of body length, head thrashes, body bending, and dopamine (DA) contents. A weaker neurotoxicity was found in 25 nm PS-NPs compared to 50 and 100 nm PS-NPs, which might be due to preferential cellular distribution and greater polymerization capability of the smaller particles. In addition, all these PS-NPs could induce lipofuscin accumulation and apoptosis independent of particle size, suggesting that oxidative damage and mitochondrial dysfunction may not be the only way responsible for NP-induced neurotoxic effects. Furthermore, the mutant test targeting two presenilin genes (sel-12 and hop-1) showed that sel-12 and hop-1 were involved in regulation of PS-NP-induced neurodevelopmental toxicity and mitochondrial damage. In conclusion, PS-NPs could induce neurodevelopmental toxicity dependent on particle sizes mediated by mitochondrial damage and DA reduction. Enhanced expression of presenilin plays a role in PS-NP-induced oxidative stress and neurodevelopmental toxicity.
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