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Early developmental nanoplastics exposure disturbs circadian rhythms associated with stress resistance decline and modulated by DAF-16 and PRDX-2 in C. elegans
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Early developmental exposure to polystyrene nanoplastics disrupted circadian rhythm gene expression in C. elegans, reducing stress resistance in time-dependent patterns modulated by the transcription factor DAF-16 and the antioxidant enzyme PRDX-2, linking nanoplastic exposure to circadian clock dysregulation at an early life stage.
Plastics pollution is an emerging environmental problem and nanoplastics (NPs) toxicity has received great concern. This study investigated whether early developmental exposure to polystyrene NPs influence the circadian rhythms and the possible underlying mechanisms in C. elegans. We show that early developmental NPs exposure disturbs circadian rhythms in C. elegans and ASH neurons and G protein-coupled receptor kinase (GRK-2) are involved in the level of chemotaxis response. A higher bioconcentration factor in entrained worms was observed, suggesting that circadian interference results in increased NPs bioaccumulation in C. elegans. In addition, we show that reactive oxygen species produced by NPs exposure and peroxiredoxin-2 (PRDX-2) are related to the disturbed circadian rhythms. We further show that the NPs-induced circadian rhythms disruption is associated with stress resistance decline and modulated by transcription DAF-16/FOXO signaling. Because circadian rhythms are found in most living organisms and the fact that DAF-16 and PRDX-2 are evolutionarily conserved, our findings suggest a possible negative impact of NPs on circadian rhythms and stress resistance in higher organisms including humans.
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Researchers found that exposure to polystyrene nanoplastics disrupted circadian rhythms in the model organism Caenorhabditis elegans, linking the disruption to dysfunction in endolysosomal pathways and autophagy. The study suggests that nanoplastic exposure may interfere with fundamental biological timing mechanisms through stress-related cellular pathways, raising concerns about the broader biological effects of nanoplastic pollution.
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