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Nanoplastics exposure disrupts circadian rhythm associated with dysfunction of the endolysosomal pathway and autophagy in Caenorhabditis elegans
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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.
Nanoplastics (NPs), an emerging pollutant, have raised great safety concerns due to their widespread applications and continuous release into the environment, which lead to potential human and environmental risks. Recently, polystyrene NPs (100 nm; 100 mg/L) exposure has been reported to disrupt circadian rhythms under five days temperature entrainment and be associated with stress resistance decline in Caenorhabditis elegans. This study explored the possible relationship between circadian rhythm disruption and endocytosis and autophagy under polystyrene NPs exposure in C. elegans. We show that the disrupted circadian rhythm induced by NPs exposure reduced stress resistance via endocytosis and autophagy impairment. Furthermore, we found that most NPs taken up by intestinal cells were localized to early endosomes, late endosomes, and lysosomes and delivered to autophagosomes. In addition, the disruption of circadian rhythm inhibited NPs localization to these organelles. These findings indicate that NPs exposure disrupts circadian rhythm and alters its subcellular trafficking, leading to enhanced toxicity in C. elegans. Our results shed light on the prominent role of NPs exposure in circadian rhythm disruption associated with endocytosis and autophagy impairments, which may be conserved in higher animals such as humans.
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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.
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Researchers exposed Drosophila melanogaster to polyethylene microplastics over multiple generations and found that MP exposure disrupted circadian rhythm gene expression, reduced lifespan, and diminished reproductive output, suggesting fitness trade-offs mediated by metabolic and clock pathway disruption.
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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.
Size-Dependent Disruption of Lipid Metabolism by Polystyrene Micro- and Nanoplastics in Caenorhabditis elegans Revealed Through Multi-Omics and Functional Genetic Validation
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Researchers used the model organism C. elegans to study how polystyrene particles of different sizes affect lipid metabolism, finding that both 100-nanometer and 1-micrometer particles disrupted fat storage and lipid processing. Multi-omics analysis identified four core genes governing the size-dependent metabolic disruption, and elevated levels of specific lipid metabolites confirmed that microplastics can meaningfully interfere with lipid homeostasis.
Exposure to nanoplastics exacerbates light pollution hazards to mammalian
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Researchers discovered that nanoplastics can enter the brain's master clock region, called the suprachiasmatic nucleus, and disrupt circadian rhythms in mice. When nanoplastic exposure was combined with artificial light pollution, the disruption to sleep-wake cycles, metabolism, and immune function was significantly worse than from either stressor alone. The study is the first to show that nanoplastics can amplify the harmful effects of light pollution on mammalian health.
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