Ecotoxicology and environmental safety · 2026
Circular RNA signatures associated with nanoplastics-induced healthspan alterations in C. elegans.
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Wu Zifan, Zhou Chiyang, Sun Xiaoman, Zhang Xiaoxiao, Qu Man, Chen He
Аннотация
BACKGROUND: Nanoplastics have emerged as ubiquitous environmental contaminants with the capacity to perturb diverse biological processes, including organismal aging. However, the molecular underpinnings connecting nanoplastic exposure to healthspan modulation remain largely unknown.
RESULTS: Employing Caenorhabditis elegans as a model organism, we examined the effects of early-life exposure to 50 nm polystyrene (PS) and amino-modified PS (PS-NH2) nanoplastics at 1 µg/L for 72 h. While such exposure exerted no significant influence on organismal lifespan, it precipitated pronounced healthspan deterioration, manifested by diminished locomotory performance and pharyngeal pumping activity during aging. Transcriptomic and circular RNAs (circRNAs) profiling was performed in day-8 adults from control and PS groups, revealing long-lasting expression changes, including a global upregulation of circRNAs whose host genes were enriched in longevity-regulating and stress-response pathways. Several circRNAs derived from key aging-related genes were associated with the degree of healthspan decline, and qRT-PCR validation indicated stronger changes under PS-NH2 exposure.
CONCLUSIONS: Early-life nanoplastic exposure disrupts healthspan through persistent transcriptional and circRNA alterations that recapitulate molecular signatures characteristic of physiological aging. These findings highlight circRNA dysregulation as a sensitive biomarker for nanoplastics-induced healthspan impairment and provide new insights into how environmental nanoplastics influence aging processes.
RESULTS: Employing Caenorhabditis elegans as a model organism, we examined the effects of early-life exposure to 50 nm polystyrene (PS) and amino-modified PS (PS-NH2) nanoplastics at 1 µg/L for 72 h. While such exposure exerted no significant influence on organismal lifespan, it precipitated pronounced healthspan deterioration, manifested by diminished locomotory performance and pharyngeal pumping activity during aging. Transcriptomic and circular RNAs (circRNAs) profiling was performed in day-8 adults from control and PS groups, revealing long-lasting expression changes, including a global upregulation of circRNAs whose host genes were enriched in longevity-regulating and stress-response pathways. Several circRNAs derived from key aging-related genes were associated with the degree of healthspan decline, and qRT-PCR validation indicated stronger changes under PS-NH2 exposure.
CONCLUSIONS: Early-life nanoplastic exposure disrupts healthspan through persistent transcriptional and circRNA alterations that recapitulate molecular signatures characteristic of physiological aging. These findings highlight circRNA dysregulation as a sensitive biomarker for nanoplastics-induced healthspan impairment and provide new insights into how environmental nanoplastics influence aging processes.