Background: Light, a crucial abiotic factor, consistently modulates organismal physiological activities. However, artificial light at night (ALAN) presents a considerable challenge. The widespread use of blue-light-rich light-emitting diodes (LEDs) in electronic products contributes to “blue light enrichment”. With population aging, the prevalence of obesity among older adults was expected to continue to increase. ALAN potentially induced obesity and shortened lifespan. However, the underlying pathogenic mechanism remains poorly understood. Methods: In this study, we investigated the effects of blue light on aging and lipid accumulation. Transcriptome and proteome analyses were performed to explore the potential regulatory mechanisms. Based on the enrichment results, we measured markers of lipid peroxidation and oxidative stress in Caenorhabditis elegans (C. elegans). We also conducted gene knockout experiments to verify the core regulatory genes. Results: The results showed that nighttime blue light induced lipid accumulation and aging in animals. Transcriptome and proteome analyses revealed that these effects might involve lipid transport, fatty acid metabolism, and oxidoreductase activity. Based on the enrichment results, we measured markers of lipid peroxidation and oxidative stress in C. elegans. Nighttime blue light exposure increased ROS, lipofuscin, lipid levels, and DAF-16 nuclear translocation, and decreased daf-16/sod-3. Notably, sod-3 knockout further exacerbated nighttime blue-light-induced lipid accumulation and lifespan shortening. Conclusions: In conclusion, our observations in C. elegans suggest that blue light is associated with altered DAF-16/SOD-3 signaling and that SOD-3 appears to contribute to protection against blue-light-induced stress. These findings provide experimental evidence from C. elegans supporting minimizing unnecessary nighttime lighting, particularly blue light exposure.
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Cheng et al. (2026) studied this question.
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