Abstract
The nematode Caenorhabditis elegans responds to flavonoid-rich diets with improved health and longevity. The precise mechanism(s) responsible for this remains to be identified, but is believed to be linked to the highly antioxidative properties of flavonoids. This study provides a dissection of lifespan modulation by the flavonoid quercetin. In detail, quercetin was shown not to act as a simple antimicrobial agent or exclusively via radical scavenging capacities. Likewise, lifespan extension had no effect on reproduction and body length. Furthermore, neither a caloric restriction mimetic nor a sirtuin (sir-2.1) dependence was identified as a likely mode of action. However, four genes were pinpointed to be required for the quercetin derived lifespan extension, namely age-1, daf-2, unc-43 and sek-1. The latter two have, to date, not been linked to quercetin-mediated lifespan extension.
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Acknowledgments
We thank the Caenorhabditis Genetic Centre, which is funded by the National Institutes of Health National Centre for Research Resources, for supplying wild type and mutant strains.
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Supplementary Table 1 Median and maximum lifespan of untreated control compared to quercetin treated wild type C. elegans (statistical significance was calculated using the mean values presented in Table 1) (DOC 46 kb)
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Supplementary Table 2 Median and maximum lifespan from wild type and mutant C. elegans, either in the presence or absence of 200 µM quercetin (statistical significance was calculated using the mean values presented in Table 2) (DOC 44 kb)
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Pietsch, K., Saul, N., Menzel, R. et al. Quercetin mediated lifespan extension in Caenorhabditis elegans is modulated by age-1, daf-2, sek-1 and unc-43 . Biogerontology 10, 565–578 (2009). https://doi.org/10.1007/s10522-008-9199-6
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DOI: https://doi.org/10.1007/s10522-008-9199-6