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Issue 1100 coverBiogerontology: Mechanisms and Interventions Volume 1100 published April 2007
Ann. N.Y. Acad. Sci. 1100: 530–542 (2007). doi: 10.1196/annals.1395.059
Copyright © 2007 by the New York Academy of Sciences
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Part IV. Aging Interventions

Evidence for a Trade-Off between Survival and Fitness Caused by Resveratrol Treatment of Caenorhabditis elegans

JAN GRUBERa, SOON YEW TANGa AND BARRY HALLIWELLa

a Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Kent Ridge, Singapore 119260, Singapore

Key Words: Caenorhabditis elegans • aging • resveratrol • fitness • stress • trade-off

Address for correspondence: Barry Halliwell, National University of Singapore University Hall, Lee Kong Chian Wing, UHL no. 05–02G, 21 Lower Kent Ridge Road, Singapore 119077. Voice: +65-6516-3247; fax:+65-6775-2207.  bchbh{at}nus.edu.sg

Resveratrol is a naturally occurring polyphenolic compound commonly found in plant-derived products, including red wine. A large number of beneficial effects including anticarcinogenic action and protection from atherosclerotic disease have been attributed to resveratrol. Increased resveratrol intake has been suggested as an explanation for the beneficial effects of moderate red wine consumption. Resveratrol also consistently extends the mean and maximum life span in model organisms including nematode worms. It has been suggested that resveratrol exerts its life-span–extending effect through calorie restriction or hormesis mimetic effects. We have characterized the effect of resveratrol on stress resistance, developmental rate, growth, and fecundity in the nematode worm Caenorhabditis elegans in order to determine whether the beneficial effects of resveratrol on life span are associated with trade-offs in terms of early life fitness in nematodes. We find that resveratrol treatment increases stress resistance, specifically to oxidative stress, and causes a small but significant decrease in fecundity early in life without affecting overall fecundity. Resveratrol increased mean and maximum life span by delaying the onset of the exponential increase in mortality characterizing the "dying phase" in C. elegans, but did not affect the dying phase itself, suggesting that it did not act by directly affecting metabolism.






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