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Papers In Press, published online ahead of print December 9, 2002
J. Biol. Chem, 10.1074/jbc.M207939200
Submitted on August 5, 2002
Revised on December 9, 2002
Accepted on December 9, 2002

Extracellular superoxide dismutase is a major antioxidant in human fibroblasts and slows down telomere shortening

Violeta Serra, Thomas von Zglinicki, Mario Lorenz, and Gabriele Saretzki

Gerontology, University of Newcastle, Newcastle upon Tyne NE4 6BE

Corresponding Author: t.vonzglinicki{at}ncl.ac.uk

There is good evidence that telomere shortening acts as a biological clock in human fibroblasts, limiting the number of population doublings a culture can achieve. Oxidative stress also limits the growth potential of human cells, and recent data show that the effect of mild oxidative stress is mediated by an increased stress-related rate of telomere shortening. Thus, fibroblast strains have donor-specific antioxidant defence, telomere shortening rate and growth potential. We used low density gene expression array analysis of fibroblast strains with different antioxidant potential and telomere shortening rate to identify gene products responsible for these differences. Extracellular superoxide dismutase was identified as the strongest candidate, and this correlation was confirmed by Northern blotting. Overexpression of this gene in human fibroblasts with low antioxidant capacity increased total cellular superoxide dismutase activity, decreased the intracellular peroxide content, slowed down telomere shortening rate and elongated the lifespan under normoxia and hyperoxia of these cells. This result identifies extracellular superoxide dismutase as an important antioxidant gene product in human fibroblasts, confirms the causal role of oxidative stress for telomere shortening and strongly suggests that the senescence-like arrest under mild oxidative stress is telomere-driven.


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