Volume 959, Issue 1 p. 24-29

Replicative Aging, Telomeres, and Oxidative Stress

GABRIELE SARETZKI

Corresponding Author

GABRIELE SARETZKI

Department of Gerontology, University of Newcastle, Newcastle upon Tyne NE6 4BE, United Kingdom

Address for correspondence: Dr. Gabriele Saretzki, University of Newcastle, Department of Gerontology, Wolfson Research Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE6 4BE, UK. Voice: +44-0191 256 3384; fax: +44-0191 2195074; [email protected].Search for more papers by this author
THOMAS VON ZGLINICKI

THOMAS VON ZGLINICKI

Department of Gerontology, University of Newcastle, Newcastle upon Tyne NE6 4BE, United Kingdom

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First published: 24 January 2006
Citations: 207

Abstract

Aging is a very complex phenomenon, both in vivo and in vitro. Free radicals and oxidative stress have been suggested for a long time to be involved in or even to be causal for the aging process. Telomeres are special structures at the end of chromosomes. They shorten during each round of replication and this has been characterized as a mitotic counting mechanism. Our experiments show that the rate of telomere shortening in vitro is modulated by oxidative stress as well as by differences in antioxidative defence capacity between cell strains. In vivo we found a strong correlation between short telomeres in blood lymphocytes and the incidence of vascular dementia. These data suggest that parameters that characterise replicative senescence in vitro offer potential for understanding of, and intervention into, the aging process in vivo.