With the exception of stem cells, the replicative potential of somatic cells is limited due to the eventual onset of cellular senescence. It is widely thought that progressive shortening of telomeres during DNA replication contributes to the aging process, so that after a sufficient number of rounds of replication, the telomeres shorten below a critical point needed to maintain genomic integrity. Overexpression of telomerase can be associated with cellular immortalization and may contribute to cancer, although other events leading to uncapped, shortened telomeres are also associated with cancer (Cui et al., 2003; Wai, 2004). During normal development, telomerase activity may decline with age. Shorter lived species display a rapid loss of telomerase activity during development, whereas longer lived species delay this decrease in telomerase activity (Haussman et al., 2004). Increased telomere length in Caenorhabditis elegans correlates with increased life span (Joeng et al., 2004). Oxidative DNA damage from reactive oxygen species, irradiation, and various forms of stress are believed to shorten telomeres prematurely, leading to accelerated aging (Kawanishi et al., 2004; Liu et al., 2002).
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When over eighty years of age, the poet Bryant said that he had added more than ten years to his life by taking a simple exercise while dressing in the morning. Those who knew Bryant and the facts of his life never doubted the truth of this statement.