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      Physiologie des Menschen 

      Alter und Altern

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      Springer Berlin Heidelberg

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          Oxidative stress shortens telomeres.

          Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
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            Why do we age?

            The evolutionary theory of ageing explains why ageing occurs, giving valuable insight into the mechanisms underlying the complex cellular and molecular changes that contribute to senescence. Such understanding also helps to clarify how the genome shapes the ageing process, thereby aiding the study of the genetic factors that influence longevity and age-associated diseases.
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              Cellular senescence and apoptosis: how cellular responses might influence aging phenotypes

              J Campisi (2003)
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                Author and book information

                Book Chapter
                2005
                : 933-947
                10.1007/3-540-26416-7_41
                f589c825-b736-4152-afa9-c041a7d37b77
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