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DNA repair, oxidative stress and aging

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Oxidative Stress and Aging

Part of the book series: Molecular and Cell Biology Updates ((MCBU))

Summary

A major factor in the progression of senescence and of age-associated diseases is the accumulation of DNA damage. Several studies have documented an age-associated increase in oxidative DNA damage, notably 7,8 dihydro-8-oxodeoxyguanosine (8-oxodG). Although not all studies have agreed on damage accumulation in the nuclear DNA, there seems to be a consensus that the level of 8- oxodG increases with aging in mitochondrial DNA (Richter et al., 1988). Oxidative DNA damage may (1) induce genes that are involved in the regulation of cellular proliferation (an example of this would be the activation of the p53 tumor suppressor gene) or could (2) simply inactive specific genes and thereby provoke progression to senescence or malignancies. If this DNA damage is a key element in senescence, then a major goal in aging research should be to clarify the mechanism involved. One likely mechanism is that the DNA repair processes which normally remove these DNA damages, deteriorate with age and thereby permit the damage accumulation. We therefore need to investigate the change in DNA repair processes and their efficiency with increasing age.

Oxidative cellular stress can be induced in several ways, and some of these are shown in Figure 1. Exogenous or endogenous agents can be involved. There are many cellular responses to stress, and one very important pathway is that induced by DNA damage.

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© 1995 Birkhäuser Verlag Basel/Switzerland

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Bohr, V.A., Larminat, F., Taffe, B.G. (1995). DNA repair, oxidative stress and aging. In: Cutler, R.G., Packer, L., Bertram, J., Mori, A. (eds) Oxidative Stress and Aging. Molecular and Cell Biology Updates. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7337-6_12

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  • DOI: https://doi.org/10.1007/978-3-0348-7337-6_12

  • Publisher Name: Birkhäuser Basel

  • Print ISBN: 978-3-0348-7339-0

  • Online ISBN: 978-3-0348-7337-6

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