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Age and gender effects on DNA strand break repair in peripheral blood mononuclear cells

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  • Christian Garm, Syddansk Universitet, Danmark
  • Maria Moreno-Villanueva, Universität Konstanz, Tyskland
  • Alexander Bürkle, Universität Konstanz, Tyskland
  • Inge Petersen, Syddansk Universitet, Danmark
  • Vilhelm A. Bohr, Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, Danmark
  • Kaare Christensen, Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, USA
  • Tinna V. Stevnsner
Exogenous and endogenous damage to DNA is constantly challenging the stability of our genome. This DNA damage increased the frequency of errors in DNA replication, thus causing point mutations or chromosomal rearrangements and has been implicated in aging, cancer, and neurodegenerative diseases. Therefore, efficient DNA repair is vital for the maintenance of genome stability. The general notion has been that DNA repair capacity decreases with age although there are conflicting results. Here, we focused on potential age associated changes in DNA damage response and the capacities of repairing DNA single strand breaks (SSBs) and double strand breaks (DSBs) in human peripheral blood mononuclear cells (PBMCs). Of these lesions DSBs are the least frequent but the most dangerous for cells. We have measured the level of endogenous SSBs, SSB repair capacity, γ-H2AX response, and DSB repair capacity in a study population consisting of 216 individuals from a population-based sample of twins aged 40 to 77 years. Age in this range did not seem to have any effect on the SSB parameters. However, γ-H2AX response and DSB repair capacity decreased with increasing age, although the associations did not reach statistical significance after adjustment for batch effect across multiple experiments. No gender differences were observed for any of the parameters analyzed. Our findings suggest that in PBMCs the repair of SSBs is maintained until old age, whereas the response to and the repair of DSBs decrease. © 2012 The Authors Aging Cell © 2012 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.
TidsskriftAging Cell
Sider (fra-til)56-66
Antal sider16
StatusUdgivet - feb. 2013

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