• Open Access

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

Authors

  • Christian Garm,

    1. Department of Molecular Biology and Genetics, Danish Center of Molecular Gerontology and Danish Aging Research Center, University of Aarhus, Aarhus, Denmark
    2. Epidemiology Unit, The Danish Aging Research Center, Institute of Public Health, University of Southern Denmark, Odense, Denmark
    3. Departments of Clinical Biochemistry and Pharmacology and Clinical Genetics, Odense University Hospital, Odense, Denmark
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    • The authors have declared that no conflicts of interest exists.
  • Maria Moreno-Villanueva,

    1. Molecular Toxicology Group, Department of Biology, University of Konstanz, Konstanz, Germany
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  • Alexander Bürkle,

    1. Molecular Toxicology Group, Department of Biology, University of Konstanz, Konstanz, Germany
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  • Inge Petersen,

    1. Epidemiology Unit, The Danish Aging Research Center, Institute of Public Health, University of Southern Denmark, Odense, Denmark
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  • Vilhelm A. Bohr,

    1. Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA
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  • Kaare Christensen,

    1. Epidemiology Unit, The Danish Aging Research Center, Institute of Public Health, University of Southern Denmark, Odense, Denmark
    2. Departments of Clinical Biochemistry and Pharmacology and Clinical Genetics, Odense University Hospital, Odense, Denmark
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  • Tinna Stevnsner

    Corresponding author
    • Department of Molecular Biology and Genetics, Danish Center of Molecular Gerontology and Danish Aging Research Center, University of Aarhus, Aarhus, Denmark
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Correspondence

Tinna Stevnsner, Laboratory of DNA Repair and Aging, Department of Molecular Biology and Genetics, University of Aarhus, C.F. Moellers Allé 3, 8000 Aarhus C, Denmark. Tel.: +45 87155482; fax: +45 87154904; e-mail: tvs@mb.au.dk

Summary

Exogenous and endogenous damage to DNA is constantly challenging the stability of our genome. This DNA damage increase 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 40–77 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.

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