• Open Access

Lifestyle impacts on the aging-associated expression of biomarkers of DNA damage and telomere dysfunction in human blood

Authors

  • Zhangfa Song,

    1. Institute of Molecular Medicine and Max-Planck Research Group on Stem Cell Aging, University of Ulm, Ulm, Germany
    2. Department of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China
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    • These authors contributed equally.

  • Guido Von Figura,

    1. Institute of Molecular Medicine and Max-Planck Research Group on Stem Cell Aging, University of Ulm, Ulm, Germany
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    • These authors contributed equally.

  • Yan Liu,

    1. Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA
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  • Johann M. Kraus,

    1. Department of Internal Medicine I, University of Ulm, Ulm, Germany
    2. Research group of Bioinformatics and Systems Biology, Institute of Neural Information Processing University of Ulm, Ulm, Germany
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  • Chad Torrice,

    1. Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA
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  • Patric Dillon,

    1. Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA
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  • Masami Rudolph-Watabe,

    1. Department of Otorhinolaryngology, University of Ulm, Ulm, Germany
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  • Zhenyu Ju,

    1. Max-Planck-Partner Group on Stem Cell aging, Key laboratory of Human Diseases Comparative Medicine Ministry of Health Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Beijing, China
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  • Hans A. Kestler,

    1. Department of Internal Medicine I, University of Ulm, Ulm, Germany
    2. Research group of Bioinformatics and Systems Biology, Institute of Neural Information Processing University of Ulm, Ulm, Germany
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  • Hanna Sanoff,

    1. Department of Medicine, University of Virginia Charlottesville, VA, USA
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  • Karl Lenhard Rudolph

    1. Institute of Molecular Medicine and Max-Planck Research Group on Stem Cell Aging, University of Ulm, Ulm, Germany
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Hans A. Kestler, Research group of Bioinformatics and Systems Biology, Institute of Neural Information Processing, University of Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany. Tel.: +49 731 5024248; fax: +49 731 5024156 ; e-mail: hans.kestler@uni-ulm.de
K. Lenhard Rudolph, Department of Molecular Medicine, Max-Planck Research Group on Stem Cell Aging, University of Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany. Tel.: 0049 731 5036 100; fax: 0049 731 5036 102 ; e-mail: Lenhard.Rudolph@uni-ulm.de

Summary

Cellular aging is characterized by telomere shortening, which can lead to uncapping of chromosome ends (telomere dysfunction) and activation of DNA damage responses. There is some evidence that DNA damage accumulates during human aging and that lifestyle factors contribute to the accumulation of DNA damage. Recent studies have identified a set of serum markers that are induced by telomere dysfunction and DNA damage, and these markers showed an increased expression in blood during human aging. Here, we investigated the influence of lifestyle factors (such as exercise, smoking, body mass) on the aging-associated expression of serum markers of DNA damage (CRAMP, EF-1α, stathmin, n-acetyl-glucosaminidase and chitinase) in comparison with other described markers of cellular aging (p16INK4a upregulation and telomere shortening) in human peripheral blood. The study shows that lifestyle factors have an age-independent impact on the expression level of biomarkers of DNA damage. Smoking and increased body mass indices were associated with elevated levels of biomarkers of DNA damage independent of the age of the individuals. In contrast, exercise was associated with an age-independent reduction in the expression of biomarkers of DNA damage in human blood. The expression of biomarkers of DNA damage correlated positively with p16INK4a expression and negatively with telomere length in peripheral blood T-lymphocytes. Together, these data provide experimental evidence that both aging and lifestyle impact on the accumulation of DNA damage during human aging.

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