Marathon running alters the DNA base excision repair in human skeletal muscle

Zsolt Radák*, Peter Apor, Jozsef Pucsok, Istvan Berkes, Helga Ogonovszky, Gabor Pavlik, Hideko Nakamoto, Sataro Goto

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

95 Citations (Scopus)


Reactive oxygen and nitrogen species generated either as products of aerobic metabolism or as a consequence of environmental mutagens, oxidatively modify DNA. Formamidopyrimidine-DNA glycosylase (Fpg) and endonuclease III (endo III) or their functional mammalian homologues repair 7,8-dihydro-8-oxoguanine (8-oxoG) and damaged pyrimidines, respectively, to curb the deleterious effects of oxidative DNA alterations. A single bout of physical exercise can induce oxidative DNA damage. However, its effect on the activity of repair enzymes is not known. Here we report that the activity of a functional homolog of Fpg, human 8-oxoG DNA glycosylase (hOGG1), is increased significantly, as measured by the excision of 32P labeled damaged oligonucleotide, in human skeletal muscle after a marathon race. The AP site repair enzyme did not change significantly. Despite the large individual differences among the six subjects measured, data suggest that a single-bout of aerobic exercise increases the activity of hOGG1 which is responsible for the excision of 8-oxoG. The up-regulation of DNA repair enzymes might be an important part of the regular exercise induced adaptation process.

Original languageEnglish
Pages (from-to)1627-1633
Number of pages7
JournalLife Sciences
Issue number14
Publication statusPublished - 2003 Feb 21
Externally publishedYes


  • Adaptation
  • Base excision repair
  • DNA damage
  • DNA repair
  • Exercise
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)


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