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


研究成果: Article査読

98 被引用数 (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.

ジャーナルLife Sciences
出版ステータスPublished - 2003 2月 21

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学一般
  • 薬理学、毒性学および薬学(全般)


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