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

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-oxogu...

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Bibliographic Details
Published inLife sciences (1973) Vol. 72; no. 14; pp. 1627 - 1633
Main Authors Radák, Zsolt, Apor, Peter, Pucsok, Jozsef, Berkes, Istvan, Ogonovszky, Helga, Pavlik, Gabor, Nakamoto, Hideko, Goto, Sataro
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 21.02.2003
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Summary: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.
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ISSN:0024-3205
1879-0631
DOI:10.1016/S0024-3205(02)02476-1