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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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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-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.[1]

References

  1. Marathon running alters the DNA base excision repair in human skeletal muscle. Radák, Z., Apor, P., Pucsok, J., Berkes, I., Ogonovszky, H., Pavlik, G., Nakamoto, H., Goto, S. Life Sci. (2003) [Pubmed]
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