Research indicates that exposure to
hypoxia is associated with oxidative stress. In this investigation, healthy subjects were exposed to
hypoxia by inhalation of 10%
oxygen for 2h (corresponding to 5500m above sea level). The levels of strand breaks and oxidatively damaged
purine bases, measured by the comet assay, and the expression of genes involved in DNA repair of oxidatively damaged
DNA were investigated in mononuclear blood cells (MNBC) at baseline, after 2h of
hypoxia, 2h of reoxygenation, and 1 day and 8 days after the exposure. The level of strand breaks and oxidized
purine bases in MNBC increased following both the 2h of
hypoxia and the 2h reoxygenation period, whereas this effect was not observed in unexposed subjects. The expressions of oxoguanine
DNA glycosylase 1 (OGG1),
nucleoside diphosphate linked moiety X-type motif 1 (NUDT1), nei
endonuclease VIII-like 1 (NEIL1), and mutY homolog (MUTYH) were unaltered throughout the experiment in both groups of subjects, indicating that DNA repair genes are not up-regulated by the
hypoxia and reoxygenation treatment. Taken together, this report shows that inhalation of 10%
oxygen for 2h is associated with increased number of oxidized DNA lesions in MNBC, but acute
hypoxia may not inflict upon the regulation of genes involved in repair of oxidized
DNA.