The Effect of Hydrogen Peroxide-Induced Oxidative Stress on Leukocytes Depends on Age and Physical Training in Healthy Human Subjects Carrying the Same Genotypes of Antioxidant Enzymes' Gene Polymorphisms

Objectives: Reactive oxygen species account for the background levels of oxidatively damaged DNA in normal tissues. Physical exercise increases oxygen consumption and can cause oxidative stress. This stress can also involve deficient antioxidant defenses, which can be influenced by certain genetic polymorphisms. Because regular exercise is a known inducer of antioxidant enzymes, the objective of this study was to compare, by comet assay, differences in the DNA damage between apparently healthy individuals and trained aerobic sportsmen carrying the same single nucleotide polymorphisms of manganese superoxide dismutase (Val9Ala), catalase (-21A/T), glutathione peroxidase 1 (Pro198Leu), before and after exposing leukocytes from peripheral blood to hydrogen peroxide (H(2)O(2)). Methods: Athletes were compared with nonathletes after a situation that promotes reactive oxygen species increase (a race). Blood samples were submitted to genotyping and comet assay, and the athletes and nonathletes were paired according to their gender, age, and MnSOD, CAT, and GPx-1 genotypes. Results: For nonathletes, there was a positive correlation between H(2)O(2) concentrations and DNA damage levels. For athletes, these correlations showed differences between sexes, indicating that running may impose higher oxidative stress on the DNA of women than of men. Significant differences appeared for nonathletes in the comparisons between younger and older age groups after treatment with H(2)O(2\) at 250 mu M. Conclusions: This suggests that, for individuals carrying the same genotypes of antioxidant enzymes' genes, the effect of H(2)O(2)-induced oxidative stress depends mainly on age and physical training. It also suggests that aerobic physical training can reduce oxidative damages to DNA, preventing related diseases in older people. Am. J. Hum. Biol. 22:807-812,2010. (C) 2010 Wiley-Liss, Inc.