How can age and lifestyle variables affect DNA damage, repair capacity and endogenous biomarkers of oxidative stress?

• The age-related changes in OGG1 repair activity in human lymphocytes.
• DNA strand breaks increased with age with no change in FPG-sensitive sites.
• OGG1 repair activity showed to be higher in older people.
• Aerobic capacity and lipid peroxidation showed to be predictors of DNA strand breaks.

Age-related DNA damage has been regarded as one of the possible explanations of aging, and these age-related changes have been associated with lifestyle variables. Considering this, the purpose of this study was to investigate how age and lifestyle may affect DNA damage, DNA repair capacity and endogenous biomarkers of oxidative stress. Sixty-one healthy men (40 to 89 yrs) were enrolled in this study. The results showed that DNA strand breaks (DNA SBs) and DNA repair capacity were greater in the older group (> = 65 yrs) compared to the younger group (< 65 yrs) (p < 0.05). FPG-sensitive sites, total antioxidant capacity and lipid peroxidation (MDA) were not statistically different between groups. The correlation test showed that DNA damage variables were not correlated with any lifestyle variable excepting DNA SBs which was correlated with aerobic capacity (6MWT). DNA SBs and DNA repair were positively correlated with age. The multiple regression analysis revealed that the aerobic capacity (6MWT) and MDA were the predictors for the variation of DNA SBs (41.9%). In conclusion these results suggest that DNA SB damage increases with age but not FPG-sensitive sites. Moreover, base excision repair capacity increases with age without the increase of oxidative damage to DNA. The most predictable variables of DNA SBs were the aerobic capacity and MDA.