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We studied the age-dependent regulation of the expression of the antioxidant enzyme manganese superoxide dismutase (MnSOD encoded by  Sod2 ) through promoter methylation. C57Bl/6 mice were either (i) sedentary (SED), (ii) treated with the antioxidant catechin (CAT), or (iii) voluntarily exercised (EX) from weaning (1-month old; mo) to 9 mo. Then, all mice aged sedentarily and were untreated until 12 mo.  Sod2  promoter methylation was similar in all groups in 9 mo but decreased ( p  < 0.05) in 12 mo SED mice only, which was associated with an increased ( p  < 0.05) transcriptional activity  in vitro . At all ages, femoral artery endothelial function was maintained; this was due to an increased ( p  < 0.05) contribution of eNOS-derived NO in 12 mo SED mice only. CAT and EX prevented these changes in age-related endothelial function. Thus, a ROS-dependent epigenetic positive regulation of  Sod2  gene expression likely represents a defense mechanism prolonging eNOS function in aging mouse femoral arteries.

Age-Dependent Demethylation ofSod2Promoter in the Mouse Femoral Artery