Taken together, we have demonstrated that, in GLO1 Tg rats, age-related acceleration in glycative and oxidative stress was mitigated and age-related endothelial dysfunction was ameliorated, concomitant with attenuation of age-related eNOS (Thr495) phosphorylation and eNOS (Ser1177) dephosphorylation, resulting in increased NO bioavailability and amelioration of endothelial dysfunction. Here, GLO1 is linked to endothelial dysfunction.