DOI: 10.36347/sjams.2017.v05i09.030

Pages: 3634-3653

Diabetes mellitus (DM) is one of the most common non-communicable diseases globally. Serum uric acid is a strong reducing agent and in humans, over half the antioxidant capacity of blood plasma comes from it. It is widely accepted that uric acid in humans is a major antioxidant that protects cardiac, vascular, and neural cells from oxidative injury, by scavenging hydroxyl radical, singlet oxygen, and peroxynitrite. Hyperuricemia in diabetes leads to endothelial dysfunction and nitric oxide (NO) inhibition. Uric acid reacts directly with nitric oxide in a rapid irreversible reaction resulting in the formation of 6-amino uracil and depletion of NO, which is an endothelial cell derived relaxing factor (EDRF). The probable mechanism by which uric acid may endanger organ damage is through endothelial dysfunction.