Diabetes is associated with chronic micro- and macrovascular complications. Oxidative stress has been defined as ‘a “shift in the pro-oxidant – antioxidant balance in the pro-oxidant direction’.” Oxidant stress may initiate and exacerbate vascular (endothelial) damage through excess production of reactive oxygen species, depletion of nitric oxide, and damage to lipids, proteins, and DNA. Experimental results and theoretical constructs suggest oxidative stress is increased in diabetes, at least in some tissues, though not all studies are supportive. Potential markers of oxidation and glycoxidation are discussed. Pharmacological suppression of intracellular oxidative stress has prevented adverse biochemical and functional changes in cultured cells and animal models, and in some cases surrogate end-points of vascular damage in humans. Definitive clinical studies are awaited.