Abstract
A substantial amount of evidence has demonstrated that diabetes is highly associated with oxidative stress and endothelial dysfunction. 1-3 Diabetics are characterized by low plasma level of both enzymatic and non-enzymatic antioxidant defences, which make their cells prone to oxidative attack. 4 It is also well recognised that endothelial dysfunction, which is present even in people at risk of developing diabetes, is strongly connected with oxidative stress and considered as a preliminary risk factor for the development of atherosclerosis and cardiovascular disease.5,6 Infact, Diabetes itself is currently recognized as an oxidative stress disorder. 7 Oxidative stress per se is characterized by high accumulation of reactive oxygen species (ROS) that cannot be coerced by the endogenous circulating neutralizing agents and antioxidants. Hyperglycemia can induce oxidative stress through four mechanisms: increased production of advanced glycation end-products (AGEs); increased flux through the polyol/aldose pathway; activation of protein kinase C (PKC); and increased flux through the hexosamine pathway Excessive superoxide production by the mitochondrial transport chain during hyperglycemia may be the initiating factor of all the above-mentioned processes.8(Figure 1)
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