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Role of free Radicals

Diabetes Mellitus

Diabetes mellitus is a common disorder, caused by hyperglycaemia resulting from a deficiency in insulin secretion or action. Diabetes mellitus is associated with increased risk of complications including retinopathy, kidney failure, nerve damage, circulatory problems, heart disease and stroke. Animal studies have suggested that reactive radicals contribute to the destruction of pancreatic islet cells in the pathogenesis of insulin dependent diabetes mellitus. Toxic amounts of reactive oxygen intermediates are released by endothelial cells and infiltrating macrophages during islet inflammation. Islet cells are thought to have deficient defense system against free radical attack, making them susceptible to reactive oxygen intermediates, leading to the destruction of the cells. Impaired ascorbic acid metabolism has also been implicated in diabetes. Ascorbate is required for the regeneration of vitamin E in vivo and may be oxidized to dehydroascorbic acid, which can disrupt cell structures and act as a neurotoxin. In healthy tissues dehydroascorbic acid is generally recycled back to ascorbic acid. Increased exposure to high levels of dehydroascorbic acid and low levels of ascorbic acid results in increased susceptibility of the cell to oxidative damage. Other research suggests that high glucose levels in diabetes interfere with ascorbic acid uptake, resulting in low levels of ascorbate in cells.

References

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  2. Kinalski M. Sledziewski A. Telejko B. Kowalska I. Kretowski A. Zarzycki W. Kinalska I. Lipid peroxidation, antioxidant defence and acid-base status in cord blood at birth: the influence of diabetes. Hormone & Metabolic Research. 33(4):227-31, 2001

  3. Peiro C. Lafuente N. Matesanz N. Cercas E. Llergo JL. Vallejo S. Rodriguez-Manas L. Sanchez-Ferrer CF. High glucose induces cell death of cultured human aortic smooth muscle cells through the formation of hydrogen peroxide. British Journal of Pharmacology. 133(7):967-74, 2001

  4. Ha H. Lee HB. Reactive oxygen species as glucose signaling molecules in mesangial cells cultured under high glucose. Kidney International - Supplement. 77:S19-25, 2000

  5. Aljada A. Garg R. Ghanim H. Mohanty P. Hamouda W. Assian E. Dandona P. Nuclear factor-kappaB suppressive and inhibitor-kappaB stimulatory effects of troglitazone in obese patients with type 2 diabetes: evidence of an antiinflammatory action?. Journal of Clinical Endocrinology & Metabolism. 86(7):3250-6, 2001

  6. Uemura S. Matsushita H. Li W. Glassford AJ. Asagami T. Lee KH. Harrison DG. Tsao PS. Diabetes mellitus enhances vascular matrix metalloproteinase activity: role of oxidative stress. Circulation Research. 88(12):1291-8, 2001

  7. Yamagishi SI. Edelstein D. Du XL. Brownlee M. Hyperglycemia potentiates collagen-induced platelet activation through mitochondrial superoxide overproduction. Diabetes. 50(6):1491-4, 2001

  8. Cosentino F. Luscher TF. Effects of blood pressure and glucose on endothelial function. Current Hypertension Reports. 3(1):79-88, 2001

  9. Aydin A. Orhan H. Sayal A. Ozata M. Sahin G. Isimer A. Oxidative stress and nitric oxide related parameters in type II diabetes mellitus: effects of glycemic control. Clinical Biochemistry. 34(1):65-70, 2001

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