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.

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