engleski

Cytotoxic mechanisms in the etiology of diabetes mellitus

Insulin-dependent diabetes mellitus (IDDM) results from a chronic autoimmune destruction of the pancreatic  -cells. Despite well-recognized role of the cellular immune system, it has become apparent that multiple effector molecules participate in the complex sequence of  -cell destruction. Recent evidence suggests that oxidative damage, resulting from both cytokine-induced production of toxic free radicals and low antioxidant capacity of the  -cell plays a significant role in the pathogenesis of IDDM. However, the production of common toxic free radicals (e.g. nitric oxide and/or reactive oxygen species), including its potentially different origin, is still an uncertain model for the specific  -cell injury. Possible role of antioxidant molecules in the etiology of diabetes received little attention so far, despite the pronounced diabetogenic action of the oxidative derivatives of ascorbic, and, particularly, uric acid. Our research evaluated the oxidant vs. antioxidant balance in the progression of diabetes mellitus. Results indicate that prediabetic condition, apart from well-established immunological and metabolic alterations, could be associated with biochemical changes revealing complex disturbances of the antioxidant defense system. Possible implications of these phenomena would at best be elucidated by studying the physiologically relevant mechanisms of the production of highly selective  -cytotoxins from the antioxidant compounds, and their influence on the  -cell function. The research on this topic is currently in progress in our laboratory.

diabetes; etiology; cytotoxic mechanisms

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