The role of oxidative stress in diabetic complications

Authors: Niedowicz, Dana¹; Daleke, David²

Source: Cell Biochemistry and Biophysics, Volume 43, Number 2, June 2005 , pp. 289-330(42)

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Abstract:

The morbidity and mortality associated with diabetes is the result of the myriad complications related to the disease. One of the most explored hypotheses to explain the onset of complications is a hyperglycemia-induced increase in oxidative stress. Reactive oxygen species (ROS) are produced by oxidative phosphorylation, nicotinamide adenine dinucleotide phosphate oxidase (NADPH), xanthine oxidase, the uncoupling of lipoxygenases, cytochrome P450 monooxygenases, and glucose autoxidation. Once formed, ROS deplete antioxidant defenses, rendering the affected cells and tissues more susceptible to oxidative damage. Lipid, DNA, and protein are the cellular targets for oxidation, leading to changes in cellular structure and function. Recent evidence suggests ROS are also important as second messengers in the regulation of intracellular signaling pathways and, ultimately, gene expression. This review explores the production of ROS and the propagation and consequences of oxidative stress in diabetes.

Keywords: Antioxidants, diabetes mellitus; free radicals; glucose autoxidation; lipid asymmetry; lipid oxidation; NADPH oxidase; oxidative phosphorylation; protein kinase C

Document Type: Research article

DOI: http://dx.doi.org/10.1385/CBB:43:2:289

Affiliations: 1: Department of Biochemistry and Molecular Biology, Medical Sciences Program, Indiana University, 47405, Bloomington, IN, 2: Department of Biochemistry and Molecular Biology, Medical Sciences Program, Indiana University, 47405, Bloomington, IN, Email: daleked@indiana.edu

Publication date: 2005-06-01