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Review Oxidative Stress and Cell Dysfunction in Diabetes: Role of ROS Produced by Mitochondria and NAD(P)H Oxidase.
Sang Soo Kim, Seok Man Son
Diabetes & Metabolism Journal 2008;32(5):389-398
DOI: https://doi.org/10.4093/kdj.2008.32.5.389
Published online: October 1, 2008
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1Department of Internal Medicine, Pusan National University School of Medicine, Korea.
2Diabetes Center, Pusan National University Yangsan Hospital. Korea.

Oxidative stress has been considered to be a major contributor to the pathogenesis of the diabetic macrovascular and microvascular complications. In the absence of an appropriate antioxidant defense mechanism, increased oxidative stress leads to the activation of stress-sensitive intracellular signaling pathways and the formation of gene products that cause damage and contribute to the late complications ofdiabetes. The source of reactive oxygen species (ROS) in the pancreatic beta cells and insulin sensitive cells has postulated to be the mitochondrial electron transport chain. NAD(P)H oxidase-dependent ROS production is also important as the source both in pancreatic beta cells and other cells. NAD(P)H oxidase mediated ROS can alter parameters of signal transduction, insulin secretion, insulin action, cell proliferation and cell death. Additionally, oxidative stress as the pathogenic mechanism linking insulin resistance with dysfunction of both pancreatic beta cells and endothelial cells, eventually leads to diabetes and its complications. Further investigation of the mechanisms and its therapeutic interventions based on focusing NAD(P)H oxidase associated ROS production in the islet cells and other islet cells are needed

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    Oxidative Stress and Cell Dysfunction in Diabetes: Role of ROS Produced by Mitochondria and NAD(P)H Oxidase.
    Korean Diabetes J. 2008;32(5):389-398.   Published online October 1, 2008
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Kim SS, Son SM. Oxidative Stress and Cell Dysfunction in Diabetes: Role of ROS Produced by Mitochondria and NAD(P)H Oxidase.. Diabetes Metab J. 2008;32(5):389-398.
DOI: https://doi.org/10.4093/kdj.2008.32.5.389.

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