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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Editorial Board Member: Gillery, Philippe / Kazmierczak, Steven / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Whitfield, John B.

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Oxidative stress and diabetes mellitus

Hui Yang1 / Xun Jin1 / Christopher Wai Kei Lam2 / Sheng-Kai Yan1, 3

1Department of Laboratory Medicine, China-Japan Friendship Hospital, Ministry of Health, Beijing, P.R. China

2Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau, P.R. China

3Guang Zhou Improve Medical Instruments Co., Ltd, Guangzhou, P.R. China

Corresponding author: Dr. Sheng-Kai Yan, Department of Laboratory Medicine, China-Japan Friendship Hospital, Ministry of Health, No. 2 East Yinghua Road, Chaoyang District, Beijing 100029, P.R. China Phone: +86-10-84205213, Fax: +86-10-64288578,

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 49, Issue 11, Pages 1773–1782, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: 10.1515/cclm.2011.250, August 2011

Publication History

Received:
2010-09-02
Accepted:
2011-06-01
Published Online:
2011-08-03

Abstract

Increasing evidences have suggested that oxidative stress plays a major role in the pathogenesis of diabetes mellitus (DM). Oxidative stress also appears to be the pathogenic factor in underlying diabetic complications. Reactive oxygen species (ROS) are generated by environmental factors, such as ionizing radiation and chemical carcinogens, and also by endogenous processes, including energy metabolism in mitochondria. ROS produced either endogenously or exogenously can attack lipids, proteins and nucleic acids simultaneously in living cells. There are many potential mechanisms whereby excess glucose metabolites traveling along these pathways might promote the development of DM complication and cause pancreatic β cell damage. However, all these pathways have in common the formation of ROS, that, in excess and over time, causes chronic oxidative stress, which in turn causes defective insulin gene expression and insulin secretion as well as increased apoptosis. Various methods for determining biomarkers of cellular oxidative stress have been developed, and some have been proposed for sensitive assessment of antioxidant defense and oxidative damage in diabetes and its complications. However, their clinical utility is limited by less than optimal standardization techniques and the lack of sufficient large-sized, multi-marker prospective trials.

Keywords: advanced glycation endproducts; diabetes mellitus; oxidative stress; reactive nitrogen species; reactive oxygen species

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