Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction

Diabetes/Metabolism Research and Reviews - Tập 22 Số 3 - Trang 198-203 - 2006
Ludovica Piconi1, Lisa Quagliaro1, Roberta Assaloni2, Roberto Da Ros2, Amabile Maier2, Gianni Zuodar2, Antonio Ceriello2
1Morpurgo-Hofman Research Laboratory on Aging, Udine, Italy
2Department of Pathology and Medicine, Experimental and Clinical, University of Udine, Chair of Internal Medicine, Udine, Italy

Tóm tắt

AbstractBackgroundIt has been previously shown that hyperglycemia enhances free radical production, inducing oxidative damage, which in its turn activates the death pathways implicated in cell apoptosis and necrosis. But the possible involvement of this pathway in the hyperglycemia‐induced apoptosis of endothelial cells has not yet been reported.MethodsTo verify a possible connection between mitochondrial ROS production and apoptosis induced by both stable and oscillating high glucose, SOD, MnTBAP and TTFA was added to HUVEC cell culture medium. We measured nitrotyrosine and 8OHdG as oxidative stress parameters and Bcl‐2 expression and Caspase‐3 expression and activity as apoptosis indicators.ResultsOur results show that hyperglycemia, both stable or oscillating, increases oxidative stress and endothelial cell apoptosis through ROS overproduction at the mitochondrial transport chain level.ConclusionThe prevention of mitochondrial oxidative damage seems to be a future important therapeutic strategy in diabetes. Copyright © 2006 John Wiley & Sons, Ltd.

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Diabetes/Metabolism Research and Reviews

Tập 22 Số 3

198-203

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