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

  1. Ludovica Piconi1,
  2. Lisa Quagliaro1,
  3. Roberta Assaloni2,
  4. Roberto Da Ros2,
  5. Amabile Maier2,
  6. Gianni Zuodar2,
  7. Antonio Ceriello2,*

Article first published online: 2 FEB 2006

DOI: 10.1002/dmrr.613

Issue

Diabetes/Metabolism Research and Reviews

Diabetes/Metabolism Research and Reviews

Volume 22, Issue 3, pages 198–203, May/June 2006

Additional Information

How to Cite

Piconi, L., Quagliaro, L., Assaloni, R., Da Ros, R., Maier, A., Zuodar, G. and Ceriello, A. (2006), Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction. Diabetes/Metabolism Research and Reviews, 22: 198–203. doi: 10.1002/dmrr.613

Author Information

  1. 1

    Morpurgo-Hofman Research Laboratory on Aging, Udine, Italy

  2. 2

    Department of Pathology and Medicine, Experimental and Clinical, University of Udine, Chair of Internal Medicine, Udine, Italy

*Chair of Internal Medicine, University of Udine, P.le S. Maria della Misericordia, 33100 Udine, Italy.

Publication History

  1. Issue published online: 2 MAY 2006
  2. Article first published online: 2 FEB 2006
  3. Manuscript Accepted: 15 NOV 2005
  4. Manuscript Revised: 17 JUN 2005
  5. Manuscript Received: 1 DEC 2004

Funded by

  • Novartis Pharma, Basel, Switzerland

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Keywords:

  • intermittent glucose;
  • endothelium;
  • oxidative stress;
  • apoptosis;
  • mitochondria

Abstract

Background

It 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.

Methods

To 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.

Results

Our results show that hyperglycemia, both stable or oscillating, increases oxidative stress and endothelial cell apoptosis through ROS overproduction at the mitochondrial transport chain level.

Conclusion

The 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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