© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Effects of vitamin E on the endothelium: equivocal? 
-tocopherol and endothelial dysfunction
Department of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 2013 Milan, Italy
* Tel.: +39-02-5835-8280; fax: +39-02-7004-26106 francesco.visioli@unimi.it
Received 22 May 2001; accepted 29 May 2001
| The first 150 words of the full text of this article appear below. |
See article by Bauersachs et al. [5] (pages 344–350) in this issue.
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1. Introduction |
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‘Endothelial dysfunction’ refers to a common complication of atherosclerosis, when impaired vasorelaxation due to reduced endothelial-derived nitric oxide (EDNO) bioactivity results in altered endothelial function [1,2]. In addition to atherosclerosis, evidence is accumulating of a dysfunctional endothelium and defective vasomotion in congestive heart failure patients [3–5].
Oxidative stress — the excessive production of reactive oxygen species (ROS) that overcomes antioxidant defense mechanisms in cells — plays an important role in endothelial dysfunction. Our current knowledge suggests that endothelial dysfunction is due to either (or both) a reduced production of EDNO or to its accelerated reaction with other species, notably ROS, of which the superoxide anion is the most widely studied [6]. Thus far, the three most widely studied sources of vascular ROS are reactions catalyzed by xantine oxidoreductase, NADH/NADPH oxidase, and NO synthase (NOS) [7,8]
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2. Do we need more NO? No! |
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3. Which strategy should we choose? |
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4. Are we carrying out biologically relevant experiments? |
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5. Conclusion |
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