Editorials |
From the Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine (W.F.G.), Medical University Graz, Austria; and the Institute of Physiology and Pathophysiology, Division of Cardiovascular Physiology (M.H.), University of Heidelberg, Germany.
Correspondence to Wolfgang F. Graier, PhD, Molecular and Cellular Physiology Research Unit, Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Medical University Graz, Harrachgasse 21/III, A-8010 Graz, Austria. E-mail wolfgang.graier@meduni-graz.at
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
About a decade ago everyone who read, at least occasionally, the science part of the local newspapers or followed popular science broadcasts "knew" that reactive oxygen species (ROS) are dangerous. They were thought to be bad, really bad, and many looking for a healthier lifestyle took action against these nasty small molecules accused of harming lipids and proteins by taking antioxidants like vitamin E. Food industry teamed up with pharmaceutical companies and brought up functional food enriched or supplemented with trustful antioxidants in the fight against ROS, which seemed to be produced under pathological conditions with just one mission: to damage the body. Things have changed during recent years, and there is emerging evidence that ROS are not only continuously produced even in healthy individuals but also exert important physiological functions. While we are still in-between a period that provides exciting new findings on the physiology of ROS, one can already summarize our present knowledge rather accurately by citing Paracelsus adage of "Dosis (sola) facit venenum" (tertio defensio, 1538).
See accompanying article on page 1774
The present work of Edwards et al1 is one of these exciting new reports that open our eyes to recognize the good side of the previously dammed ROS. This article deals with the effect of hydrogen peroxide (H2O2) on endothelium-derived hyperpolarization and is quite remarkable in several ways:
First, the article is focused on EDHF (formerly termed endothelium-derived hyperpolarizing factor), a nitric oxide (NO) and prostacyclin-independent phenomenon of endothelium-dependent
Related Article:
Arterioscler Thromb Vasc Biol 2008 28: 1774-1781.
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2008 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |