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- December 1, 2008 |
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"Nox, Nox, Knocking: The Emerging Roles of NADPH Oxidases in Vascular Physiology & Disease"Dr. Grant Drummond (biography)
English - 2006-09-16 - 48 minutes
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Summary :
"Despite the bad press about reactive oxygen species, they are not always that bad," says Dr. Drummond. "In fact they are critical for cell signaling processes." What happens when oxygen free radicals/reactive oxygen species are overproduced, and what are the potential implications for lowering oxidative stress in the vasculature?
All of the known cardiovascular risk factors are associated with increased production of reactive oxygen species in the vascular wall, and in vitro studies show that addition of reactive oxygen species to isolated blood vessels and cultured vascular cells can mimic many of the cellular and biochemical processes that occur in the onset of vascular disease. Are reactive oxygen species then the molecular link between cardiovascular risk factors and cardiovascular disease? In the past few years there has been an interest in antioxidant therapy, however large clinical trials on the effects of antioxidants such as vitamin E on cardiovascular outcomes show disappointing results. Dr. Drummond explains why antioxidant therapy may not be a good way to remove reactive oxygen species in blood vessels.
A number of enzymes could potentially be sources of reactive oxygen species in the blood vessel wall, however the NADPH oxidase family of enzymes is one whose function appears to be to produce superoxide anions or the "parent" species of the reactive oxygen species family. Vascular cells express at least 3 isoforms of NADPH oxidase, having different Nox catalytic subunits: Nox1, Nox2 and Nox4 (1,2). In the context of vascular disease there appears to be an upregulation of the Nox1 and Nox2-dependent isoforms of NADPH oxidase (3). Dr. Drummond further talks about the "kindling bonfire" hypothesis of vascular free radical production and how it may provide a framework for lowering oxidative stress in blood vessels through a systematic therapeutic approach.
Copyright © 2006 E-MedHosting.com Inc.
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- What are reactive oxygen species?
- Effects of overproduction of reactive oxygen species in disease states
- Clinical trials with antioxidants
- NADPH oxidase isoforms and superoxide production
- Proposed mechanisms of vascular free radical production
Bibliographic references :
1. Young-Ah Suh, Rebecca S. Arnold, Bernard Lassegue, Jing Shi, Xiangxi Xu, Dan Sorescu, Andrew B. Chung, Kathy K. Griendling and J. David LambethCell transformation by the superoxide-generating oxidase Mox1 Nature 1999;401:79.
2. Bernard Lassčgue, Dan Sorescu, Katalin Szöcs, QiQin Yin, Marjorie Akers, Yong Zhang, Sharon L. Grant, J. David Lambeth, Kathy K. Griendling Novel gp91phox Homologues in Vascular Smooth Muscle Cells: nox1 Mediates Angiotensin II–Induced Superoxide Formation and Redox-Sensitive Signaling Pathways Circulation Research. 2001;88:888.
3. Cornelius F.H. Mueller; Karine Laude; J. Scott McNally; David G. Harrison Redox Mechanisms in Blood Vessels Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:274.
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