Editorials |
From the Departments of Internal Medicine and Pharmacology, Cardiovascular Center, University of Iowa Carver College of Medicine, Iowa City.
Correspondence to Frank M. Faraci, PhD, Department of Internal Medicine, E315-GH, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242-1081. E-mail frank-faraci@uiowa.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Cells within the vessel wall have the capacity to produce a variety of reactive oxygen species (ROS: superoxide anion, hydrogen peroxide [H2O2], hydroxyl radical, etc).13 In diverse experimental models and in patients with disease, levels of ROS in blood vessels increase and contribute to vascular pathophysiology.13 Although not widely appreciated initially, it has become increasing apparent that relatively low concentrations of ROS can function as signaling molecules,47 and thus may be involved with normal regulation of vascular structure and function.
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Superoxide can be produced by multiple enzymatic and non-enzymatic sources and is the precursor for many ROS including the highly reactive hydroxyl radical (Figure). In addition to the rate of production, steady state levels of ROS are also determined by the activity of an array of antioxidant enzymes including superoxide dismutases (SOD) which convert superoxide to H2O2 (Figure).8,9 H2O2 levels are regulated by catalase and a group of glutathione peroxidases which metabolize H2O2 to water (Figure).710
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Arterioscler Thromb Vasc Biol 2006 26: 2035-2042.
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