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Hypertension. 2007;49:717-727
Published online before print February 12, 2007, doi: 10.1161/01.HYP.0000258594.87211.6b
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(Hypertension. 2007;49:717.)
© 2007 American Heart Association, Inc.


Brief Reviews

Measurement of Reactive Oxygen Species in Cardiovascular Studies

Sergey Dikalov; Kathy K. Griendling; David G. Harrison

From the Division of Cardiology (S.D., K.K.G., D.G.H.), Department of Medicine, Emory University, Atlanta, Ga; and Atlanta Veterans Administration Hospital (D.G.H.), Ga.

Correspondence to David G. Harrison, Emory University, Division of Cardiology, 319 WMB, 1639 Pierce Dr, Atlanta, GA 30322. E-mail dharr02@emory.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Several mammalian enzymes are capable of transferring electrons to molecular oxygen, sequentially forming the 1 electron-reduction product superoxide (O2·–) and the 2 electron-reduction product hydrogen peroxide (H2O2). These serve as progenitors for other reactive oxygen species (ROS), including peroxynitrite (ONOO), hypochlorous acid, the hydroxyl radical, lipid peroxides, lipid peroxy- radicals, and lipid alkoxyl radicals. Another relevant group of molecules is the reactive nitrogen species, including NO, the nitrogen dioxide radical, and the nitrosonium cation. In the cardiovascular system, the most important enzymes that produce ROS are the Nox-based reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidases, xanthine oxidase, the mitochondrial electron transport system and, under certain circumstances, NO synthase. Conditions such as hypertension, atherosclerosis, hypercholesterolemia, diabetes, and insulin resistance increase either the activity or the expression of these enzymes, leading to elevated ROS production. ROS, in turn, contribute to these disorders. As examples, virtually every aspect of atherosclerotic lesion formation is augmented by oxidative events. Via several mechanisms involving vessels, the kidney, and the central nervous system, ROS augment hypertension. ROS have been implicated in causing insulin resistance and pancreatic damage leading to diabetes. Moreover, ROS, when produced in specific subcellular compartments in controlled amounts, can act as signaling molecules to regulate normal cellular functions. These reactions have been reviewed in depth elsewhere recently.1

Given the importance of ROS and reactive nitrogen species in physiology and pathophysiology, it has become essential that methods be adapted and standardized to quantify the levels of these molecules in cells and tissues. . . . [Full Text of this Article]




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