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Extracellular SOD Inactivation in High-Volume Hypertension Role of Hydrogen Peroxide

Extracellular SOD Inactivation in High-Volume Hypertension Role of Hydrogen Peroxide Editorial Extracellular SOD Inactivation in High-Volume Hypertension Role of Hydrogen Peroxide Tohru Fukai / / xcessive reactive oxygen species (ROS), especially blood pressure in ecSOD mice and ecSOD mice is not superoxide anion (O ), contribute to the pathogene- significantly different, but is decreased by an administration Esis of many cardiovascular diseases, including hyper- of recombinant ecSOD. This result suggests that low renin tension. The major antioxidant defense system against O is and high volume hypertension model is dependent on insuf- superoxide dismutases (SODs). In mammals, 3 isoforms of ficient amount or lack of ecSOD. Furthermore, the authors superoxide dismutase exist: the cytoplasmic CuZnSOD demonstrated that ecSOD protein level is markedly elevated (SOD1), the mitochondrial MnSOD (SOD2), and the extra- with a slight increase in ecSOD activity in the 1K1C model, cellular Cu/ZnSOD (SOD3, ecSOD). The ecSOD is the major suggesting that a large amount of ecSOD protein induced by SOD in the vascular extracellular space, and synthesized by 1K1C is inactive. To test the hypothesis that ecSOD has vascular smooth muscle cells and fibroblasts. It is secreted peroxidase activity, Jung et al examined the effects of and anchored to the extracellular matrix and endothelial cell polyethylene glycol (PEG)-catalase http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

Extracellular SOD Inactivation in High-Volume Hypertension Role of Hydrogen Peroxide

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References (22)

ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/01.ATV.0000258920.36436.8e
pmid
17301320
Publisher site
See Article on Publisher Site

Abstract

Editorial Extracellular SOD Inactivation in High-Volume Hypertension Role of Hydrogen Peroxide Tohru Fukai / / xcessive reactive oxygen species (ROS), especially blood pressure in ecSOD mice and ecSOD mice is not superoxide anion (O ), contribute to the pathogene- significantly different, but is decreased by an administration Esis of many cardiovascular diseases, including hyper- of recombinant ecSOD. This result suggests that low renin tension. The major antioxidant defense system against O is and high volume hypertension model is dependent on insuf- superoxide dismutases (SODs). In mammals, 3 isoforms of ficient amount or lack of ecSOD. Furthermore, the authors superoxide dismutase exist: the cytoplasmic CuZnSOD demonstrated that ecSOD protein level is markedly elevated (SOD1), the mitochondrial MnSOD (SOD2), and the extra- with a slight increase in ecSOD activity in the 1K1C model, cellular Cu/ZnSOD (SOD3, ecSOD). The ecSOD is the major suggesting that a large amount of ecSOD protein induced by SOD in the vascular extracellular space, and synthesized by 1K1C is inactive. To test the hypothesis that ecSOD has vascular smooth muscle cells and fibroblasts. It is secreted peroxidase activity, Jung et al examined the effects of and anchored to the extracellular matrix and endothelial cell polyethylene glycol (PEG)-catalase

Journal

Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health

Published: Mar 1, 2007

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