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(Hypertension. 2008;51:825.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

One Step Beyond

Glutathione Peroxidase and Endothelial Dysfunction

M. Julia Brosnan

From the Center for Metabolic Disease, Ordway Research Institute, Albany, NY.

Correspondence to M. Julia Brosnan, Center for Metabolic Disease, Ordway Research Institute, Center for Medical Science Building, 150 New Scotland Ave, Albany, NY 12208-3425. E-mail jbrosnan@ordwayresearch.org

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

Much evidence supports the role of increased levels of reactive oxygen species (ROS) in the pathogenesis of cardiovascular diseases, including hypertension. The increased activity and expression of the reduced nicotinamide-adenine dinucleotide phosphate oxidase observed in hypertensive populations have implicated the superoxide anion as one of the main species responsible. This view has been supported by studies demonstrating vascular-protective effects of the superoxide dismutase family, enzymes that remove superoxide anion thereby protecting the bioavailability of NO.¹ Despite this, it has proven particularly difficult to identify those genetic and environmental factors, relating to ROS metabolism, that contribute to the development of vascular dysfunction. The article by Chrissobolis et al² in this issue of Hypertension serves to remind us that we need to look one step beyond those mechanisms directly involving superoxide anion and superoxide dismutase. Indeed, hydrogen peroxide (H₂O₂), the end product of the superoxide dismutases, has been shown to have vascular reactive properties and can impair NO-mediated signaling in blood vessels by a variety of mechanisms. Looking beyond superoxide dismutase will undoubtedly help us to more comprehensively understand the roles of ROS in vascular function and disease.³ Perhaps this will assist in the identification of those elusive genes suspected, but so far undefined, in the pathogenesis of high blood pressure.

Chrissobolis et al² explored the effects of modulating the activity of glutathione peroxidase-1 (GPX1), an enzyme that catalyzes the conversion of H₂O₂ to water, on vascular function in mice. The authors demonstrated impaired endothelial function in carotid arteries . . . [Full Text of this Article]

Related Article:

Glutathione Peroxidase-1 Plays a Major Role in Protecting Against Angiotensin II–Induced Vascular Dysfunction

Sophocles Chrissobolis, Sean P. Didion, Dale A. Kinzenbaw, Laura I. Schrader, Sanjana Dayal, Steven R. Lentz, and Frank M. Faraci
Hypertension 2008 51: 872-877. [Abstract] [Full Text] [PDF]

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