Genetic determinants of vascular oxidant stress and endothelial dysfunction.

Abstract

Reactive oxygen species are products of cellular metabolism and function as normal signaling molecules in the vasculature. Overproduction of reactive oxygen species that outstrips antioxidant defenses generates oxidant stress that can lead to nitric oxide depletion and endothelial cell injury, and contributes to the pathophysiology of cardiovascular disease and myocardial dysfunction. Antioxidant enzymes that are important in limiting vascular oxidant stress include superoxide dismutases, catalase, glutathione peroxidases, and glucose-6-phosphate dehydrogenase. The relevance of deficiencies in glutathione peroxidase and glucose-6-phosphate dehydrogenase on endothelial and myocardial dysfunction will be reviewed.

• Authors: Joseph Loscalzo, Barbara Voetsch, Ronglih Liao, Jane Leopold
• Journal: Congestive heart failure (Greenwich, Conn.) (Congest Heart Fail) 2005 Mar-Apr Vol. 11 Issue 2 Pg. 73-9 ISSN: 1527-5299 [Print] United States
• PMID: 15860972 (Publication Type: Journal Article, Review)

Chemical References

• Antioxidants
• Reactive Oxygen Species
• Glucosephosphate Dehydrogenase
• Catalase
• Glutathione Peroxidase
• Superoxide Dismutase

Topics

• Antioxidants (metabolism)
• Cardiovascular Diseases (physiopathology)
• Catalase (genetics)
• Endothelium, Vascular (physiology)
• Glucosephosphate Dehydrogenase (genetics)
• Glucosephosphate Dehydrogenase Deficiency (genetics)
• Glutathione Peroxidase (genetics)
• Humans
• Oxidative Stress (genetics)
• Reactive Oxygen Species (metabolism)
• Superoxide Dismutase (genetics)