Oxidative stress, antioxidants, and endothelial function.
Endothelial dysfunction, characterized by a loss in nitric oxide bioactivity, is an early event in the development of atherosclerosis and determines future vascular complications. Emerging evidence suggests a causal role for oxidative stress in this process. Reactive oxygen species can directly inactivate nitric oxide, modulate protein function and act as cellular signaling molecules. These events contribute to the initiation and progression of endothelial dysfunction. Considerable data also indicates that antioxidant compounds limit oxidative damage and restore endothelial function. The purpose of this review is to discuss these data and suggest novel approaches for lowering the oxidative stress in the vasculature.
Schulz
Eberhard
E
Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118, USA.
Anter
Elad
E
Keaney
John F
JF
D000818:Animals; D000975:Antioxidants / Q000378:metabolism* / Q000627:therapeutic use; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000201:enzymology / Q000503:physiopathology*; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000201:enzymology; D019255:NADPH Oxidases / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism*; D014969:Xanthine Oxidase / Q000378:metabolism
D000975:Antioxidants; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D014969:Xanthine Oxidase; D019255:NADPH Oxidases