title: Oxidative stress and endothelial function: therapeutic interventions.
abstract: Cardiovascular risk factors, such as hypertension, hypercholesterolemia, diabetes mellitus, or chronic smoking, stimulate the production of reactive oxygen species (ROS) in the vascular wall. Oxidative stress and endothelial dysfunction in the coronary and peripheral circulation have important prognostic implications for subsequent cardiovascular events. The pathophysiologic causes of oxidative stress are likely to involve changes in a number of different enzyme systems. Reactive oxygen species (ROS) are produced by various oxidase enzymes, including nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, xanthine oxidase, uncoupled endothelial NO synthase (eNOS), cyclooxygenase, glucose oxidase, and lipooxygenase, and mitochondrial electron transport. Decreased NO production due to changes in the expression and activity of eNOS and increased degradation of NO, by reaction with superoxide account for the reduction in endothelium-dependent vascular relaxation. Recently, a variety of antioxidants have been extensively studied in clinical trials for the prevention and treatment of atherosclerosis. In small clinical studies both vitamins C and E may improve endothelial function in high-risk patients. However, larger interventional trials have been controversial, suggesting potential harm in certain high-risk populations. Antihypertensive and hypolipidemic medications exhibit well-documented antioxidant effects and improve endothelial function. However, the discussion of recent patents with the novel antioxidant strategies are required to clarify the role of antioxidant intervention in vascular diseases.
authors.affiliation: 1st Cardiology Department, Athens University Medical School, Hippokration Hospital, Vasilissis Sofias, Greece. drtousoulis@hotmail.com
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Alexandros
authors.initials: A
authors.lastname: Briasoulis
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Papageorgiou
authors.forename: Costas
authors.initials: C
authors.lastname: Tsioufis
authors.forename: Eleftherios
authors.initials: E
authors.lastname: Tsiamis
authors.forename: Kostas
authors.initials: K
authors.lastname: Toutouzas
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D009569:Nitric Oxide / Q000096:biosynthesis / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010330:Patents as Topic; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D009569:Nitric Oxide