title: NADH/NADPH oxidase p22 phox C242T polymorphism and lipid peroxidation in coronary artery disease.
abstract: The nicotinamide adenine dinucleotide (NADH)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system is a major source of superoxide anion (.O2-) production in the human vasculature and may therefore influence lipid peroxidation and severity of atherosclerosis. This study aimed to investigate a hypothetical influence of the p22 phox C242T polymorphism on the generation of malondialdehyde (MDA), extent and clinical onset of coronary artery disease (CAD) in patients. We studied 108 male Caucasians with angiographically documented CAD and 45 controls free of vascular disease under 60 years of age. p22 phox C242T genotypes and MDA levels were determined. Additional information was obtained from each subject on classic risk factors and clinical events of CAD. Genotype distribution in CAD-patients and controls was thymine-thymine (TT): 13.8% (13.3%), cytosine-thymine (CT): 46.3% (53.3%) and cytosine-cytosine (CC): 39.8% (33.3%), respectively. No significant influence was seen of the p22 phox C242T polymorphism on corresponding mean MDA levels in both groups. Furthermore, age at onset of first time angina pectoris (AP) and myocardial infarction (MCI) was not significantly different between genotype groups. It is concluded that the C242T polymorphism of the p22 phox gene is not associated with lipid peroxidation as measured by MDA, and is not a genetic risk marker for CAD Caucasians.
authors.affiliation: Department of Surgery, Division of Cardiac Surgery, Atherosclerosis Research Group, Karl-Franzens University School of Medicine, Graz, Austria.
authors.forename: O
authors.initials: O
authors.lastname: Stanger
authors.forename: W
authors.initials: W
authors.lastname: Renner
authors.forename: G
authors.initials: G
authors.lastname: Khoschsorur
authors.forename: B
authors.initials: B
authors.lastname: Rigler
authors.forename: T C
authors.initials: TC
authors.lastname: Wascher
mesh_terms: D000328:Adult; D017668:Age of Onset; D000787:Angina Pectoris / Q000503:physiopathology; D000792:Angiography; D003324:Coronary Artery Disease / Q000235:genetics* / Q000473:pathology*; D005838:Genotype; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D026901:Membrane Transport Proteins; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology; D009243:NAD / Q000235:genetics / Q000378:metabolism; D009247:NADH, NADPH Oxidoreductases / Q000235:genetics* / Q000378:metabolism; D009252:NADPH Dehydrogenase / Q000235:genetics*; D019255:NADPH Oxidases / Q000235:genetics* / Q000378:metabolism; D010750:Phosphoproteins / Q000235:genetics*; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D012307:Risk Factors
chemical_list: D026901:Membrane Transport Proteins; D010750:Phosphoproteins; D009243:NAD; D008315:Malondialdehyde; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases; C086986:CYBA protein, human; D009252:NADPH Dehydrogenase