NADH/NADPH oxidase p22 phox C242T polymorphism and lipid peroxidation in coronary artery disease

被引:27
作者
Stanger, O
Renner, W
Khoschsorur, G
Rigler, B
Wascher, TC
机构
[1] Karl Franzens Univ Graz, Sch Med, Dept Surg, Div Cardiac Surg,Atherosclerosis Res Grp, A-8036 Graz, Austria
[2] Karl Franzens Univ Graz, Sch Med, Dept Med, Div Angiol & Genet Res, A-8036 Graz, Austria
[3] Karl Franzens Univ Graz, Sch Med, Dept Med, Diabet Angiopathy Res Grp, A-8036 Graz, Austria
[4] Karl Franzens Univ Graz, Sch Med, Dept Lab Med, A-8036 Graz, Austria
来源
CLINICAL PHYSIOLOGY | 2001年 / 21卷 / 06期
关键词
atherosclerosis; coronary disease; free radicals; gene expression;
D O I
10.1046/j.1365-2281.2001.00381.x
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The nicotinamide adenine dinucleotide (NADH)/ nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system is a major source of superoxide anion (O-2(-)) 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.
引用
收藏
页码:718 / 722
页数:5
相关论文
共 16 条
[2]   SULFITE STIMULATES NADPH OXIDASE OF HUMAN NEUTROPHILS TO PRODUCE ACTIVE OXYGEN RADICALS VIA PROTEIN-KINASE-C AND CA2+/CALMODULIN PATHWAYS [J].
BECKSPEIER, I ;
LIESE, JG ;
BELOHRADSKY, BH ;
GODLESKI, JJ .
FREE RADICAL BIOLOGY AND MEDICINE, 1993, 14 (06) :661-668
[3]   RELATIONSHIP BETWEEN THE EXTENT OF CORONARY-ARTERY DISEASE AND INDICATORS OF FREE-RADICAL ACTIVITY [J].
BRIDGES, AB ;
SCOTT, NA ;
PRINGLE, TH ;
MCNEILL, GP ;
BELCH, JJF .
CLINICAL CARDIOLOGY, 1992, 15 (03) :169-174
[4]  
Cai H, 1999, EUR J CLIN INVEST, V29, P744
[5]   Cloning and sequencing of the bovine flavocytochrome b subunit proteins, gp91-phox and p22-phox:: comparison with other known flavocytochrome b sequences [J].
Davis, AR ;
Mascolo, PL ;
Bunger, PL ;
Sipes, KM ;
Quinn, MT .
JOURNAL OF LEUKOCYTE BIOLOGY, 1998, 64 (01) :114-123
[6]   HUMAN NEUTROPHIL CYTOCHROME-B LIGHT CHAIN (P22-PHOX) - GENE STRUCTURE, CHROMOSOMAL LOCATION, AND MUTATIONS IN CYTOCHROME-NEGATIVE AUTOSOMAL RECESSIVE CHRONIC GRANULOMATOUS-DISEASE [J].
DINAUER, MC ;
PIERCE, EA ;
BRUNS, GAP ;
CURNUTTE, JT ;
ORKIN, SH .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (05) :1729-1737
[7]   p22phox mRNA expression and NADPH oxidase activity are increased in aortas from hypertensive rats [J].
Fukui, T ;
Ishizaka, N ;
Rajagopalan, S ;
Lauren, JB ;
Capers, Q ;
Taylor, WR ;
Harrison, DG ;
deLeon, H ;
Wilcox, JN ;
Griendling, KK .
CIRCULATION RESEARCH, 1997, 80 (01) :45-51
[8]   The p22 phox A640G gene polymorphism but not the C242T gene variation is associated with coronary heart disease in younger individuals [J].
Gardemann, A ;
Mages, P ;
Katz, N ;
Tillmanns, H ;
Haberbosch, W .
ATHEROSCLEROSIS, 1999, 145 (02) :315-323
[9]  
HALLIWELL B, 1993, HAEMOSTASIS, V23, P118
[10]   Polymorphism of the NADH/NADPH oxidase p22 phox gene in patients with coronary artery disease [J].
Inoue, N ;
Kawashima, S ;
Kanazawa, K ;
Yamada, S ;
Akita, H ;
Yokoyama, M .
CIRCULATION, 1998, 97 (02) :135-137