Oxidative stress as a mediator of cardiovascular disease

被引:291
作者
Elahi, Maqsood M. [2 ]
Kong, Yu Xiang [3 ]
Matata, Bashir M. [1 ]
机构
[1] Liverpool Heart & Chest Hosp NHS Trust, Liverpool, Merseyside, England
[2] BUPA Hosp, Wessex Cardiothorac Ctr, Southampton, Hants, England
[3] St Vincents Hosp, Dept Cardiothorac Surg, Melbourne, Vic, Australia
基金
日本学术振兴会;
关键词
molecular mediators; redox; NO synthase; the cyclooxygenases; NAD(P)H oxidase isoforms; NF-KAPPA-B; NITRIC-OXIDE SYNTHASE; SMOOTH-MUSCLE-CELLS; LOW-DENSITY-LIPOPROTEIN; MONOCYTE CHEMOATTRACTANT PROTEIN-1; POSTOPERATIVE ATRIAL-FIBRILLATION; OXYGEN SPECIES PRODUCTION; CORONARY-ARTERY-DISEASE; HUMAN ENDOTHELIAL-CELLS; TOLL-LIKE RECEPTOR-4;
D O I
10.4161/oxim.2.5.9441
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
During physiological processes molecules undergo chemical changes involving reducing and oxidizing reactions. A molecule with an unpaired electron can combine with a molecule capable of donating an electron. The donation of an electron is termed as oxidation whereas the gaining of an electron is called reduction. Reduction and oxidation can render the reduced molecule unstable and make it free to react with other molecules to cause damage to cellular and sub-cellular components such as membranes, proteins and DNA. In this paper, we have discussed the formation of reactive oxidant species originating from a variety of sources such as nitric oxide (NO) synthase (NOS), xanthine oxidases (XO), the cyclooxygenases, nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase isoforms and metal-catalyzed reactions. In addition, we present a treatise on the physiological defences such as specialized enzymes and antioxidants that maintain reduction-oxidation (redox) balance.-We have also given an account of how enzymes and antioxidants can be exhausted by the excessive production of reactive oxidant species (ROS) resulting in oxidative stress/nitrosative stress, a process that is an important mediator of cell damage. Important aspects of redox imbalance that triggers the activity of a number of signaling pathways including transcription factors activity, a process that is ubiquitous in cardiovascular disease related to ischemia/reperfusion injury have also been presented.
引用
收藏
页码:259 / 269
页数:11
相关论文
共 150 条
[91]   Heat shock and the activation of AP-1 and inhibition of NF-κB DNA-binding activity:: possible role of intracellular redox status [J].
Mattson, D ;
Bradbury, CM ;
Bisht, KS ;
Curry, HA ;
Spitz, DR ;
Gius, D .
INTERNATIONAL JOURNAL OF HYPERTHERMIA, 2004, 20 (02) :224-233
[92]   Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox [J].
Maytin, M ;
Siwik, DA ;
Ito, M ;
Xiao, L ;
Sawyer, DB ;
Liao, R ;
Colucci, WS .
CIRCULATION, 2004, 109 (09) :1168-1171
[93]   Nitric oxide in the human respiratory cycle [J].
McMahon, TJ ;
Moon, RE ;
Luschinger, BP ;
Carraway, MS ;
Stone, AE ;
Stolp, BW ;
Gow, AJ ;
Pawloski, JR ;
Watke, P ;
Singel, DJ ;
Piantadosi, CA ;
Stamler, JS .
NATURE MEDICINE, 2002, 8 (07) :711-717
[94]  
Meier B, 1996, ADV EXP MED BIOL, V387, P113
[95]   Nuclear factor κB:: a potential therapeutic target in atherosclerosis and thrombosis [J].
Monaco, C ;
Paleolog, E .
CARDIOVASCULAR RESEARCH, 2004, 61 (04) :671-682
[96]   Interaction of genetic deficiency of endothelial nitric oxide, gender, and pregnancy in vascular response to injury in mice [J].
Moroi, M ;
Zhang, L ;
Yasuda, T ;
Virmani, R ;
Gold, HK ;
Fishman, MC ;
Huang, PL .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (06) :1225-1232
[97]   Complex III releases superoxide to both sides of the inner mitochondrial membrane [J].
Muller, FL ;
Liu, YH ;
Van Remmen, H .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (47) :49064-49073
[98]   Oxidative stress markers are associated with persistent atrial fibrillation [J].
Neuman, Robert B. ;
Bloom, Heather L. ;
Shukrullah, Irfan ;
Darrow, Lyndsey A. ;
Kleinbaum, David ;
Jones, Dean P. ;
Dudley, Samuel C., Jr. .
CLINICAL CHEMISTRY, 2007, 53 (09) :1652-1657
[99]   Calorie restriction promotes mitochondrial biogenesis by inducing the expression of eNOS [J].
Nisoli, E ;
Tonello, C ;
Cardile, A ;
Cozzi, V ;
Bracale, R ;
Tedesco, L ;
Falcone, S ;
Valerio, A ;
Cantoni, O ;
Clementi, E ;
Moncada, S ;
Carruba, MO .
SCIENCE, 2005, 310 (5746) :314-317
[100]   Post-operative atrial fibrillation and oxidative stress - A novel causal mechanism or another biochemical epiphenomenon? [J].
Oral, Hakan .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2008, 51 (01) :75-76