Oxidative Stress and Antioxidant Defense

被引:3706
作者
Birben, Esra [1 ]
Sahiner, Umit Murat [1 ]
Sackesen, Cansin [1 ]
Erzurum, Serpil [2 ,3 ]
Kalayci, Omer [1 ]
机构
[1] Hacettepe Univ, Sch Med, Pediat Allergy & Asthma Unit, TR-06600 Ankara, Turkey
[2] Cleveland Clin, Lerner Res Inst, Dept Pathobiol, Cleveland, OH 44106 USA
[3] Cleveland Clin, Resp Inst, Cleveland, OH 44106 USA
关键词
antioxidant; oxidant; oxidative stress; reactive oxygen species; redox;
D O I
10.1097/WOX.0b013e3182439613
中图分类号
R392 [医学免疫学];
学科分类号
100102 [免疫学];
摘要
Reactive oxygen species (ROS) are produced by living organisms as a result of normal cellular metabolism and environmental factors, such as air pollutants or cigarette smoke. ROS are highly reactive molecules and can damage cell structures such as carbohydrates, nucleic acids, lipids, and proteins and alter their functions. The shift in the balance between oxidants and antioxidants in favor of oxidants is termed "oxidative stress." Regulation of reducing and oxidizing (redox) state is critical for cell viability, activation, proliferation, and organ function. Aerobic organisms have integrated antioxidant systems, which include enzymatic and nonenzymatic antioxidants that are usually effective in blocking harmful effects of ROS. However, in pathological conditions, the antioxidant systems can be overwhelmed. Oxidative stress contributes to many pathological conditions and diseases, including cancer, neurological disorders, atherosclerosis, hypertension, ischemia/perfusion, diabetes, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma. In this review, we summarize the cellular oxidant and antioxidant systems and discuss the cellular effects and mechanisms of the oxidative stress.
引用
收藏
页码:9 / 19
页数:11
相关论文
共 147 条
[71]
Superoxide anion production is increased in a model of genetic hypertension - Role of the endothelium [J].
Kerr, S ;
Brosnan, MJ ;
McIntyre, M ;
Reid, JL ;
Dominiczak, AF ;
Hamilton, CA .
HYPERTENSION, 1999, 33 (06) :1353-1358
[72]
Superoxide dismutases in the lung and human lung diseases [J].
Kinnula, VL ;
Crapo, JD .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 167 (12) :1600-1619
[73]
Cell specific expression of peroxiredoxins in human lung and pulmonary sarcoidosis [J].
Kinnula, VL ;
Lehtonen, S ;
Kaarteenaho-Wiik, R ;
Lakari, E ;
Pääkkö, P ;
Kang, SW ;
Rhee, SG ;
Soini, Y .
THORAX, 2002, 57 (02) :157-164
[74]
Kinnula Vuokko L., 2005, Current Drug Targets - Inflammation and Allergy, V4, P465, DOI 10.2174/1568010054526368
[75]
Mechanisms of protection of catalase by NADPH - Kinetics and stoichiometry [J].
Kirkman, HN ;
Rolfo, M ;
Ferraris, AM ;
Gaetani, GF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (20) :13908-13914
[76]
Redox regulation of c-Jun DNA binding by reversible S-glutathiolation [J].
Klatt, P ;
Molina, EP ;
De Lacoba, MG ;
Padilla, CA ;
Martínez-Galisteo, E ;
Bárcena, JA ;
Lamas, S .
FASEB JOURNAL, 1999, 13 (12) :1481-1490
[77]
Myeloperoxidase: friend and foe [J].
Klebanoff, SJ .
JOURNAL OF LEUKOCYTE BIOLOGY, 2005, 77 (05) :598-625
[78]
THE OXYGEN FREE-RADICAL SYSTEM - FROM EQUATIONS THROUGH MEMBRANE-PROTEIN INTERACTIONS TO CARDIOVASCULAR INJURY AND PROTECTION [J].
KUKREJA, RC ;
HESS, ML .
CARDIOVASCULAR RESEARCH, 1992, 26 (07) :641-655
[79]
Hypochlorous acid produced by the myeloperoxidase system of human phagocytes induces covalent cross-links between DNA and protein [J].
Kulcharyk, PA ;
Heinecke, JW .
BIOCHEMISTRY, 2001, 40 (12) :3648-3656
[80]
Parallel evolutionary pathways for glutathione transferases: Structure and mechanism of the mitochondrial class kappa enzyme rGSTK1-1 [J].
Ladner, JE ;
Parsons, JF ;
Rife, CL ;
Gilliland, GL ;
Armstrong, RN .
BIOCHEMISTRY, 2004, 43 (02) :352-361