Systems biology of antioxidants

被引:32
作者
Andriantsitohaina, Ramaroson [2 ]
Duluc, Lucie [2 ]
Garcia-Rodriguez, Julio C. [3 ]
Gil-Del Valle, Lizette [4 ]
Guevara-Garcia, Mariela [5 ]
Simard, Gilles [2 ]
Soleti, Raffaella [2 ]
Su, Ding-Feng [6 ]
Velasquez-Perez, Luis [7 ]
Wilson, John X. [8 ]
Laher, Ismail [1 ]
机构
[1] Univ British Columbia, Fac Med, Dept Pharmacol & Therapeut, Vancouver, BC V6T 1Z4, Canada
[2] INSERM, U1063, F-49100 Angers, France
[3] Natl Ctr Anim Breeding CENPALAB, Havana, Cuba
[4] Inst Pedro Kouri, Havana, Cuba
[5] Biopharmaceut Labs LABIOFAM, Dept Res & Dev, Havana, Cuba
[6] Second Mil Med Univ, Dept Pharmacol, Shanghai 200433, Peoples R China
[7] Univ Havana, Ctr Res & Rehabil Hereditary Ataxias Carlos J Fin, Holguin 80100, Cuba
[8] SUNY Buffalo, Dept Exercise & Nutr Sci, Buffalo, NY 14214 USA
基金
美国国家卫生研究院;
关键词
antioxidant; ataxia; diabetes; free radical; mitochondrion; sepsis; stroke; MITOCHONDRIAL SUPEROXIDE OVERPRODUCTION; OXYGEN SPECIES PRODUCTION; OXIDATIVE STRESS; NITRIC-OXIDE; COMPLEX-I; FREE-RADICALS; CARDIOVASCULAR-DISEASE; MOLECULAR-MECHANISMS; HIGH GLUCOSE; CELL-DEATH;
D O I
10.1042/CS20110643
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Understanding the role of oxidative injury will allow for therapy with agents that scavenge ROS (reactive oxygen species) and antioxidants in the management of several diseases related to free radical damage. The majority of free radicals are generated by mitochondria as a consequence of the mitochondrial cycle, whereas free radical accumulation is limited by the action of a variety of antioxidant processes that reside in every cell. In the present review, we provide an overview of the mitochondrial generation of ROS and discuss the role of ROS in the regulation of endothelial and adipocyte function. Moreover, we also discuss recent findings on the role of ROS in sepsis, cerebral ataxia and stroke. These results provide avenues for the therapeutic potential of antioxidants in a variety of diseases.
引用
收藏
页码:173 / 192
页数:20
相关论文
共 133 条
[31]   Intracellular signaling by reactive oxygen species during hypoxia in cardiomyocytes [J].
Duranteau, J ;
Chandel, NS ;
Kulisz, A ;
Shao, ZH ;
Schumacker, PT .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (19) :11619-11624
[32]   A signalling role for 4-hydroxy-2-nonenal in regulation of mitochondrial uncoupling [J].
Echtay, KS ;
Esteves, TC ;
Pakay, JL ;
Jekabsons, MB ;
Lambert, AJ ;
Portero-Otín, M ;
Pamplona, R ;
Vidal-Puig, AJ ;
Wang, S ;
Roebuck, SJ ;
Brand, MD .
EMBO JOURNAL, 2003, 22 (16) :4103-4110
[33]   Oxidative stress in the context of acute cerebrovascular stroke [J].
El Kossi, MMH ;
Zakhary, MM .
STROKE, 2000, 31 (08) :1889-1892
[34]   Oxidative stress and stress-activated signaling pathways: A unifying hypothesis of type 2 diabetes [J].
Evans, JL ;
Goldfine, ID ;
Maddux, BA ;
Grodsky, GM .
ENDOCRINE REVIEWS, 2002, 23 (05) :599-622
[35]   Crosstalk signaling between mitochondrial Ca2+ and ROS [J].
Feissner, Robert F. ;
Skalska, Jolanta ;
Gaum, Winston E. ;
Sheu, Shey-Shing .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2009, 14 :1197-1218
[36]   Mechanisms of organ dysfunction in critical illness: report from a Round Table Conference held in Brussels [J].
Fink, MP ;
Evans, TW .
INTENSIVE CARE MEDICINE, 2002, 28 (03) :369-375
[37]   p66Shc protein, oxidative stress, and cardiovascular complications of diabetes: the missing link [J].
Francia, Pietro ;
Cosentino, Francesco ;
Schiavoni, Marzia ;
Huang, Yale ;
Perna, Enrico ;
Camici, Giovani G. ;
Luescher, Thomas F. ;
Volpe, Massimo .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2009, 87 (09) :885-891
[38]   The mitochondria-targeted anti-oxidant mitoquinone decreases liver damage in a phase II study of hepatitis C patients [J].
Gane, Edward J. ;
Weilert, Frank ;
Orr, David W. ;
Keogh, Geraldine F. ;
Gibson, Michael ;
Lockhart, Michelle M. ;
Frampton, Christopher M. ;
Taylor, Kenneth M. ;
Smith, Robin A. J. ;
Murphy, Michael P. .
LIVER INTERNATIONAL, 2010, 30 (07) :1019-1026
[39]   Electron transfer between cytochrome c and p66Shc generates reactive oxygen species that trigger mitochondrial apoptosis [J].
Giorgio, M ;
Migliaccio, E ;
Orsini, F ;
Paolucci, D ;
Moroni, M ;
Contursi, C ;
Pelliccia, G ;
Luzi, L ;
Minucci, S ;
Marcaccio, M ;
Pinton, P ;
Rizzuto, R ;
Bernardi, P ;
Paolucci, F ;
Pelicci, PG .
CELL, 2005, 122 (02) :221-233
[40]   The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance [J].
Goossens, Gijs H. .
PHYSIOLOGY & BEHAVIOR, 2008, 94 (02) :206-218