Role of ROS and RNS Sources in Physiological and Pathological Conditions

被引:1001
作者
Di Meo, Sergio [1 ]
Reed, Tanea T. [2 ]
Venditti, Paola [1 ]
Manuel Victor, Victor [3 ]
机构
[1] Univ Napoli Federico II, Dipartimento Biol, I-80126 Naples, Italy
[2] Eastern Kentucky Univ, Dept Chem, Richmond, KY 40475 USA
[3] Fdn Promot Hlth & Biomed Res Valencian Reg FISABI, Univ Hosp Dr Peset, Serv Endocrinol, E-46010 Valencia, Spain
关键词
ENDOPLASMIC-RETICULUM STRESS; NITRIC-OXIDE SYNTHASE; INDUCED OXIDATIVE STRESS; BETA-AMYLOID PEPTIDE; MITOCHONDRIAL PERMEABILITY TRANSITION; NICOTINAMIDE-ADENINE-DINUCLEOTIDE; APOLIPOPROTEIN-E GENOTYPE; INSULIN-DEGRADING ENZYME; ONSET ALZHEIMERS-DISEASE; ELECTRON-SPIN-RESONANCE;
D O I
10.1155/2016/1245049
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
There is significant evidence that, in living systems, free radicals and other reactive oxygen and nitrogen species play a double role, because they can cause oxidative damage and tissue dysfunction and serve as molecular signals activating stress responses that are beneficial to the organism. Mitochondria have been thought to both play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction through several mechanisms, including stimulation of opening of permeability transition pores. Until recently, the functional significance of ROS sources different from mitochondria has received lesser attention. However, the most recent data, besides confirming the mitochondrial role in tissue oxidative stress and protection, show interplay between mitochondria and other ROS cellular sources, so that activation of one can lead to activation of other sources. Thus, it is currently accepted that in various conditions all cellular sources of ROS provide significant contribution to processes that oxidatively damage tissues and assure their survival, through mechanisms such as autophagy and apoptosis.
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共 545 条
[11]   LIPID-PEROXIDATION AND SCAVENGER ENZYMES DURING EXERCISE - ADAPTIVE RESPONSE TO TRAINING [J].
ALESSIO, HM ;
GOLDFARB, AH .
JOURNAL OF APPLIED PHYSIOLOGY, 1988, 64 (04) :1333-1336
[12]   MDA CONTENT INCREASES IN FAST-TWITCH AND SLOW-TWITCH SKELETAL-MUSCLE WITH INTENSITY OF EXERCISE IN A RAT [J].
ALESSIO, HM ;
GOLDFARB, AH ;
CUTLER, RG .
AMERICAN JOURNAL OF PHYSIOLOGY, 1988, 255 (06) :C874-C877
[13]   Clinical findings in nondemented mutation carriers predisposed to Alzheimer's disease: a model of mild cognitive impairment [J].
Almkvist, O ;
Axelman, K ;
Basun, H ;
Jensen, M ;
Viitanen, M ;
Wahlund, LO ;
Lannfelt, L .
ACTA NEUROLOGICA SCANDINAVICA, 2003, 107 :77-82
[14]  
AMBROSIO G, 1993, J BIOL CHEM, V268, P18532
[15]   Mitochondrial metabolism of reactive oxygen species [J].
Andreyev, AI ;
Kushnareva, YE ;
Starkov, AA .
BIOCHEMISTRY-MOSCOW, 2005, 70 (02) :200-214
[16]  
ANGERMULLER S, 1987, EUR J CELL BIOL, V45, P137
[17]   Peroxisomes Are Oxidative Organelles [J].
Antonenkov, Vasily D. ;
Grunau, Silke ;
Ohlmeier, Steffen ;
Hiltunen, J. Kalervo .
ANTIOXIDANTS & REDOX SIGNALING, 2010, 13 (04) :525-537
[18]   Apoptosis induced by exposure to a low steady-state concentration of H2O2 is a consequence of lysosomal rupture [J].
Antunes, F ;
Cadenas, E ;
Brunk, UT .
BIOCHEMICAL JOURNAL, 2001, 356 :549-555
[19]   Synchronized whole cell oscillations in mitochondrial metabolism triggered by a local release of reactive oxygen species in cardiac myocytes [J].
Aon, MA ;
Cortassa, S ;
Marbán, E ;
O'Rourke, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (45) :44735-44744
[20]   Molecular Strategies for Targeting Antioxidants to Mitochondria: Therapeutic Implications [J].
Apostolova, Nadezda ;
Victor, Victor M. .
ANTIOXIDANTS & REDOX SIGNALING, 2015, 22 (08) :686-729