Oxygen, reactive oxygen species and tissue damage

被引:500
作者
Bergamini, CM
Gambetti, S
Dondi, A
Cervellati, C
机构
[1] Univ Ferrara, Sch Med, Dept Biochem & Mol Biol, I-44100 Ferrara, Italy
[2] Univ Ferrara, Sch Med, Interdisciplinary Ctr Study Inflammat, I-44100 Ferrara, Italy
关键词
oxygen; reactive oxygen species; oxygen derived radicals; radical scavengers; physiology; oxidative damage; alterations in cell structures;
D O I
10.2174/1381612043384664
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The diatomic molecule of oxygen contains two uncoupled electrons and can therefore undergo reduction, yielding several different oxygen metabolites, which are collectively called Reactive Oxygen Species or ROS. They are invariably produced in aerobic environments through a variety of mechanisms, which include electron "leakage" during biologic oxidations. action of flavin dehydrogenases and specific membrane associated secretion, as well as by physical activation of oxygen by irradiation, e.g. UV sun-light. Organisms have developed efficient protective mechanisms against excessive accumulation of ROS, which include superoxide anion, hydrogen peroxide and hydroxyl radical, since all these metabolites are highly reactive and affect almost every kind of organism, either directly or through conversion into other derivatives, notably NO-derived radicals or RNS. Depending on their tissue concentration they can either exert beneficial physiologic effects (control of gene expression and mitogenesis) or damage cell structures, including lipids and membranes, proteins and nucleic acids, leading to cell death. In this brief overview we summarize the present state-of-the-art. restricting the discussion to the role of ROS in physiology and pathology, not taking into account RNS. Discussion will focus on basic chemical and biochemical features of ROS, underlining how ROS can promote severe diseases, including neoplastic, cardiovascular and neurodegenerative diseases. This brief discussion should clarify the present huge interest in ROS, in the perspective to develop new and specific therapeutic approaches.
引用
收藏
页码:1611 / 1626
页数:16
相关论文
共 109 条
[1]   Inactivation of aconitase and oxoglutarate dehydrogenase in skeletal muscle in vitro by superoxide anions and/or nitric oxide [J].
Andersson, U ;
Leighton, B ;
Young, ME ;
Blomstrand, E ;
Newsholme, EA .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 249 (02) :512-516
[2]  
[Anonymous], 1990, INORG CHEM
[3]   ENERGY CHARGE OF ADENYLATE POOL AS A REGULATORY PARAMETER . INTERACTION WITH FEEDBACK MODIFIERS [J].
ATKINSON, DE .
BIOCHEMISTRY, 1968, 7 (11) :4030-&
[4]   Roles of superoxide radical anion in signal transduction mediated by reversible regulation of protein-tyrosine phosphatase 1B [J].
Barrett, WC ;
DeGnore, JP ;
Keng, YF ;
Zhang, ZY ;
Yim, MB ;
Chock, PB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (49) :34543-34546
[5]   Role of oxidative stress in diabetic complications - A new perspective on an old paradigm [J].
Baynes, JW ;
Thorpe, SR .
DIABETES, 1999, 48 (01) :1-9
[6]   The free radical theory of aging matures [J].
Beckman, KB ;
Ames, BN .
PHYSIOLOGICAL REVIEWS, 1998, 78 (02) :547-581
[7]   Covalent modification of epithelial fatty acid-binding protein by 4-hydroxynonenal in vitro and in vivo -: Evidence for a role in antioxidant biology [J].
Bennaars-Eiden, A ;
Higgins, L ;
Hertzel, AV ;
Kapphahn, RJ ;
Ferrington, DA ;
Bernlohr, DA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (52) :50693-50702
[8]  
Benzie IFF, 1999, METHOD ENZYMOL, V299, P15
[9]   Protein oxidation in aging, disease, and oxidative stress [J].
Berlett, BS ;
Stadtman, ER .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (33) :20313-20316
[10]   Identification and quantification of major Maillard cross-links in human serum albumin and lens protein - Evidence for glucosepane as the dominant compound [J].
Biemel, KM ;
Friedl, DA ;
Lederer, MO .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (28) :24907-24915