FREE-RADICALS AS MEDIATORS OF TISSUE-INJURY AND DISEASE

被引:1252
作者
KEHRER, JP
机构
[1] Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX
关键词
FREE RADICALS; OXYGEN RADICALS; INFLAMMATION; RHEUMATOID ARTHRITIS; ATHEROSCLEROSIS; CANCER; REPERFUSION INJURY; OXYGEN TOXICITY; QUINONES; METAL CHELATES; NITRO COMPOUNDS; BIPYRIDILIUM COMPOUNDS;
D O I
10.3109/10408449309104073
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
A radical is any molecule that contains one or more unpaired electrons. Radicals are normally generated in many metabolic pathways. Some of these radicals can exist in a free form and subsequently interact with various tissue components resulting in dysfunction. The potential role of oxygen- or xenobiotic-derived free radicals in the pathology of several human diseases has stimulated extensive research linking the toxicity of numerous xenobiotics and disease processes to a free radical mechanism. However, because free radical-mediated changes are pervasive and often poorly understood, the question of whether such species are a major cause of tissue injury and human disease remains equivocal. This review discusses cellular sources of various radical species and their reactions with vital cellular constituents. Examples of purported free radical-mediated disorders are discussed in detail to provide insights into the controversy over whether free radicals are important mediators of tissue injury.
引用
收藏
页码:21 / 48
页数:28
相关论文
共 161 条
[61]   SUPEROXIDE-MEDIATED MODIFICATION OF LOW-DENSITY-LIPOPROTEIN BY ARTERIAL SMOOTH-MUSCLE CELLS [J].
HEINECKE, JW ;
BAKER, L ;
ROSEN, H ;
CHAIT, A .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 77 (03) :757-761
[62]   ENHANCED MACROPHAGE DEGRADATION OF LOW-DENSITY LIPOPROTEIN PREVIOUSLY INCUBATED WITH CULTURED ENDOTHELIAL-CELLS - RECOGNITION BY RECEPTORS FOR ACETYLATED LOW-DENSITY LIPOPROTEINS [J].
HENRIKSEN, T ;
MAHONEY, EM ;
STEINBERG, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1981, 78 (10) :6499-6503
[63]   LIPOPROTEIN OXIDATION AND LIPOPROTEIN-INDUCED CYTO-TOXICITY [J].
HESSLER, JR ;
MOREL, DW ;
LEWIS, LJ ;
CHISOLM, GM .
ARTERIOSCLEROSIS, 1983, 3 (03) :215-222
[64]   LEUKOCYTIC OXYGEN ACTIVATION AND MICROBICIDAL OXIDATIVE TOXINS [J].
HURST, JK ;
BARRETTE, WC .
CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1989, 24 (04) :271-328
[65]   OXYGEN TOLERANCE IN NEONATAL RATS - ROLE OF SUBCELLULAR SUPEROXIDE GENERATION [J].
ISCHIROPOULOS, H ;
NADZIEJKO, CE ;
KUMAE, T ;
KIKKAWA, Y .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (06) :L411-L420
[66]  
JAKOBY WB, 1990, J BIOL CHEM, V265, P20715
[67]   OXYGEN-TOXICITY AND REACTIVE OXYGEN METABOLITES IN MAMMALS [J].
JAMIESON, D .
FREE RADICAL BIOLOGY AND MEDICINE, 1989, 7 (01) :87-108
[68]   THE RELATION OF FREE-RADICAL PRODUCTION TO HYPEROXIA [J].
JAMIESON, D ;
CHANCE, B ;
CADENAS, E ;
BOVERIS, A .
ANNUAL REVIEW OF PHYSIOLOGY, 1986, 48 :703-719
[69]   MALONDIALDEHYDE AND THIOBARBITURIC ACID-REACTIVITY AS DIAGNOSTIC INDEXES OF LIPID-PEROXIDATION AND PEROXIDATIVE TISSUE-INJURY [J].
JANERO, DR .
FREE RADICAL BIOLOGY AND MEDICINE, 1990, 9 (06) :515-540
[70]   OXIDATIVE CROSS-LINKING OF IMMUNE-COMPLEXES BY HUMAN POLYMORPHONUCLEAR LEUKOCYTES [J].
JASIN, HE .
JOURNAL OF CLINICAL INVESTIGATION, 1988, 81 (01) :6-15