OXYGEN RADICALS, INFLAMMATION, AND ARTHRITIS - PATHOPHYSIOLOGICAL CONSIDERATIONS AND IMPLICATIONS FOR TREATMENT

被引:170
作者
GREENWALD, RA
机构
[1] LONG ISL JEWISH MED CTR, B206A SCHWARTZ RES CTR, DIV RHEUMATOL, NEW HYDE PK, NY 11042 USA
[2] YESHIVA UNIV ALBERT EINSTEIN COLL MED, MED, BRONX, NY 10461 USA
关键词
OXYGEN RADICAL; SUPEROXIDE; HYDROXYL RADICAL; INFLAMMATION;
D O I
10.1016/0049-0172(91)90018-U
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
A vast amount of circumstantial evidence implicates oxygen-derived free radicals, especially superoxide and hydroxyl radical (and to lesser extent, hydrogen peroxide), as mediators of inflammation and/or tissue destruction in inflammatory and arthritic disorders. The substrates for radical generation, namely properly stimulated phagocytic cells, transition metal catalysts, and (to a limited extent) ischemia, are all amply present, although there is no particular rheumatic disease in which a consistent abnormality of radical generation has been identified. These radical species can clearly degrade hyaluronic acid, modify collagen and perhaps proteoglycan structure and/or synthesis, alter and interact with immunoglobulins, activate enzymes and inactivate their inhibitors, and possibly participate in chemotaxis. In most situations, however, there is ample scavenging ability to detoxify these radicals before they hit their target, and many rheumatic disease drugs can decrease their production and/or effects. Despite the apparent sufficiency of natural scavengers and the lack of direct evidence that oxygen radicals are pathogenetically important, substantial pharmaceutical effort is still being made to develop free radical scavengers as therapeutic agents. Although individual free radicals die out quickly, rheumatologic interest in them has been sustained for nearly two decades. © 1991.
引用
收藏
页码:219 / 240
页数:22
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