Oxygen radicals, inflammation, and arthritis: Pathophysiological considerations and implications for treatment
Identifieur interne : 002F20 ( Main/Exploration ); précédent : 002F19; suivant : 002F21Oxygen radicals, inflammation, and arthritis: Pathophysiological considerations and implications for treatment
Auteurs : Robert A. Greenwald [États-Unis]Source :
- Seminars in Arthritis and Rheumatism [ 0049-0172 ] ; 1991.
English descriptors
- Teeft :
- Acta, Agents actions, Aggregation, Anion, Antiinflammatory, Antioxidant, Antirheumatic drugs, Arthritic, Arthritic disorders, Arthritis, Arthritis rheum, Articular cartilage, Auranofin, Biochem, Biochem biophys, Biochim biophys acta, Biol, Biol chem, Biophys, Cartilage, Catalase, Chemotactic, Clin, Collagen, Collagen synthesis, Collagenase, Cuzn, Degradation, Direct evidence, Dismutase, Elastase, Ferrous, Free iron, Free radicals, Free radicals biol, Gingival proteoglycans, Gold compounds, Greenwald, Human disease, Hurst, Hyaluronic, Hyaluronic acid, Hyde park, Hydrogen peroxide, Hydroxyl, Hydroxyl radicals, Hypochlorous acid, Immune complexes, Immunoglobulin, Inflamed, Inflamed joints, Inflammation, Inflammatory, Inhibitor, Joint fluid, Leukocyte, Lipid, Lipid peroxidation, Long island jewish, Lymphocyte, Macromolecule, Mccord, Mediator, Metal ions, Molecular oxygen, Monocyte, Neutrophil, Nsaid, Odfr, Odfr generation, Other hand, Oxidant, Oxidase, Oxygen radicals, Pathogenesis, Peroxidation, Peroxide, Phagocytic, Phagocytic cells, Physiological conditions, Pmns, Polymer, Polymorphonuclear, Polymorphonuclear leukocytes, Possible role, Proteoglycan, Proteoglycan synthesis, Proteoglycans, Radical generation, Radical species, Reactive, Rheum, Rheumatic diseases, Rheumatoid, Rheumatoid arthritis, Rheumatol, Scavenger, Singlet, Singlet oxygen, Such radicals, Superoxide, Superoxide anion, Superoxide dismutase, Superoxide dismutases, Superoxide generation, Superoxide production, Synovial, Synovial fluid, Target tissues, Therapeutic agents, Tissue damage, Vivo, Xanthine, Xanthine oxidase.
Abstract
Abstract: 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.
Url:
DOI: 10.1016/0049-0172(91)90018-U
Affiliations:
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Greenwald</name><affiliation wicri:level="2"><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Long Island Jewish Medical Center, New Hyde Park</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Seminars in Arthritis and Rheumatism</title><title level="j" type="abbrev">YSARH</title><idno type="ISSN">0049-0172</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="219">219</biblScope><biblScope unit="page" to="240">240</biblScope></imprint><idno type="ISSN">0049-0172</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0049-0172</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acta</term><term>Agents actions</term><term>Aggregation</term><term>Anion</term><term>Antiinflammatory</term><term>Antioxidant</term><term>Antirheumatic drugs</term><term>Arthritic</term><term>Arthritic disorders</term><term>Arthritis</term><term>Arthritis rheum</term><term>Articular cartilage</term><term>Auranofin</term><term>Biochem</term><term>Biochem biophys</term><term>Biochim biophys acta</term><term>Biol</term><term>Biol chem</term><term>Biophys</term><term>Cartilage</term><term>Catalase</term><term>Chemotactic</term><term>Clin</term><term>Collagen</term><term>Collagen synthesis</term><term>Collagenase</term><term>Cuzn</term><term>Degradation</term><term>Direct evidence</term><term>Dismutase</term><term>Elastase</term><term>Ferrous</term><term>Free iron</term><term>Free radicals</term><term>Free radicals biol</term><term>Gingival proteoglycans</term><term>Gold compounds</term><term>Greenwald</term><term>Human disease</term><term>Hurst</term><term>Hyaluronic</term><term>Hyaluronic acid</term><term>Hyde park</term><term>Hydrogen peroxide</term><term>Hydroxyl</term><term>Hydroxyl radicals</term><term>Hypochlorous acid</term><term>Immune complexes</term><term>Immunoglobulin</term><term>Inflamed</term><term>Inflamed joints</term><term>Inflammation</term><term>Inflammatory</term><term>Inhibitor</term><term>Joint fluid</term><term>Leukocyte</term><term>Lipid</term><term>Lipid peroxidation</term><term>Long island jewish</term><term>Lymphocyte</term><term>Macromolecule</term><term>Mccord</term><term>Mediator</term><term>Metal ions</term><term>Molecular oxygen</term><term>Monocyte</term><term>Neutrophil</term><term>Nsaid</term><term>Odfr</term><term>Odfr generation</term><term>Other hand</term><term>Oxidant</term><term>Oxidase</term><term>Oxygen radicals</term><term>Pathogenesis</term><term>Peroxidation</term><term>Peroxide</term><term>Phagocytic</term><term>Phagocytic cells</term><term>Physiological conditions</term><term>Pmns</term><term>Polymer</term><term>Polymorphonuclear</term><term>Polymorphonuclear leukocytes</term><term>Possible role</term><term>Proteoglycan</term><term>Proteoglycan synthesis</term><term>Proteoglycans</term><term>Radical generation</term><term>Radical species</term><term>Reactive</term><term>Rheum</term><term>Rheumatic diseases</term><term>Rheumatoid</term><term>Rheumatoid arthritis</term><term>Rheumatol</term><term>Scavenger</term><term>Singlet</term><term>Singlet oxygen</term><term>Such radicals</term><term>Superoxide</term><term>Superoxide anion</term><term>Superoxide dismutase</term><term>Superoxide dismutases</term><term>Superoxide generation</term><term>Superoxide production</term><term>Synovial</term><term>Synovial fluid</term><term>Target tissues</term><term>Therapeutic agents</term><term>Tissue damage</term><term>Vivo</term><term>Xanthine</term><term>Xanthine oxidase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: 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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Greenwald, Robert A" sort="Greenwald, Robert A" uniqKey="Greenwald R" first="Robert A." last="Greenwald">Robert A. Greenwald</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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