Oxygen radicals, inflammation, and arthritis: pathophysiological considerations and implications for treatment.

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 inflammation and/or tissue destruction in inflammatory arthritic disorders. The substrates for generation, namely properly stimulated phagocytic cells, transition metal catalysts, (to a limited extent) ischemia, are all amply present, although there is no particular rheumatic disease which consistent abnormality generation has been identified. These species can clearly degrade hyaluronic acid, modify collagen perhaps proteoglycan structure synthesis, alter interact with immunoglobulins, activate enzymes inactivate their inhibitors, possibly participate chemotaxis. In most situations, however, ample scavenging ability detoxify these radicals before they hit target, many drugs decrease production effects. Despite the apparent sufficiency natural scavengers lack direct that oxygen pathogenetically important, substantial pharmaceutical effort still being made develop therapeutic agents. Although individual die out quickly, rheumatologic interest them sustained nearly two decades.