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      Oxygen-derived free radicals in postischemic tissue injury.

      The New England journal of medicine

      Animals, Calcium, metabolism, Coronary Disease, Free Radicals, Humans, Intestines, blood supply, Ischemia, pathology, Shock, Superoxides, Transplantation, Xanthine Dehydrogenase, Xanthine Oxidase

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          Abstract

          It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury. Although there are certainly multiple components to clinical ischemic and reperfusion injury, it appears likely that free-radical production may make a major contribution at certain stages in the progression of the injury. The primary source of superoxide in reperfused reoxygenated tissues appears to be the enzyme xanthine oxidase, released during ischemia by a calcium-triggered proteolytic attack on xanthine dehydrogenase. Reperfused tissues are protected in a variety of laboratory models by scavengers of superoxide radicals or hydroxyl radicals or by allopurinol or other inhibitors of xanthine oxidase. Dysfunction induced by free radicals may thus be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.

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          Journal
          2981404
          10.1056/NEJM198501173120305

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