Contrasting Features of Peroxide Metabolism in Heart and Liver
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Abstract
Peroxides arise in the course of normal aerobic metabolism as products and by-products of various oxidases and in association with electron transfer reactions of hemoproteins, flavoproteins and other redox active molecules. Because peroxides are mediators of oxidative injury, cellular systems capable of detoxifying and eliminating these compounds are an essential feature of aerobic life. By the catalatic and peroxidatic activities of catalase, glutathione peroxidase, and other proteins present in mammalian cells, peroxides are effectively maintained at nontoxic levels under conditions of normal metabolism. However, in instances of enhanced peroxide production, such as occurs in association with the inflammatory response (1), the metabolism of redox cycling agents (2), and reoxygenation and reperfusion following periods of hypoxia and ischemia (3), cellular peroxide levels may exceed the capacity of these detoxication systems and result in oxidative injury and cell death. Under some conditions, such as hypoxia, the detoxication mechanisms are compromised so that even normal peroxide production can be toxic (4).
Keywords
Glutathione Peroxidase Oxidative Injury Heart Cell Aldehyde Oxidase Sulfite OxidasePreview
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