Cardiac Defense Mechanisms against Oxidative Damage: The Role of Superoxide Dismutase and Glutathione-Related Enzymes
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Abstract
Cardiomyopathy resulting from oxidative damage inflicted by hyperoxia or administration of antineoplastic agents, such as adriamycin, has been well documented (1,2). The heart is the organ continuously exposed to highly oxygenated blood from the lung. Within aeroboically living cells including the cardiac cell, molecular oxygen is reduced by a number of pathways to produce reactive oxygen species, such as superoxide anion radical (O2 -), hydrogen peroxide (H2O2), hydroxyl radical (OH.) and oxygen-centered radicals of organic compounds (ROO. and RO.) (3). There is increasing evidence that these reactive oxygen species are involved in processes of cellular oxidative damage (4–7). Biological importance of reactive intermediates generating from radical-initiated peroxidative breakdown of polyunsaturated fatty acids, e.g. hydroxyalkenals, has also been implied in propagation of oxidative damage as well as in mutagenic effects and inflammatory responces (8).
Keywords
Xanthine Oxidase Keshan Disease Perfusion Time Electron Spin Reso Reoxygenation InjuryPreview
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