Abstract
Oxygen-derived free radicals have been implicated as possible mediators in the development of tissue injury induced by ischemia and reperfusion.1,2 Furthermore, lipid peroxidation mediated by free radicals is believed to be one of the important causes of cell membrane destruction and cell damage.3 The ischemia itself causes tissue damage and eventual death, but further injuries can occur while oxygen reintroduced to the tissue. Much evidence suggests that free radical and active oxygens including superoxide, hydrogen peroxide, hydroxyl radical, and singlet oxygen, contribute to the tissue injury. At least five possible sources are under investigation for the production of the active oxygen species: 1)the hypoxanthine-xanthine oxidase system; 2)the activated polymorphonuclear leukocytes; 3) the disrupted mitochondrial electron transport system; 4)the metabolism of arachidona te via the lipoxygenase pathway, and 5) vascular endothelial cell.
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© 1992 Springer Science+Business Media New York
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Yoshikawa, T. et al. (1992). Ischemia-Reperfusion Injury and Free Radical Involvement in Gastric Mucosal Disorders. In: Goldstick, T.K., McCabe, M., Maguire, D.J. (eds) Oxygen Transport to Tissue XIII. Advances in Experimental Medicine and Biology, vol 316. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3404-4_27
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DOI: https://doi.org/10.1007/978-1-4615-3404-4_27
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