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Tissue Iron Overload and Mechanisms of Iron-Catalyzed Oxidative Injury

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Book cover Free Radicals in Diagnostic Medicine

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 366))

Abstract

Tissue iron overload causes cell damage and organ dysfunction. The mechanisms of iron uptake by tissues and the probable biochemical pathways of iron-derived tissue injury will be reviewed. The iron-overload states are the initial clinical setting where the contribution of iron-catalyzed oxidative injury to the pathogenesis of a clinical disease has been appreciated. When viewed from the perspective of oxidative injury, the iron-overload syndromes also provide a model of tissue injury that is applicable to other disease states, including inflammation, ischemia-reperfusion injury, and anthracycline-induced cardiac toxicity. The goal of this chapter will be to provide a brief clinical overview of the iron-overload states, review the mechanisms of tissue iron uptake in normal and pathologic situations, the likely cellular targets and reactions of iron-catalyzed oxidative injury, and the clinical therapy of the iron-overload syndromes. The potential role of iron-catalyzed oxidative injury in the myocardial damage resulting from ischemia and reperfusion, and from anthracycline administration will also be discussed.

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Lesnefsky, E.J. (1994). Tissue Iron Overload and Mechanisms of Iron-Catalyzed Oxidative Injury. In: Armstrong, D. (eds) Free Radicals in Diagnostic Medicine. Advances in Experimental Medicine and Biology, vol 366. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1833-4_10

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  • DOI: https://doi.org/10.1007/978-1-4615-1833-4_10

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