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Identification of Thiolic Sarcolemmal Proteins as a Primary Target of Iron Toxicity in Cultured Heart Cells

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Progress in Iron Research

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 356))

Abstract

Damage to the heart is one of the most critical manifestations of transfusional iron overload. Because at present no experimental model is available to simulate iron-induced heart disease in the intact animal, we have employed rat myocardial cells in culture for studying the harmful effects of iron and the protective effects of iron chelation(1-4). Our previous studies have shown that iron toxicity in myocyte cultures is associated with profound, and reproducible changes in contractility and electophysiologic behaviour (5,6); that these abnormalities are associated with a marked increase in lipid peroxidation reflected in a change in composition of membrane lipids and an increased production of malondialdehyde (4,7); that these alterations may be prevented, or reversed by deferoxamine or the selective application of pharmacologic stimulants such as caffeine or calcium and; that iron toxicity may be significantly modified by the use of antioxidants such as α-tocopherol, by ascorbic acid, or by simultaneous hypoxia.

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© 1994 Springer Science+Business Media New York

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Link, G., Pinson, A., Hershko, C. (1994). Identification of Thiolic Sarcolemmal Proteins as a Primary Target of Iron Toxicity in Cultured Heart Cells. In: Hershko, C., Konijn, A.M., Aisen, P. (eds) Progress in Iron Research. Advances in Experimental Medicine and Biology, vol 356. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2554-7_28

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  • DOI: https://doi.org/10.1007/978-1-4615-2554-7_28

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-6090-2

  • Online ISBN: 978-1-4615-2554-7

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