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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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
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