Iron Redistribution and Lipid Peroxidation in the Cold Ischaemic Kidney
Oxygen-derived free radicals may play an important role in the damage which occurs to organs subjected to extended periods of cold storage followed by reperfusion with oxygenated blood upon transplantation into the recipient1. One damaging radical-mediated process is the peroxidation of membrane-bound polyunsaturated fatty acids and we have previously demonstrated significant elevations in lipid peroxidation markers in kidneys subjected to cold storage and autotransplantation2. Iron is required for the initiation of lipid peroxidation3 which may be the consequence of highly reactive OH. radical formation from O 2 .- and H2O2 via the Haber-Weiss reaction or direct attack on polyunsaturated fatty acids by iron complexes with oxygen4. In addition, iron also catalyses the decomposition of lipid hydroperoxides (LOOH) to alkoxy (LO.) and peroxy (LOO.) radicals which stimulate the chain reaction of lipid peroxidation4. In order to minimize the likelihood of these damaging reactions, iron is transported and stored in specific proteins. However, a small pool of iron exists in the cell as low molecular weight chelates5 which are able to exert catalytic activity.
KeywordsCold Storage Chelatable Iron Cold Ischaemia Rabbit Kidney Total Iron Content
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