Intracellular iron redistribution. An important determinant of reperfusion damage to rabbit kidneys.

These studies were designed to examine the possible role of low molecular weight intracellular iron chelates (desferrioxamine-available (DFX-A) iron) in the damage which occurs during cold storage and subsequent reperfusion of kidneys. The level of DFX-A iron increased significantly (P less than 0.005) in the cortex of rabbit kidneys rendered cold ischaemic (CI) for 24 hr and the amount of iron available for DFX chelation increased significantly (P less than 0.05) in both the cortex and medulla of kidneys stored for 48 or 72 hr compared with fresh non-ischaemic controls. During ex vivo reperfusion of the organs with an oxygenated asanguinous perfusate, DFX-A iron returned rapidly to pre-ischaemic levels in 24 hr CI kidneys, but remained elevated following 48 and 72 hr CI (P less than 0.05 compared with 24 hr CI kidneys after 5 min reperfusion), returning to control levels only after 30 min reperfusion. There was no concurrent increase in total iron levels, indicating that a redistribution of iron to more accessible pools had occurred within the tissue. We suggest that decompartmentalization of intracellular iron during ischaemia and raised DFX-A iron levels over an extended period during subsequent reperfusion are responsible for increased catalysis of oxygen-derived free radical-mediated lipid peroxidation, and are an important factor in the deterioration of physiological function observed in rabbit kidneys following extended periods of cold storage.