Intracellular free iron content of rat liver tissue after cold ischemia

TRANSPLANTABLE ORGANS are usually stored in a preservation medium, such as University of Wisconsin (UW) solution, under hypothermic conditions due to the energy deficiency. During cold storage significant cellular alterations may occur. Rauen et al have described that the preservation injury to cultured liver endothelial cells and hepatocytes is mediated by the formation of reactive oxygen species (ROS) through energy-dependent mechanisms that occur independent of hypoxia and subsequent reoxygenation. Damage to cultured hepatocytes was prevented when the cells were preincubated with desferrioxamine, suggesting iron-dependent generation of ROS. Kozlov et al have provided evidence that intracellular free iron in the liver represents an intermediate step in the transport of iron from blood transferrin to the site of synthesis of iron-containing molecules such as ferritin. Detected by electron paramagnetic resonance (EPR) spectroscopy as paramagnetic complexes in presence of desferioxamine, this transit pool consists of low-molecular weight (LMW) iron compounds able to participate in ROS generation. In the present paper, we examine the effect of cold ischemia on the intracellular free iron content of rat liver tissue.