Ischemia-Reperfusion Injury in the Transplanted Kidney Based on Purine Metabolism Markers and Activity of the Antioxidant System

The pathophysiology of ischemia and reperfusion stress linked with the generation of reactive oxygen species (ROS), as well as the activation of antioxidant defense mechanisms are an integral part of non-immune factors implicated in the early and delayed graft function (DGF). Oxygen free radicals are central mediators of cellular injury that occurs upon postischaemic reperfusion. Studies on the mechanisms of reperfusion injury in the cold-preserved kidney transplant model have suggested an important role for free radicals generated at reperfusion from oxygen by activated xanthine oxidase. Generation of ROS is the main mechanism inducing ischemic/reperfusion damage of the organ. Oxygen burst is a trigger for complex biochemical reactions leading to generation of oxygenated lipids and changes in microcirculation with recruitment of neutrophils to the graft. Recently, radical generation has been measured in postischaemic tissues using electron paramagnetic resonance spectroscopy. Electron paramagnetic resonance techniques have demonstrated that presence of oxygen burst after postischaemic reperfusion of the graft (Hirayama et al.,2004). Moreover, it has been shown that free radical generation is correlated with the activity of the anti-oxidative system. Many markers have been researched to prove the presence of ROS in the transplanted tissue including malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT). They are involved in protection against free radicals. Elucidation of inter-relations between these factors is important for our understanding of the phenomena and for implementation of perioperative procedures aimed at prolonging graft survival. Organ preservation seeks to ensure the functional viability of transplanted organs. Preservation during ischemia includes steps against acidosis, steps to maintain cell volume and for optimal utilization of anaerobic energy reserves. Previous studies have demonstrated that apart from ischemic damage, additional tissue injury evolves as a result of reperfusion and reoxygenation (Tilney et al., 2001). Energy-dependent processes occurring during cold ischemia of the graft require adequate levels of ATP and other high-energy compounds generated in the majority during oxidative catabolism of various substrates. Because oxygen is required for such reactions, the ability to maintain adequate levels of high-energy phosphates would appear to depend on oxygen delivery to graft cells (Chien et al., 2001a). Oxygen delivery during reperfusion is