Superoxide anion as a marker of ischemia-reperfusion injury of the transplanted kidney

Reactive oxygen species (ROS) are considered to be important factors involved in the pathophysiology of renal ischemia-reperfusion injury. ROS-induced alterations of proteins, carbohydrates, DNA, and lipid membranes lead to cell and organ dysfunction. Several antioxidant defense mechanisms exist to prevent or limit oxidant injury. Cellular Cu-Zn superoxide dismutase, catalase, and cellular glutathione peroxidase (cGSH-Px) are enzyme ROS scavengers, implicated in the protection against kidney damage resulting from ischemia-reperfusion injury. Reduced glutathione, a cosubstrate of cGSH-Px, have been shown to display a reductive properties without the contribution of enzymes. We examined superoxide anion (O(2)(-)) production by neutrophils, without and with stimulation using opsonized zymosan, in the whole blood of renal transplant patients before and after (5 and 15 minutes) reperfusion. The mean O(2)(-) concentration after reperfusion was statistically significantly higher than that before reperfusion.