INTRODUCTION
As a result of ischemia occurring in tissues for various reasons, cellular energy stores are emptied, and cell death occurs as a result of the accumulation of toxic metabolites. It is necessary to provide blood flow to ischemic tissue for both regeneration of the cell and removal of toxic metabolites. Reperfusion injury occurs during the re-bleeding period following the ischemia period. Free oxygen radical (ROS) derivatives, which are rapidly formed by the presentation of molecular oxygen into the cell, are one of the most causing factors1. Ischemia-reperfusion (I / R) damage in tissues may be caused clinically by transplantation surgery, aortic cross clamp applications, tourniquet application, free tissue transfers, acute compartment syndrome, and replantation of the amputated extremity2,3. During ischemia, toxic oxygen radicals are produced in ischemic tissue. After reperfusion, free oxygen radicals and superoxide radicals cause endothelial damage and increased vascular permeability. In addition, activated adhesion molecules and cytokines also initiate the systemic inflammatory response 4.