Study of Superoxide Dysmutase Isozyme Activities in Hepatitis C Virus-Positive Cirrhotic Liver Transplant Recipients

p S h 1 t THE FORMATION OF reactive oxygen species following ischemia-reperfusion causes hepatocellular injury during transplantation. It has been suggested that hepatitis C virus may cause oxidative stress in infected cells. Oxidative stress develops when reactive oxygen forms are produced in excess and factors preventing their harmful effects fail to occur. Enzymatic antioxidant defense mechanism in the organism include superoxide dysmutase (SOD), which protects cells from toxic effects of superoxide radicals. Superoxide dysmutase activity has been related to the pathogenesis of hepatitis C virus by excessive superoxide radical production by NADPHoxidase. Three types of SOD isozymes—Cu,=Zn-SOD, Mn-SOD, and extracellular SOD (EC-SOD)— can catalyze dysmutation of superoxide radicals. Whereas MnSOD and EC-SOD are localized in the mitochondrial matrix and on the outer cell membrane surface respectively, Cu, Zn-SOD resides in the cytosol. In the present tudy, we studied perioperative SOD isozymes Cu, n-SOD and Mn-SOD activity in 22 patients with hepaitis C virus who received liver transplants.