THE EFFECT OF HYDROGEN PEROXIDE ON TRYPSINOGEN ACTIVATION AND APOPTOSIS IN EXPERIMENTAL ACUTE PANCREATITIS

Abstract

Role of free oxygen radicals in the pathogenesis of acute pancreatitis has not been studied thoroughly in the literature. In addition to the direct toxic effect of free oxygen radicals on acinar cells, these agents may activate pancreatic enzymes and, in turn, add to the parenchymal injury. In this study we aimed to study the effect of introductal perfusion of hydrogen peroxide, a member of free oxygen radical family, on the activation of trypsinogen and induction of apoptosis in pancreatic parenchyma. Twenty Sprague-Dawley rats were randomly divided into two groups. Bile-pancreatic duct was cannulated close to the liver in all animals and perfused through the duodenum with %0.9 NaCI solution in group 1 and 250(M hydrogen peroxide in group 2 at 0.5 ml/h for 3 hours. Serum amylase and lipase levels were measured for the diagnosis of acute pancreatitis; serum and urine trypsinogen activation peptide levels measured for the determination of trypsinogen activation. Tissue samples were obtained for the evaluation of apoptosis. Mann Whitney U test was used for statistical analysis. Hydrogen peroxide perfusion induced acute pancreatitis with high serum amylase and lipase levels. There were no statistical differences in serum and urine trypsinogen activation peptide levels between the two groups. Apopitosis has not been detected in both groups. We concluded that hydrogen peroxide induced acute pancreatitis in our study. In this model, trypsiongen activation has not been detected in serum and urine after 3 hours of hydrogen peroxide perfusion. No increase in apopitosis has been found in hydrogen peroxide group when compared with control group.