Studies on oxygen-derived free radicals in acute pancreatic damage in rats--pancreatic damage experimentally induced by diethyldithiocarbamate

In order to investigate the role of the oxygen-derived free radicals in the pathogenesis of acute pancreatitis, an experimentally induced pancreatic damage was prepared in rats by the injection of diethyldithiocarbamate (DDC), which was known to be an inhibitor of Cu, Zn-superoxide dismutase (SOD). Male Wistar rats weighing 200-250 g received a single subcutaneous injection of DDC at a dose of 1000 mg/kg. Serum activities of amylase were significantly increased at 3 and 5 hours after the injection of DDC. Thiobarbituric acid reactants (TBA reactants) concentrations in the pancreatic tissue were increased at 30 minutes after the injection of DDC. At 7 hours after the injections of DDC, focal necrosis and degeneration of pancreatic acinar cells were observed. Peroral administration of allopurinol, an inhibitor of xanthine oxidase, before the injection of DDC suppressed the increase of TBA reactants concentration in the pancreatic tissue, but did not suppress the increase of serum activities of amylase. These results indicate that oxygen-derived free radicals may play an important role in the pathogenesis of acute pancreatic damage. However, since allopurinol did not suppress the increase of serum activities of amylase, further examination is needed to analyze the mechanism of DDC-induced pancreatic damage.