Minor role of oxidative stress during intermediate phase of acute pancreatitis in rats

Reactive oxygen species have been implicated in the pathogenesis of acute p ancreatitis. Few studies have focused on the loss of endogenous antioxidant s and molecular oxidative damage. Two acute pancreatitis models in rats; ta urocholate (3% intraductal infusion) and cerulein (10 mug/kg/h), were used to study markers of oxidative stress: Glutathiune, ascorbic acid, and their oxidized forms (glutathione disulfide and dehydroascorbic acid), malondial dehyde, and 4-hydroxynoneal in plasma and pancreas, as well as 7-hydro-8-ox o-2'-deoxyguanosine in pancreas. Tn both models, pancreatic glutathione dep leted by 36-46% and pancreatic ascorbic acid depleted by 36-40% (p < .05). In the taurocholate model, plasma glutathione was depicted by 34% (p < .05) , but there were no significant changes in plasma ascorbic acid or in plasm a and pancreas dehydroascorbic acid, malondialdehyde, and 3-hydroxynoneal, and no significant changes in the pancreas glutathione disulfide/glutathion e ratio. While pancreas glutathione disulfide/ glutathione ratio increased in the cerulein model, there were no significant changes in plasma glutathi one, plasma, or pancreas ascorbic acid, dehydroascorbic acid, 4-hydroxynone al, and malondialdehyde, or in pancreas 7-hydro-8-oxo-2'-deoxyguanosine. Re active oxygen species have a minor role in the intermediate stages of pancr eatitis models. (C) 2001 Elsevier Science Inc.