Oxygen-Derived Free Radicals in Cerulein-Induced Acute Pancreatitis

Abstract

Conscious rats were treated with a supramaximal dose of 5.10(-6)g.kg-1.h-1 of cerulein for periods of 3 and 12 h. In both groups of animals typical features of acute oedematous pancreatitis were proved by biochemical and histologic examinations. The most important finding of our study was the decrease of superoxide dismutase (SOD) activity in pancreatic tissue, accompanied by a slight increase of this scavenger enzyme in serum of rats stimulated with cerulein during 3 h. Parallelly, evident elevation of malondialdehyde (MDA) concentration in pancreatic tissue was noted. After the 12-h infusion of cerulein we were not able to detect any SOD activity in pancreatic tissue, whereas this activity appeared in ascitic fluid of tested animals. Further increase of MDA concentration in pancreatic tissue, in comparison with 3-h pancreatitis, was found. These data suggest that in 3-h and 12-h cerulein-induced pancreatitis the oxygen-derived free radicals mediate the increased lipid peroxidation in pancreatic tissue. We think that the depletion of the scavenger enzyme SOD may be responsible for such a disturbance of lipid metabolism.

Reactive oxygen species inactivation improves pancreatic capillary blood flow in caerulein-induced pancreatitis in rats

“…Also the serum amylase increase in group 2 was statistically reduced in the presence of the PBN. These findings are in accord with reports of gluthatione depletion 25 , decrease of superoxide dismutase activity in the pancreatic tissue and elevation malondialdehyde concentration 26 (a by-product of lipid peroxidation) seen during caerulein-induced pancreatitis. During the effort to produce and secret pancreatic enzymes by caerulein hyperstimulation, a disturb in the oxidantantioxidant balance may occur in the pancreatic cell.…”

Useful Markers for Predicting Severity and Monitoring Progression of Acute Pancreatitis

“…Polyunsaturated fatty acids of cell membranes undergo degradation to form lipid hydroperoxides by lipid peroxidation. End products include malondialdehyde and thiobarbituric acid reactive substances, which have been detected in pancreatic tissue in highly elevated concentrations shortly after induction of experimental pancreatitis [89,90]. Neutrophils, monocytes, eosinophils and macrophages are the major source of oxygen free radicals in the later course of acute pancreatitis [88].…”

Elevated protein carbonyls as plasma markers of oxidative stress in acute pancreatitis

“…Experimentally induced pancreatitis in rats and mice is associated with decreased pancreatic levels of glutathione [8][9][10] and antioxidant enzymes such as superoxide dismutase [11, Winterbourn/Bonham/Buss/Abu-Zidan/ Windsor 12] and elevated concentrations of lipid peroxidation markers [8,[12][13][14][15]. Formation of protein carbonyls (products of protein oxidation) in pancreatic tissue has been seen as an early event [16,17].…”