Oxygen Radicals Mediate Depletion of Pancreatic Sulfhydryl Compounds in Rats with Cerulein-Induced Acute Pancreatitis

Abstract

Acute edematous pancreatitis was induced in conscious rats by intravenous infusion of cerulein at a supramaximal dose of 7.5 μg/kg/h during 6 h. The most important finding of our study was a marked decrease in the protein and non-protein content of sulfhydryl groups parallel to an evident elevation in the malondialdehyde concentration in pancreatic tissue. The presented data suggest that in cerulein-induced acute pancreatitis in rats, oxygen radicals mediate increased peroxidation reactions which are accompanied by depletion of nonenzymatic sulfhydryl-containing free radical scavengers. The above phenomenon contributes to a disturbance in thiol metabolism resulting in serious diminution of pancreatic protein sulfhydryl compounds.

Glutathione monoethyl ester ameliorates caerulein-induced pancreatitis in the mouse.

“…Nonaka et al (23) found increased indices of pancreatic lipid peroxidation in mice fed a choline-deficient, ethionine-supplemented diet. In the caerulein model of acute pancreatitis, recent studies have described elevations in several indices of oxidant stress, such as malondialdehyde (24,25), conjugated dienes (24), and chemiluminescence (26).…”

Novel antioxidant ameliorates the fibrosis and inflammation of cerulein-induced chronic pancreatitis in a mouse model

“…Dabrowski and Chwiecko [29] and Neuschwander-Tetri et al [30] showed a marked decrease in pancreatic GSH content at an early stage of cerulein-induced pancreatitis in rats and mice, respectively. Similarly, Schoenberg et al [7] observed a significant reduction of GSH in ceruleinand sodium taurocholate-induced pancreatitis in rats.…”

Hydrogen Sulfide, Nitric Oxide and a Molecular Mass 66 u Substance in the Exhaled Breath of Chronic Pancreatitis Patients

“…Braganza [13] claimed that oxidative stress may play a role in the development of pancreatic inflammation. An increase in oxidative stress, as measured by increased lipid peroxidation and decreased antioxidant defenses, occurs in a number of experimental models of pancreatitis mainly in those studying acute pancreatic inflammation [14][15][16] . An increase in lipoperoxidation has also been reported in pancreatic juice and in resected pancreatic tissue samples of patients with CP [17,18] ; the decrease of the efficiency of plasma antioxidant defenses seems to correlate with the severity of pathological tissue changes [19][20][21][22][23] .…”