Changes in Lipid Peroxide and Oxygen Radical Scavengers in Cerulein-Induced Acute Pancreatitis

Abstract

The role of free radicals in the development of cerulein-induced pancreatitis was evaluated by measuring the activity of the endogenous scavengers, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHpx), as indicators of the defense system, and the level of lipid peroxide (LPO) in the pancreas, as an indicator of the offense system. Acute pancreatitis was induced by 5 hourly intraperitoneal administrations of cerulein (50 μg/kg body weight), in 0.9% NaCl, to mice. The presence of acute pancreatitis was confirmed by changes in serum amylase levels and in typical microscopical features. Regarding the changes in the levels of endogenous scavengers, the SOD level was decreased significantly from a basal level of 52.6 ± 3.94 to 43.1 ± 2.79 mU/μg DNA at 6 h (p < 0.01) to 38.8 ± 5.18 mU/μg DNA at 9 h (p < 0.05) and to 31.7 ± 3.10 mU/μg DNA at 12 h (p < 0.01) after the first intraperitoneal cerulein injection. The CAT level also decreased significantly from a basal level of 7.80 ± 0.27 to 5.86 ± 0.46 mU/μg DNA at 9 h (p < 0.01) and to 4.52 ± 0.21 mU/μg DNA at 12 h (p < 0.01). GSHpx increased from a basal level of 6.80 ± 0.43 to 7.58 ± 0.50 mU/μg DNA at 9 h and to 10.2 ± 0.52 mU/μg DNA at 12 h after the first intraperitoneal cerulein injection. The LPO level increased from a basal level of 1.11 ± 0.48 to 7.22 ± 1.75 nmol/ml at 3.5 h(p < 0.05), 5.40 ± 1.50 nmol/ml at 6 h(p < 0.05), 3.86 ± 1.07 nmol/ml at 9 h (p < 0.05) and 3.18 ± 1.18 nmol/ml at 12 h (p < 0.01) after the first intraperitoneal cerulein injection. These results indicate that tissue imbalances of the offense system, indicated by changes in the level of LPO, and of the defense system, indicated by changes in the levels of SOD and CAT, might result in the development of tissue damage induced by oxygen-derived free radicals.

The Dynamics of the Oxidant-Antioxidant Balance in the Early Phase of Human Acute Biliary Pancreatitis

“…Most studies published so far, using animal models, showed rapid increases in concentrations of peroxidation products both in pancreatic tissue and serum, with peak changes during the first 6 h after induction of pancreatitis [8,9,[27][28][29][30]. Results of the very few studies in human AP published so far confirmed the presence of similar, but somewhat less dynamic, disturbances of the oxidantantioxidant balance [14][15][16].…”

Free radicals and the pancreatic acinar cells: role in physiology and pathology

“…Oxidative stress was documented in pancreatic tissue by detecting generation of ROS with chemiluminescence (Gough et al 1990) or fluorescence (Urunuela et al 2002) and accumulation of products of ROS-mediated lipid peroxidation (Nonaka et al 1989b(Nonaka et al , 1990Guyan et al 1990; Schoenberg et al , 1995Tsai et al 1998;Rau et al 2000) and protein modification (Reinheckel et al 1998), with concomitant depletion of low molecular weight antioxidants (Neuschwander-Tetri et al 1994;Luthen et al 1995;Tsai et al 1998;Schulz et al 1999;Kruse et al 2001;Rau et al 2001;Rahman et al 2004). It was also confirmed by ESR spectroscopy using spin traps (Nonaka et al 1989a).…”

The Natural Flavonoid Quercetin Ameliorates Cerulein-Induced Acute Pancreatitis in Mice

“…1,6,26,27) TNF-a, IL-1b, and IL-6 were found to be enhanced in both experimental pancreatitis as well as in pancreatitis patients. [28][29][30] TNF-a plays a pivotal role in severe acute pancreatitis, acting early in the disease course.…”