Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

K Batcioglu,M Esrefoglu,M Gul,A.B Uyumlu

doi:10.1590/s0100-879x2009000900001

K Batcioglu, M Esrefoglu + Show 2 more

Open Access

https://doi.org/10.1590/s0100-879x2009000900001

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Abstract

The aim of this study was to evaluate the role of oxidative damage in pancreatitis-induced hepatic injury. Thirty-five rats were divided into five groups (each of 7 rats): control, cerulein (100 microg/kg body weight), cerulein and pentoxifylline (12 mg/kg body weight), cerulein plus L-NAME (10 mg/kg body weight) and cerulein plus L-arginine (160 mg/kg body weight). The degree of hepatic cell degeneration differed significantly between groups. Mean malondialdehyde levels were 7.00 +/- 2.29, 20.89 +/- 10.13, 11.52 +/- 4.60, 18.69 +/- 8.56, and 8.58 +/- 3.68 nmol/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Mean catalase activity was 3.20 +/- 0.83, 1.09 +/- 0.35, 2.05 +/- 0.91, 1.70 +/- 0.60, and 2.85 +/- 0.47 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively, and mean glutathione peroxidase activity was 0.72 +/- 0.25, 0.33 +/- 0.09, 0.37 +/- 0.04, 0.34 +/- 0.07 and 0.42 +/- 0.1 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Cerulein-induced liver damage was accompanied by a significant increase in tissue malondialdehyde levels (P < 0.05) and a significant decrease in catalase (P < 0.05) and GPx activities (P < 0.05). L-arginine and pentoxifylline, but not L-NAME, protected against this damage. Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancreatitis-induced hepatic damage.

Highlights

Acute pancreatitis (AP) is an inflammatory disease with pathophysiological mechanisms that have not been thoroughly elucidated and few, if any, effective treatments
Nitric oxide (NO) is a free radical that is synthesized during the reaction of L-arginine with oxygen, a reaction that is catalyzed by NO synthase (NOS) enzymes
To evaluate the effect of these agents, the rats were divided into three additional groups (N = 7): the first group was treated with cerulein (100 μg/kg body weight) and pentoxifylline (Sigma-Aldrich; 12 mg/kg body weight), the second group was treated with the same dose of cerulein plus L-arginine (Sigma-Aldrich; 160 mg/kg body weight), and the third group received the same dose of cerulein plus L-NAME (Sigma-Aldrich; 10 mg/kg body weight)

Summary

Introduction

Acute pancreatitis (AP) is an inflammatory disease with pathophysiological mechanisms that have not been thoroughly elucidated and few, if any, effective treatments. AP is characterized by edema, hemorrhage and necrosis of the pancreas related to tissue damage in the pancreas and its adjacent tissues, such as the liver. This damage is caused by the activation of normally inactive digestive enzymes owing to some etiologic factor [1]. Oxidative stress caused by free radicals has been proposed as a common mechanism for pancreatic injury in alcohol, gallstone and ischemic pancreatitis [4], as well as in other experimental models of acute pancreatitis [5]. Schoenberg et al [6] have shown that the concentration of malondialdehyde in the pancreas increases during edematous acute pancreatitis, indicating free radical-mediated lipid peroxidation. In the presence of a superoxide radical, excess NO is converted to an even more toxic molecule, peroxynitrite (ONOO−), which directly damages proteins and decomposes to other toxic products, such as nitronium ion, nitrogen dioxide gas and hydroxyl radicals [7]

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