Aminotriazole attenuated carbon tetrachloride-induced oxidative liver injury in mice

被引：28

作者：

Deng, Xinyu ^{[1
]}

Wu, Kunwei ^{[1
]}

Wan, Jingyuan ^{[2
]}

Li, Longjiang ^{[1
]}

Jiang, Rong ^{[3
]}

Jia, Mengying ^{[1
]}

Jing, Yuping ^{[1
]}

Zhang, Li ^{[1
]}

机构：

[1] Chongqing Med Univ, Dept Pathophysiol, Chongqing, Peoples R China

[2] Chongqing Med Univ, Dept Pharmacol, Chongqing, Peoples R China

[3] Chongqing Med Univ, Lab Stem Cell & Tissue Engn, Chongqing, Peoples R China

来源：

FOOD AND CHEMICAL TOXICOLOGY | 2012年 / 50卷 / 09期

关键词：

Aminotriazole; Catalase; Carbon tetrachloride; Oxidative stress; Acute liver injury; INDUCED LIPID-PEROXIDATION; CATALASE ACTIVITY; FREE-RADICALS; CYTOCHROME-P450; HEPATOTOXICITY; STRESS; ANTIOXIDANTS; INFLAMMATION; INHIBITION; MECHANISMS;

D O I：

10.1016/j.fct.2012.05.052

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Carbon tetrachloride (CCl4) has been used extensively to study xenobiotic-induced oxidative liver injury. Catalase (CAT) is a major antioxidant enzyme while aminotriazole (ATZ) is commonly used as a CAT inhibitor. In the present study, the effects of ATZ on CCl4-induced liver injury were investigated. Our experimental data showed that pretreatment with ATZ significantly decreased CCl4-induced elevation of serum aspartate transaminase (AST) and alanine transaminase (ALT) and improved hepatic histopathological abnormality. ATZ dose-dependently inhibited the activity of CAT, but it reduced the content of H2O2 and the levels of malondialdehyde (MDA) in liver tissues. ATZ decreased plasma level of pro-inflammatory cytokines (TNF-alpha. and IL-6) and reduced hepatic levels of myeloperoxidase (MPO). In addition, posttreatment with ATZ also decreased the level of ALT and AST. These data indicated that ATZ effectively alleviated CCl4-induced oxidative liver damage. These findings suggested that ATZ might have potential value in preventing oxidative liver injury. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：3073 / 3078

页数：6

共 39 条

[1] Myeloperoxidase and elastase are only expressed by neutrophils in normal and in inflammed liver [J].

Amanzada, Ahmad ;

Malik, Ihtzaz Ahmed ;

Nischwitz, Martin ;

Sultan, Sadaf ;

Naz, Naila ;

Ramadori, Giuliano .

HISTOCHEMISTRY AND CELL BIOLOGY, 2011, 135 (03) :305-315

[2] Human myeloperoxidase in innate and acquired immunity [J].

Arnhold, Juergen ;

Flemmig, Joerg .

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2010, 500 (01) :92-106

[3] The role of inflammatory cells and cytochrome P450 in the potentiation of CCl4-induced liver injury by a single dose of retinol [J].

Badger, DA ;

Sauer, JM ;

Hoglen, NC ;

Jolley, CS ;

Sipes, IG .

TOXICOLOGY AND APPLIED PHARMACOLOGY, 1996, 141 (02) :507-519

[4] Carbon tetrachloride-induced lipid peroxidation: eicosanoid formation and their regulation by antioxidant nutrients [J].

Basu, S .

TOXICOLOGY, 2003, 189 (1-2) :113-127

[5]

Cesaratto Laura, 2004, Ann Hepatol, V3, P86

[6] Catalase transgenic mice: characterization and sensitivity to oxidative stress [J].

Chen, XL ;

Liang, HY ;

Van Remmen, H ;

Vijg, J ;

Richardson, A .

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2004, 422 (02) :197-210

[7] Serum and liver concentrations of tumor necrosis factor α and interleukin-1β following administration of carbon tetrachloride to male rats [J].

DeCicco, LA ;

Rikans, LE ;

Tutor, CG ;

Hornbrook, KR .

TOXICOLOGY LETTERS, 1998, 98 (1-2) :115-121

[8] Free radicals in the physiological control of cell function [J].

Dröge, W .

PHYSIOLOGICAL REVIEWS, 2002, 82 (01) :47-95

[9] Activation of catalase by apelin prevents oxidative stress-linked cardiac hypertrophy [J].

Foussal, Camille ;

Lairez, Olivier ;

Calise, Denis ;

Pathak, Atul ;

Guilbeau-Frugier, Celine ;

Valet, Philippe ;

Parini, Angelo ;

Kunduzova, Oksana .

FEBS LETTERS, 2010, 584 (11) :2363-2370

[10] The wanderings of a free radical [J].

Halliwell, Barry .

FREE RADICAL BIOLOGY AND MEDICINE, 2009, 46 (05) :531-542

← 1 2 3 4 →