Hepatoprotective role and antioxidant capacity of selenium on arsenic-induced liver injury in rats

被引:141
作者
Messarah, Mahfoud [1 ]
Klibet, Fahima [2 ]
Boumendjel, Amel [2 ]
Abdennour, Cherif [2 ]
Bouzerna, Noureddine [2 ]
Boulakoud, Mohamed Salah [1 ]
El Feki, Abdelfattah [3 ]
机构
[1] Badji Mokhtar Univ, Fac Sci, Anim Ecophysiol Lab, Annaba, Serbia
[2] Badji Mokhtar Univ, Fac Sci, Appl Biochem & Microbiol Lab, Annaba, Serbia
[3] Fac Sci, Anim Ecophysiol Lab, Sfax 3018, Tunisia
关键词
Arsenic; Antioxidant enzymes; Liver; Oxidative stress; Rat; Selenium; INDUCED OXIDATIVE STRESS; LIPID-PEROXIDATION; ALPHA-TOCOPHEROL; FREE-RADICALS; DIETARY SUPPLEMENTATION; PROTECTIVE ROLE; NERVOUS-SYSTEM; GLUTATHIONE; EXPOSURE; ACID;
D O I
10.1016/j.etp.2010.08.002
中图分类号
R36 [病理学];
学科分类号
100103 [病原生物学];
摘要
The present study was undertaken to evaluate the protective effect of selenium against arsenic-induced oxidative damage in experimental rats. Males were randomly divided into four groups where the first was served as a control, whereas the remaining groups were respectively treated with sodium selenite (3 mg/kg b.w.), sodium arsenite (5.55 mg/kg b.w.)and a combination of sodium arsenite and sodium selenite. Changes in liver enzyme activities, thiobarbituric acid reactive substances (TBARS) level, antioxidants and reduced glutathione (GSH) contents were determined after 3 weeks experimental period. Exposure of rats to As caused a significant increase in liver TBARS compared to control, but the co-administration of Se was effective in reducing its level. The activities of glutathione peroxidase (GPx) and glutathione-S-transferase (GST) of As-treated group were found lower compared to the control and the Se-treated group. The co-administration of Se had an additive protective effect on liver enzyme activities compared to As-treated animals. On the other hand, a significant increase in plasmatic activities of AST, ALT and ALP was observed in As-treated group. The latter was also exhibited a decrease in body weight and an increase in liver weight compared to the control. The co-administration of Se has decreased the activities of AST, AST and ALP and improved the antioxidant status as well. Liver histological studies have confirmed the changes observed in biochemical parameters and proved the beneficial role of Se. To conclude, results suggest that As exposure enhanced an oxidative stress by disturbing the tissue antioxidant defense system, but the Se co-administration protected liver tissues against As intoxication probably owing to its antioxidant properties. (C) 2010 Elsevier GmbH. All rights reserved.
引用
收藏
页码:167 / 174
页数:8
相关论文
共 100 条
[1]
Afzal Mohammed, 2002, Methods Mol Biol, V186, P117
[2]
Oxidative stress by inorganic arsenic: modulation by thyroid hormones in rat [J].
Allen, T ;
Rana, SVS .
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY, 2003, 135 (02) :157-162
[3]
[Anonymous], 2001, ARS DRINK WAT 2001 U
[4]
[Anonymous], 1984, METHODS ENZYMOL, DOI DOI 10.1016/S0076-6879(78)52032-6]
[5]
How is inorganic arsenic detoxified? [J].
Aposhian, HV ;
Zakharyan, RA ;
Wildfang, EK ;
Healy, SM ;
Gailer, J ;
Radabaugh, TR ;
Bogdan, GM ;
Powell, LA ;
Aposhian, MM .
ARSENIC EXPOSURE AND HEALTH EFFECTS, 1999, :289-297
[6]
Aposhian HV., 1989, Rev Biochem Toxicol, V10, P265
[7]
Binding of α-tocopherylquinone, an oxidized form of α-tocopherol, to glutathione-S-transferase in the liver cytosol [J].
Arita, M ;
Sato, Y ;
Arai, H ;
Inoue, K .
FEBS LETTERS, 1998, 436 (03) :424-426
[8]
In vitro tissue specificity for arsine and arsenite toxicity in the rat [J].
Ayala-Fierro, F ;
Barber, DS ;
Rael, LT ;
Carter, DE .
TOXICOLOGICAL SCIENCES, 1999, 52 (01) :122-129
[9]
Arsenic induces oxidant stress and NF-kappa B activation in cultured aortic endothelial cells [J].
Barchowsky, A ;
Dudek, EJ ;
Treadwell, MD ;
Wetterharn, KE .
FREE RADICAL BIOLOGY AND MEDICINE, 1996, 21 (06) :783-790
[10]
Effect of selenium on rat thioredoxin reductase activity - Increase by supranutritional selenium and decrease by selenium deficiency [J].
Berggren, MM ;
Mangin, JF ;
Gasdaska, JR ;
Powis, G .
BIOCHEMICAL PHARMACOLOGY, 1999, 57 (02) :187-193