Silymarin increases antioxidant enzymes in alloxan-induced diabetes in rat pancreas

被引:136
作者
Soto, C
Recoba, R
Barrón, H
Alvarez, C
Favari, L
机构
[1] Univ Autonoma Metropolitana Xochimilco, Dept Sistemas Biol, Mexico City 04960, DF, Mexico
[2] IPN, Ctr Invest & Estudios Avanzados, Secc Externa Farmacol, Mexico City 07738, DF, Mexico
来源
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY | 2003年 / 136卷 / 03期
关键词
superoxide dismutase; glutathione peroxidase; catalase; lipid peroxidation; free radicals; pancreatic damage; hyperglycemia; defense mechanisms;
D O I
10.1016/S1532-0456(03)00214-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of this study was to analyze the effect of the flavonoid silymarin, a free radical scavenger that prevents lipoperoxidation, on the pancreatic activity of superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and catalase (CAT) in rats with alloxan-induced diabetes mellitus. Alloxan intoxicated rats were treated with silymarin in two manners, simultaneously (four or eight doses) or 20 days after alloxan administration for 9 weeks. Alloxan elicited a transient increase in the activity of the three enzymes, which decreased after 5 days of treatment. On its own, silymarin significantly increased the activity of these enzymes. Simultaneous treatment with alloxan and silymarin also induced an increment in the activity of the enzymes followed by a delayed decrease (four doses). However, a longer treatment with silymarin (eight doses) induced a more sustained effect. Interestingly, silymarin treatment recovered to control values for the activity of the three-antioxidant enzymes that were significantly diminished after 20 days of alloxan administration. It is suggested that the protective effect of silymarin on pancreatic damage induced by alloxan may be due to an increase in the activity of antioxidant enzymes that, in addition to the glutathione system, constitute the more important defense mechanisms against damage by free radicals. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:205 / 212
页数:8
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