Protective effects of erdosteine against doxorubicin-induced cardiomyopathy in rats

被引:96
作者
Fadillioglu, E
Erdogan, H
Sögüt, S
Kuku, I
机构
[1] Inonu Univ, Fac Med, Dept Physiol, Malatya, Turkey
[2] Inonu Univ, Fac Med, Dept Biochem, Malatya, Turkey
[3] Inonu Univ, Fac Med, Dept Haematol, Malatya, Turkey
关键词
doxorubicin; erdosteine; cardiotoxicity; oxidants; antioxidants; lipid peroxidation; catalase; superoxide dismutase; glutathione peroxidase;
D O I
10.1002/jat.889
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The usefulness of doxorubicin (DXR) is limited by its cardiotoxicity. In order to improve future DXR therapy by using a new antioxidant agent, an experimental study was designed. This study was undertaken to determine whether DXR-induced cardiotoxicity is prevented by erdosteine, a mucolytic agent showing antioxidant properties. Three groups of male Sprague-Dawley rats (60 days old) were used: one group was untreated as a control; the other groups were treated with DXR (single i.p. dosage of 20 mg kg(-1) body wt.) or DXR plus erdosteine (10 mg kg(-1) day(-1), orally), respectively. The DXR treatment without erdosteine increased antioxidant enzyme activities and also increased lipid peroxidation in myocardial tissue. The rats treated with DXR plus erdosteine produced a significant decrease in lipid peroxidation in comparison with control and DXR groups. Furthermore, erdosteine administration led to an increase in antioxidant enzyme activities in comparison with the control group. Erdosteine treatment also increased the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in comparison with the DXR group. There was no significant difference in lipid peroxidation of myocardial tissue between control and DXR plus erdosteine-treated rats. It was concluded that erdosteine caused an increase in the activities of antioxidant enzymes, especially GSH-Px and CAT, protecting the heart tissue sufficiently from oxidative damage to membrane lipids and other cellular components induced by DXR. Copyright (C) 2003 John Wiley Sons, Ltd.
引用
收藏
页码:71 / 74
页数:4
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