Matsuda A, Kimura M, Itokawa Y
Development Laboratories, Nippon Hoechst Marion Roussel Ltd., Shiga, Japan.
Biol Trace Elem Res. 1997 May;57(2):157-67. doi: 10.1007/BF02778199.
The influence of selenium (Se) deficiency on the acute cardiotoxicity induced by the anticancer drug adriamycin (ADR) has been studied in rats by electrocardiography. Two categories were formed by feeding groups of rats a Se-supplemented and a Se-deficient diet. The supplemented animals were taken as normals. The two categories were treated with iv injections of saline solution containing ADR at doses of 0, 7.5, and 15 mg/kg body wt. The cardiac Se concentration and glutathione peroxidase (GSH-Px) activity in the Se-deficient groups were < 2% lower than in the normals. The normal groups showed significant widening of the SaT and QaT durations when given 15 mg/kg ADR. The Se-deficient groups exhibited a dose-dependent widening of the SaT and QaT duration at 7.5 and 15 mg/kg and narrowing of the PQ duration at 15 mg/kg ADR. No heart rate or QRS duration changes were detected in both categories. Our results suggest that an imbalance of the antioxidant system is associated with Se deficiency and that Se plays a role in preventing the cardiac functional disorder attributable to oxygen free radical formation induced by ADR.
通过心电图研究了缺硒对大鼠体内抗癌药物阿霉素（ADR）所致急性心脏毒性的影响。通过给大鼠喂食补硒饮食和缺硒饮食形成两组。喂食补硒饮食的动物作为正常组。两组均静脉注射含0、7.5和15mg/kg体重ADR的盐溶液。缺硒组的心脏硒浓度和谷胱甘肽过氧化物酶（GSH-Px）活性比正常组低<2%。正常组给予15mg/kg ADR时，SaT和QaT间期显著延长。缺硒组在给予7.5和15mg/kg ADR时，SaT和QaT间期呈剂量依赖性延长，在给予15mg/kg ADR时PQ间期缩短。两组均未检测到心率或QRS间期变化。我们的结果表明，抗氧化系统失衡与缺硒有关，并且硒在预防ADR诱导的氧自由基形成所致心脏功能障碍中起作用。
