BIOCHEMICAL-MECHANISMS OF OXFENICINE CARDIOTOXICITY
BIOCHEMICAL-MECHANISMS OF OXFENICINE CARDIOTOXICITY
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DOI：
10.1159/000138390
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发表时间：
1988-04-01
期刊：
影响因子：
3.1
通讯作者：
WEBER, E
中科院分区：
文献类型：
--
作者：
BACHMANN, E;WEBER, E
Oxfenicine（S-4-OH-苯基-甘氨酸）被认为是一种刺激心脏碳水化合物利用从而减少氧需求的化合物，特别是在缺血性心脏病中。对大鼠口服给药数周，导致心脏、肝脏和肾脏重量增加。这种药物破坏了线粒体代谢，减少了所有三个器官的耗氧量和解偶联氧化磷酸化。心肌线粒体肌酸磷酸激酶被抑制，线粒体肌酸含量增加。心肌细胞膜功能（Ca uptke以及Na/K-、Mg-和Ca-ATP酶）受到抑制。在所有三个器官中，脂质（磷脂和甘油三酯）以及游离脂肪酸显示出一过性蓄积。
Oxfenicine (S-4-OH-phenyl-glycine) was proposed as a compound which would stimulate carbohydrate utilization in the heart and thus reduce oxygen requirement, especially in ischemic heart disease. Oral administration to rats for several weeks gave rise to an increase in heart, liver and kidney weights. The drug damaged mitochondrial metabolism, reducing oxygen consumption and uncoupling oxidative phosphorylation in all three organs. In heart mitochondria creatine phosphate kinase was inhibited and the creatine content of the mitochondria increased. Myocyte membrane functions (Ca uptke as well as Na/K-, Mg- and Ca-ATPases) were inhibited. In all three organs lipids (phospholipids and triglycerides) as well as free fatty acids showed a transient accumulation.