摘要
为探讨铬对实验性心肌损伤的保护作用机制，选用Ｗｉｓｔａｒ大鼠腹肢内注射铬，尾静脉注射阿霉素，复制动物模型，用荧光偏振法测定心肌线粒体膜流动性，低温电子自旋共振技术测定心肌及肝脏自由基含量，同时观察抗氧化酶及心肌酶活性变化。结果表明单纯注射阿霉素大鼠心肌线粒体膜流动性降低，血清ＬＤＨ及ＣＰＫ活性增强，心肌及肝脏自由基含量升高，全血、心肌及肝脏ＧＳＨ－Ｐｘ活性降低，血清ＳＯＤ活性增强，心肌及肝脏ＳＯＤ活性降低。铬保护的大鼠心肌线粒体膜流动性改善，ＬＤＨ及ＣＰＫ释放减少，心肌及肝脏自由基含量降低，ＧＳＨ－Ｐｘ活性增强。维持膜的稳定性，增强抗氧化功能。可能是铬抗心肌损伤的重要机制。
In order to investigate the protecting mechanism of chromium on experimental myocardial injury , the animal models of myocardiopathy in rats were reconstructed with chromium , selenium and adri- amycin. The membrane lipid fludity (FLU) of myocadial mitochondria was determined with fluorescent polarimetry. The free radicals of myocardium and liver were measured by using low-temperature elec- tronic spin resonance (ESR ) technique. At the same time ,LDH ,CPK ,GSH-Px and SOD activities were observed. The results showed that in rats received adriamycin (2mg/kg ,once a week , for 7 weeks ) , the membrane lipid fluidity of myocardial mitochondria was decreased ,but LDH and CPK activities in serum were increasted. The contents of free radicals in myocardium and liver were markedly increased, but GSH-Px activities were decreased in blood ,myocardium and liver. SOD activities rose in serum ,but re- duced in myocardium and liver. In rats received chromium or selenium and adriamycin , the FLU im- proved ,LDH and CPK release reduced. The contents of free radicals were markedly decreased ,but GSH- Px activities were increased. These results indicated to keep normal function of membrane and to in- crease antioxidation function might be the important protected mechanism of chromium on experimental myocardial injury.
出处
《中国地方病学杂志》
CAS
CSCD
1997年第6期321-325,共5页
Chinese Jouranl of Endemiology
基金
国家自然基金
关键词
心肌损伤
阿霉素
铬
心肌保护
微量元素
Myocardial injury Adriamycin Chromium Membrane lipid fluidity Free rad- icals
