风湿性心脏病心肌线粒体DNA^（4977）的定量研究  

Quantitative study of myocardlal mitochondrialDNA4977deletion in rheumatic heart disease and its sig-nificance

作　　者：钱伟[1] 谢毅[1] 张宝仁[1] 朱家麟[1] 郝家骅[1] 陈如坤[1] 蔡凯华[1] 吴小舟[1] 

机构地区：[1]上海第二军医大学长海医院胸心外科,复旦大学遗传工程国家重点实验室

出　　处：《中华医学杂志》1995年第8期473-475,共3页National Medical Journal of China

摘　　要：为了探讨风湿性心脏病（风心病）心肌慢性缺血、缺氧损害心肌功能的机理，作者采用聚合酶链反应（ＰＣＲ）技术检测了１６例风心病患者心肌线粒体ＤＮＡ４９７７片段（ｍｔＤＮＡ４９７７）缺失率，同时测定了心肌丙二醛（ＭＤＡ）含量和超氧化物歧化酶（ＳＯＤ）活性。ＰＣＲ结果显示：正常对照组（ｎ＝１０）、年龄＞４５岁，ｍｔＤＮＡ４９７７缺失水平低，缺失率最高为０．００４２％，风心思音ｍｔＤＮＡ４９７７均有缺失，缺失率为０．０２％～１．２６％，明显高于对照组。由于ｍｔＤＮＡ４９７７缺夫导致氧化磷酸化复合物的蛋白质基因丢失，使氧化磷酸化抑制，ＡＴＰ合成减少，致使心肌功能恢复较差，另外．氧自由基可导致ｍｔＤＮＡ的损伤并产生缺失，风心病心肌ＭＤＡ含量增加，ＳＯＤ活力下降，表明心肌氧自由基量增加，序在ｍｔＤＮＡ４９７７缺失的内部条件。o better understand the mechaenisms of cardiacfunction damaged by chronic hypoxemia in rheumaticheart disease, we investigated the level of the 4977base pair mitochondrial DNA (mtDNA4977) deletion in16 patients with rheumatic heart disease (RHD)by us-ing polymerase chain reaction (PCR). Myocardial mal-ondialdehyde(SOD) activity was also measured. Incontrol group, mtDNA4977 deletion appeared after 45years old and reached a maximum of 0. 0042%. Ahigher level of mtDNA4977 deletion to. 02 %～1. 26 %)was found in RHD group. Because mtDNA4977deletionremoves 8 genes coding for subunits of complexes ofrespiratory chain, its deletion can inhibit oxidativephosphorylation, reduce ATP production and hinderthe recovery of cardiac function. In addition, myocar-dial MDA content increased and SOD activity decreasedin the RHD group as compared with the control group.This indicates that the generation of oxygen free radi-cals enhances and the elimilation of free radicals re-duces. Oxygen free radical can be an important factorin myocardialmitochondrial DNA injury and lead tomrtochondrial DNA deletion.

关 键 词：风湿性心脏病 心肌 线粒体 DNA 聚合酶链反应 

分 类 号：R541.202[医药卫生—心血管疾病]