脑梗塞患者外周红细胞Cu/Zn SOD水平变化的观察  

Observation on SOD—1 in Cytosols and Membranes of Peripheral Erythrocytes from Patients with Cerebral Infarction

作　　者：吴怀志[1] 王洛夫[2] 赵明敏[3] 

机构地区：[1]中国人民解放军123医院 [2]蚌埠医学院核医学教研室 [3]蚌埠医学院药理教研室

出　　处：《微循环学杂志》1993年第1期16-17,共2页Chinese Journal of Microcirculation

摘　　要：本文报告18例脑梗塞患者及50例正常人外周RBC胞液及其胞膜SOD—1(Cu/Zn—SOD)放免测定值,结果表明94.44％的脑梗塞患者红细胞液SOD—1呈极显著性降低(P<0.001),提示脑梗塞病理过程中红细胞内氧自由基(O_2^-)产生异常。胞外O_2^-可通过RBC膜阴离子通道进入胞内增多,引起胞内SOD—1歧化作用而耗损增加,导致RBC胞液SOD—1降低。本文还观察10例脑梗塞患者RBC膜SOD—1含量未见明显变化,并就RBC内O_2^-产生异常的机理作简要论述。The valves of Cu/Zn SOD (Cu/Zn superoxide dismutase, SOD—1) in RBC cytosols and membranes were measured by radioimmunoassay in 50 normal subjects and 18 patients with cerebral infarction. The data obtained indicated that the SOD—1 in RBC cytosols decreased significantly (P<0.001) in 94.44％ of cerebral infarction, suggesting that intracellular oxygen radicals produced abnormalities in the pathological process of cerebral infarction. It is that extracelullar O_2 could pass through the erythrocyte membranes entering cells via anion channel. The consumption of intracelullar SOD—1 was increased by dismutation. But, no significant changes SOD—1 in erythrocyte membranes were observated (in 10 patients with cerebral infarction). Also, the mechanism of intracelullar oxygen radicals produced abnormalities are discussed in this report.

关 键 词：脑梗塞 红细胞 Cu/ZnSOD 放免测定 

分 类 号：R743.33[医药卫生—神经病学与精神病学]