脑血管疾病患者外周红细胞及其胞膜Cu/ZnSOD水平变化的观察

OBSERVATION ON THE Cu/Zn SOD IN CYTOSOLS AND MEMBRANES OF PERIPHERAL ERYTHROCYTES FROM THE PATIENTS WITH CEREBRAL VASCULAR DISEASE

本文报道50名健康人及33例脑血管疾病患者外周红细胞及其胞膜铜锌超氧化物歧化酶Cu/Zn SOD放免测定值。结果表明94％患者红细胞胞液Cu/Zn SOD呈极显著性降低(P<0.001),提示缺血性损伤病理过程中红细胞内超氧阴离子自由基(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,从而引起胞内SOD歧化作用而耗损增加。本文测定18例脑血栓形成患者红细胞膜Cu/ZnSOD含量未见明显变化(0.2>P>0.1),可能由于细胞间隙胞外SOD(EC-SOD)及RBC膜本身具有防御氧自由基作用有关,从而保护了RBC膜Cu/ZnSOD于平衡状态。本文还就其作用机理作了简要论述。

The values of Cu/Zn superoxidc dismutase (Cu/Zn SOD, SOD-1)in RBG cytosols and membranes were measured by radioimmunoassay in 50 normal subjects and 33 patients with cerebral vascular disease. The data obtained indicated that the SOD-1 in RBC cytosols decreased significantly ( P<0.001 ) in 94% of cerebral vascular disease, suggesting that intracellulular. oxygen radicals produced abnormalities in the pathological process of ischemic injury. It is that extracellular O2- could pass through the erythrocyte membranes entering cells via anion channel. The consumption of intracellular SOD-1 was increased by dismutation. But, no significant changes of SOD-1 in RBC membranes were observed, (in 18 patients with cerebral thrombosis ), which may be related to the extracellular EC-SOD, ceruloplasmin and red cell membranes. This is because all of them defend against oxygen radicals. Therefore, the erythiocyte membranes could obtain important regulators and supplements from their surroundings, protect the SOD-1 in red cell membranes and maintain a balance. Their mechanisms of action are discussed in this report.