Shainkin-Kestenbaum R, Caruso C, Berlyne G M
Nephrology Section, Brooklyn VA Medical Center, N.Y.
Nephron. 1990;55(3):251-3. doi: 10.1159/000185970.
Superoxide dismutase (SOD) plays a major part in the destruction of oxygen-free radicals in the body. SOD activity is impaired by several trace elements including aluminium and silicon which are found in increased levels in plasma and tissues of uremic man. SOD activity was investigated in the erythrocytes of normal controls and of dialysis patients to determine if lack of SOD-protective activity could be a contributory cause to the increased hemolysis of uremia. It was found that SOD levels in red cell hemolysate were significantly lower in dialysis patients (41.4 +/- 9.1 units/100 ml) compared to control (49.3 +/- 7.2 units/100 ml) (U = 7.3; p less than 0.005). When expressed per 100 ml of whole blood SOD levels were 3.25 +/- 0.93 units/100 ml in dialysis patients and 6.46 +/- 0.99 units/100 ml in controls (U = 96; p less than 0.001). It is concluded that inhibition of SOD activity in the erythrocytes of dialysis patients may contribute to their anemia.
超氧化物歧化酶(SOD)在体内氧自由基的破坏过程中起主要作用。SOD活性会受到包括铝和硅在内的几种微量元素的损害,这些元素在尿毒症患者的血浆和组织中的含量会升高。对正常对照组和透析患者的红细胞中的SOD活性进行了研究,以确定缺乏SOD保护活性是否可能是导致尿毒症患者溶血增加的一个促成因素。结果发现,与对照组(49.3±7.2单位/100毫升)相比,透析患者红细胞溶血产物中的SOD水平显著降低(41.4±9.1单位/100毫升)(U = 7.3;p<0.005)。以每100毫升全血计算,透析患者的SOD水平为3.25±0.93单位/100毫升,对照组为6.46±0.99单位/100毫升(U = 96;p<0.001)。得出的结论是,透析患者红细胞中SOD活性的抑制可能是导致其贫血的原因之一。