Ohara T, Asaki S, Toyota T
Third Department of Internal Medicine, School of Medicine, Tohoku University, Sendai, Japan.
Nihon Shokakibyo Gakkai Zasshi. 1990 Jan;87(1):1-7.
In the experimental stress ulcer models of guinea pig superoxide dismutase-like plasma substance increased in plasma. Upon chromatography on heparin-Sepharose, this substance was separated into three fractions; A, without affinity for heparin; B, with intermediate affinity for heparin; C, with relatively strong heparin affinity, and the fraction C was specifically increased by a stress and a heparin injection. Analysis by a polyacrylamide gel electrophoresis (PAGE) of the fraction C revealed SOD activity, whose molecular weight was 135 K in a native state. The fraction C seemed to be the same as extracellular superoxide dismutase (EC-SOD) reported by Marklund. Assuming to the releasing potency of heparin, the major part of EC-SOD in the vasculature was most likely located on endothelial-cell surface. A pathophysiological role of EC-SOD released into plasma seemed to be an indicator of endothelial-cell damage by free radicals of endothelial cells and polymorphonuclear neutrophils (PMNs).
在豚鼠实验性应激性溃疡模型中，血浆中超氧化物歧化酶样血浆物质增加。在肝素-琼脂糖柱上进行层析时，该物质被分离为三个组分；A组对肝素无亲和力；B组对肝素有中等亲和力；C组对肝素有相对较强的亲和力，并且应激和注射肝素后C组分特异性增加。对C组分进行聚丙烯酰胺凝胶电泳（PAGE）分析显示具有超氧化物歧化酶（SOD）活性，其天然状态下的分子量为135kDa。C组分似乎与Marklund报道的细胞外超氧化物歧化酶（EC-SOD）相同。根据肝素的释放能力推测，脉管系统中EC-SOD的主要部分很可能位于内皮细胞表面。释放到血浆中的EC-SOD的病理生理作用似乎是内皮细胞和多形核中性粒细胞（PMN）自由基对内皮细胞损伤的一个指标。
