Jones O T
Biochemistry Department, Bristol University, UK.
Mol Chem Neuropathol. 1993 May-Jun;19(1-2):177-84. doi: 10.1007/BF03160177.
Superoxide is produced by phagocytic cells at rates sufficient to have cytocidal effects. A wide variety of receptor-dependent and -independent agonists triggers this respiratory burst, including immunoglobin aggregates, complement fragments, and leukotriene B4. Lower rates of O2-. production are triggered by addition of specific cytokines into B-lymphocytes, endothelial cells, fibroblasts, and kidney mesangial cells; low concentration of radicals may act as signals for proliferation or other changes. The NADPH oxidase of phagocytes, characterized by the presence of FAD and a low potential cytochrome b, is organized to transfer electrons electrogenically across the plasma membrane from NADPH to O2. A proton channel permits movement of compensating H+.
吞噬细胞产生超氧化物的速率足以产生细胞杀伤作用。多种受体依赖性和非依赖性激动剂可触发这种呼吸爆发,包括免疫球蛋白聚集体、补体片段和白三烯B4。向B淋巴细胞、内皮细胞、成纤维细胞和肾系膜细胞中添加特定细胞因子可触发较低速率的O2-产生;低浓度的自由基可能作为增殖或其他变化的信号。吞噬细胞的NADPH氧化酶以含有FAD和低电位细胞色素b为特征,其作用是将电子从NADPH经电化学方式穿过质膜传递给O2。质子通道允许补偿性H+的移动。