Polymorphonuclear leukocyte-mediated, antibody-dependent, cellular cytotoxicity against tumor cells: dependence on oxygen and the respiratory burst.
Polymorphonuclear leukocyte-mediated, antibody-dependent, cellular cytotoxicity against tumor cells: dependence on oxygen and the respiratory burst.
复制标题
多形核白细胞介导的、抗体依赖性的针对肿瘤细胞的细胞毒性：依赖于氧气和呼吸爆发。
DOI：
10.4049/jimmunol.123.1.55
复制
发表时间：
1979
影响因子：
4.4
通讯作者：
Z. J. Lucas
中科院分区：
文献类型：
--
作者：
D. Hafeman;Z. J. Lucas
进行实验以确定1）在多形核白细胞（PMN）中超氧阴离子（O2-）产生的呼吸爆发是否在抗体依赖性杀伤肿瘤细胞期间触发，以及2）O2-产生是否是细胞毒性所必需的。呼吸爆发的三个参数（1- 14 C-葡萄糖氧化，耗氧量和O2-释放）增加2.5至7.3倍，在杀死抗体引发的肿瘤细胞的人PMN。添加过氧化氢酶和超氧化物歧化酶没有抑制溶解，可能是因为这些酶无法扩散到杀伤细胞和靶细胞之间的质膜间隙。细胞毒性需氧的证据是异戊巴比妥或保泰松的浓度足以抑制PMN的氰化物不敏感呼吸也抑制细胞毒性。此外，缺氧条件抑制细胞毒性从29%至73%。对氧气的需求最可能与O2生成有关，而不是线粒体呼吸，因为氰化物和叠氮化物，抑制线粒体呼吸，增加细胞毒性。
Experiments were done to determine 1) whether the respiratory burst of superoxide anion (O2-) production in polymorphonuclear leukocytes (PMN) is triggered during antibody-dependent killing of tumor cells and 2) whether O2- production is essential for cytotoxicity. Three parameters of the respiratory burst (1-14C-glucose oxidation, oxygen consumption, and O2- release) were increased 2.5- to 7.3-fold during killing of antibody-primed tumor cells by human PMN. Added catalase and superoxide dismutase did not inhibit lysis, possibly because these enzymes were unable to diffuse into the inter-plasma-membrane space between killer and target cells. Evidence for an O2- requirement for cytotoxicity was the fact that concentrations of amobarbital or phenylbutazone sufficient to inhibit the cyanide-insensitive respiration of PMN also inhibited cytotoxicity. Also, hypoxic conditions inhibited cytotoxicity from 29 to 73%. The requirement for oxygen was most likely related to O2- generation and not mitochondrial respiration since cyanide and azide, which inhibit mitochondrial respiration, increased cytotoxicity.