Oliver J M, Berlin R D, Baehner R L, Boxer L A
Br J Haematol. 1977 Nov;37(3):311-22. doi: 10.1111/j.1365-2141.1977.tb01001.x.
Microtubule assembly in human polmorphonuclear leucocytes is a dynamic process that can be initiated by binding of the plant lectin Concanavalin A to surface receptors. Colchicine inhibits lectin-induced microtubule assembly and promotes the movement of Concanavalin A into surface caps. Inhibition of microtubule assembly and enhanced Concanavalin A cap formation also follow treatment of normal leucocytes with two specific glutathione-oxidizing agents, 'diamide' and tertiary butylhydroperoxide. Our objective here was to determine if microtubule inhibition is mediated via glutathione disulphide or via hydrogen peroxide that is generated in Concanavalin A-treated leucocytes and may accumulate when cells are depleted of reduced glutathione. We show that exogenous hydrogen peroxide induces Concanavalin A capping on normal polymorphonuclear leucocytes but only at concentrations that simultaneously oxidize glutathione. We also show that 'diamide' and tertiary butylhydroperoxide cause Concanavalin A cap formation in leucocytes from patients with chronic granulomatous disease. These cells cannot generate significant amounts of superoxide or hydrogen peroxide. Thus, it seems likely that the reversible inhibition of microtubule assembly and function caused by glutathione oxidants requires only increased glutathione disulphide and is not dependent on subsequent accumulation of other metabolites.
人多形核白细胞中的微管组装是一个动态过程，可由植物凝集素伴刀豆球蛋白A与表面受体结合引发。秋水仙碱抑制凝集素诱导的微管组装，并促进伴刀豆球蛋白A向表面帽的移动。用两种特定的谷胱甘肽氧化剂“二酰胺”和叔丁基过氧化氢处理正常白细胞后，也会出现微管组装抑制和伴刀豆球蛋白A帽形成增强的情况。我们在此的目的是确定微管抑制是通过二硫化谷胱甘肽介导，还是通过在伴刀豆球蛋白A处理的白细胞中产生且在细胞内还原型谷胱甘肽耗尽时可能积累的过氧化氢介导。我们发现外源性过氧化氢可诱导正常多形核白细胞上伴刀豆球蛋白A帽的形成，但仅在同时氧化谷胱甘肽的浓度下才会出现。我们还发现“二酰胺”和叔丁基过氧化氢可导致慢性肉芽肿病患者白细胞中伴刀豆球蛋白A帽的形成。这些细胞无法产生大量的超氧化物或过氧化氢。因此，谷胱甘肽氧化剂对微管组装和功能的可逆抑制似乎仅需要增加二硫化谷胱甘肽，而不依赖于其他代谢产物的后续积累。
