Schweinzer E, Goldenberg H
Institut für Medizinische Chemie, Universität Wien, Austria.
Eur J Biochem. 1992 Jun 15;206(3):807-12. doi: 10.1111/j.1432-1033.1992.tb16988.x.
Transmembrane reduction of extracellular oxidants by K562 and U937 leukemic cells was stimulated by catalytic amounts of ascorbate or dehydroascorbate. This stimulation was not due to transport of ascorbate in different redox states in and out of the cells. The membrane redox cycle was strictly dependent on the presence of the cells at every stage, and showed high affinity for ascorbate with simple linear kinetics. Metabolic inhibitors and sulfhydryl reagents inhibited this stimulation. Ascorbate uptake was also dependent on oxidation, but in a very different manner and with much lower affinity for ascorbate. The uptake was non-saturable in the concentration range used. There was some release of ascorbate from the cells, which cannot account for an appreciable part of the reduction of extracellular electron acceptors.
K562和U937白血病细胞对细胞外氧化剂的跨膜还原作用可被催化量的抗坏血酸或脱氢抗坏血酸所刺激。这种刺激并非源于处于不同氧化还原状态的抗坏血酸进出细胞的转运。膜氧化还原循环在每个阶段都严格依赖于细胞的存在，并且对抗坏血酸表现出高亲和力以及简单的线性动力学。代谢抑制剂和巯基试剂会抑制这种刺激作用。抗坏血酸的摄取也依赖于氧化作用，但方式截然不同，且对抗坏血酸的亲和力低得多。在所使用的浓度范围内，摄取是不饱和的。细胞有一些抗坏血酸的释放，但这并不能解释细胞外电子受体还原的可观部分。
