Ascorbate-mediated transmembrane electron transport and ascorbate uptake in leukemic cell lines are two different processes.
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.
Schweinzer
E
E
Institut für Medizinische Chemie, Universität Wien, Austria.
Goldenberg
H
H
D001205:Ascorbic Acid / Q000378:metabolism / Q000494:pharmacology*; D001692:Biological Transport; D002462:Cell Membrane / Q000378:metabolism*; D003470:Culture Media; D003683:Dehydroascorbic Acid / Q000494:pharmacology; D004579:Electron Transport / Q000187:drug effects*; D005292:Ferricyanides / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D004915:Leukemia, Erythroblastic, Acute / Q000378:metabolism*; D016403:Lymphoma, Large B-Cell, Diffuse / Q000378:metabolism*; D010084:Oxidation-Reduction; D014407:Tumor Cells, Cultured
D003470:Culture Media; D005292:Ferricyanides; C007931:hexacyanoferrate III; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid