Abstract
Ascorbate is stabilized in the presence of HL-60 cells. This stabilization has been questioned as a simple chemical effect. Further properties and controls about the enzymatic nature of this stabilization are described and discussed. Our results showed that cAMP derivatives and cAMP-increasing agents stimulated the ability of HL-60 cells to stabilize ascorbate. On the other hand, tunicamycin, a glycosylation-interfering agent, inhibited this ability. These data, together with hormonal regulation, support the hypothesis of an enzymatic redox system located at the plasma membrane as being responsible for the extracellular ascorbate stabilization by HL-60 cells.
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