J OURNAOFL B IOLOGICACLH EMISTRY 33, NVol.. 267, Issue of November 25, pp. 23568-23574,1992
in U. S. A.
of Ascorbic Acid Transport in Human Neutrophils
(Received for publication, May 22, 1992)
Philip Washko and Mark Levine$
From the Laboratory
of Cell Biology and Genetics, National Institute of Diabetes and Digestiue and Kidney Diseuses, National
of Health, Bethesda, Maryland 20892
Because of the structural similarity between glucose
and ascorbic acid, we investigated the effect of glucose
on uptake and accumulation of ascorbic acid in isolated
normal human neutrophils. Ascorbic acid accumulation
was determined using high-performance liquid
chromatography with coulometric electrochemical detection,
in conjunction with liquid scintillation spectrometry.
Ascorbic acid accumulation in neutrophils is
mediated by a high and a low affinity transport activity.
In neutrophils from different volunteers, glucose
inhibited uptake and accumulation of ascorbic acid by
both transport activities 3-9-fold. The mechanism of
inhibition was different for each transport activity:
inhibition of the high affinity transport activity was
noncompetitive, while inhibition of the low affinity
activity was competitive. Glucose-induced inhibition
of both ascorbic acid transport activities occurred in
neutrophils of all donors tested and was fully reversible.
Although the mechanism of ascorbic acid accumulation
appeared to be different than that for glucose
transport, other monosaccharides and glucose transport
inhibitors also inhibited ascorbic acid accumulation.
These are the first data to suggest that ascorbic
acid accumulation in neutrophils can be regulated by
compounds of similar structure.