AJP - Renal Physiology, Vol 256, Issue 1 52-F56, Copyright © 1989 by American Physiological Society
Renal metabolism of the oxidized form of ascorbic acid (dehydro-L-ascorbic acid)
R. C. Rose
Department of Surgery, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
We evaluated whether specific transport and metabolic properties exist in
rat and guinea pig kidney for handling the immediate oxidative product of
ascorbic acid, dehydro-L-ascorbic acid. Isolated tubules were used to
measure uptake of 10 microM [14C]-dehydro-L-ascorbic acid over an 8-min
incubation period. Uptake did not show dependence on the bathing media
electrolyte composition but was inhibited to some extent by glucose. In
tubules of both animal species the majority of 14C label present in the
tissue extract was in the reduced form. No degredative enzymatic effect on
dehydro-L-ascorbic acid is evident. Thirty-six percent of the
[14C]dehydro-L-ascorbic acid reduced by the tubules was released during an
8-min incubation. Recently formed ascorbic acid is not substantially bound
to cellular components. A factor necessary for dehydro-L-ascorbic acid
reduction in renal cortex was found primarily in the 55-70% ammonium
sulfate fraction. It is retained by mol wt 12,000 dialysis tubing, is heat
labile, pH sensitive, inhibited by thiol reagents, and is most active in
the presence of NADPH and glutathione. It has a molecular weight between
that of blue dextran and cytochrome c as indicated by gel chromatography.
We suggest that a cytosolic enzyme functions in reduction of
dehydro-L-ascorbic acid and thereby is important in maintaining the redox
state of ascorbic acid derived from the glomerular filtrate or from
peritubular fluid.
