Renal metabolism of the oxidized form of ascorbic acid (dehydro-L-ascorbic acid).

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.