ABSTRACT
Hypoxanthine is oxidized to xanthine, and xanthine to uric acid by the enzyme xanthine oxidase, which has been found in liver and in milk. A genetic lesion in primates and in Dalmatian dogs is responsible for loss of the enzyme uricase; this causes uric acid to be the end product of purine metabolism. Proctor has suggested that the resulting accumulation of uric acid may be of benefit to species which have lost the ability to synthesize ascorbic acid from simple sugars. Berger et al. studied the urinary clearance rates of both ascorbic acid and uric acid in human subjects. It would seem that ascorbic acid may decrease plasma uric acid levels in two ways: by inhibiting the synthesis of uric acid from xanthine and by increasing the renal excretion of uric acid. If so, uric acid levels will tend to rise in ascorbic acid deficiency.
