Abstract
In most mammals, uric acid is converted into allantoin by the enzyme uricase, which does not occur in man and apes. Thus, the urinary end product of purine metabolism in man and apes is uric acid, whereas it is allantoin in most mammals. An attempt to produce an animal model for research into hyperuricemia was made by Johnson1, who blocked the activity of hepatic uricase in rats by a selective enzyme inhibitor, oxonic acid (oxonate). Particularly the amide of oxonic acid (allantoxanamide) has been described as an effective inhibitor of uricase activity in vitro and in vivo. Hropot2 demonstrated that the prolonged duration of action of allantoxanamide as compared to oxonic acid is due to its elimination kinetics. Allantoxanamide was eliminated by the kidneys with a half-life of 25.4 min, which was double that of oxonate during the first 30 min after administration. The purpose of this study was to establish an appropriate screening method for evaluating antiuricopathic drugs in the allantoxanamide-treated rat.
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