Abstract
PURINE metabolism in man has been studied extensively since the time of Garrod. Its end product is a readily measurable purine, uric acid, which reflects overall purine metabolism and, in uricotelic organisms, the major pathway of nitrogen excretion as well. In addition, gout, an important disease of purine metabolism, has been recognized since antiquity and has been identified with urate since Wollaston's studies in 1797 on tophaceous chemistry. In contrast, the study of pyrimidine metabolism has languished. The products of pyrimidine catabolism, largely carbon dioxide and ammonia, are submerged in the anonymity of these large metabolic pools. The only known . . .
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