Abstract

The de novo synthesis and subsequent utilization of nucleotide by anabolic and catabolic pathways in the chick embryo have been studied using formate-¹⁴C and glycine-1-¹⁴C. The normal embryo produces soluble nucleotide far in excess of its requirement for polynucleotide synthesis, the major portion of newly synthesized purine being catabolized to uric acid largely via deamination and subsequent oxidation of guanine and its soluble anabolites. The untreated embryo thus appears to provide a biochemical model for essential hyperuricemia.

The uricogenic agent 2-aminothiadiazole increases urate synthesis, presumably by inhibiting incorporation of nucleotide into nucleic acid, thus triggering a compensatory in crease in de novo synthesis.

The xanthine oxidase inhibitor 4-hydroxy[3,4-d]pyrazolopyrimidine specifically reverses the effect of aminothiadiazole upon uric acid labeling, while having no effect upon acid-soluble or nucleic acid purine. The absence, in the chick embryo, of an adequate salvage pathway for oxypurine bases is suggested as a basis for these and other observations.