The purine bases guanine and hypoxanthine (derived from adenine by events in the purine salvage pathways) are converted to xanthine and then to uric acid, which is excreted from the body (Watts 1974). The end-point of this pathway in humans and hominoid primates is unusual. Most other mammals metabolize uric acid further to yield more soluble end products, and much speculation has centered on possible roles for high uric acid levels in normal human physiology.
In parallel sequences of three reactions each, the pyrimidines thymine and uracil are converted to beta-aminoisobutyrate and beta-alanine respectively. Both of these molecules are excreted in human urine and appear to be normal end products of pyrimidine catabolism (Griffith 1986). Mitochondrial AGXT2, however, can also catalyze the transamination of both molecules with pyruvate, yielding 2-oxoacids that can be metabolized further by reactions of branched-chain amino acid and short-chain fatty acid catabolism (Tamaki et al. 2000).
Hydrolysis of phosphate bonds in nucleotides catalyzed by members of the NUDT and NTPD families of enzymes have been grouped here as well, although the physiological roles of these groups of catabolic reactions are diverse.