Hepatic Purine Enzyme Profiles and Uric Acid Overproduction in Muscular Dystrophy and in Inherited Tophaceous Gout

Summary

Although uric acid overproduction frequently, but not always, leads to gout in humans, it is not known if different biochemical aberrations in purine metabolism might be responsible for that uric acid overproduction which culminates in gout and that which does not. To investigate this possibility hepatic purine enzymes were measured in a line of chickens which overproduced uric acid but did not develop clinical gout (dystrophic) and in another line of the same strain which overproduced uric acid and developed severe tophaceous gout (dystrophic gouty). Adenosine and adenylate deaminases and nucleoside phosphorylase were elevated in both the dystrophic and dystrophic gouty chickens compared with controls. The activities of these three enzymes were not different between the dystrophic and dystrophic gouty groups. 5′-nucleotidase and adenosine kinase were elevated only in dystrophic gouty chickens. Hypoxanthine phosphoribosyltransferase was elevated in dystrophic chickens and was further elevated in dystrophic gouty chickens. To the extent that the hepatic purine enzyme activities reflect events at the molecular level, the present study demonstrates that different biochemical mechanisms may be involved in the uric acid overproduction associated with tissue atrophy (dystrophy) and inherited tophaceous gout.