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Absence of guanine deaminase from cerebellum

THE DISCOVERY that the Lesch-Nyhan syndromel of choreoathetosis, hyperuricemia, selfmutilation, and mental retardation is associated with absence of one of the enzymes of the saIvage pathway of purine metabolism2 has reawakened interest in this pathway in the brain. The missing enzyme is hypoxanthine-guanine phosphoribosyl transferase (inosinic acid pyrophosphorylase) . Affected boys are unable to convert hypoxanthine, guanine, and probably xanthine3 to their respective mononucleotides. Tissues other than brain are apparently able to tolerate this deficiency, although they may be affected by the resulting hyperuricemia and gout; the brain appears to require the enzyme for normal function. No explanation for the necessity for salvage of free purine bases in the brain has been established. Blockade of either the hypoxanthine-inosinic acid4 or the guanine-guanylic acid conversion5 could be blamed. Two recent papers have contributed to our knowledge of the special metabolism of purines in rat brain. Santos et a1.6 studied the uptake of various labeled precursors into brain RNA and concluded that both the de novo synthetic pathway (from glycine, aspartate, etc.) and the salvage pathway contributed nucleotides to a common precursor pool. They also assayed a number of enzymes concerned with these two pathways and showed that a number of possible conversions (e.g., purine nucleosides to nucleotides and xanthine and hypoxanthine to urate) did not occur in brain. Held and Wells' also studied the uptake of radioactive precursors into RNA and the relevant pools of soluble nucleotides; they were able to conclude that the de novo pathway was utilized preferentially. The symptoms of the Lesch-Nyhan syndrome point to a disturbance of function in the deep nuclei, such as striatum or pallidum. For this reason, a survey of the known enzymes of guanine metabolism in cat brain on a regional basis has been undertaken. The results are given below.