Abstract

The homozygous muscular dystrophic mice (dydy) were found to have significantly higher plasma uric acid than their heterozygous littermate controls (Dydy), and the Swiss albino mice. Because the rate of uric acid excretion did not compensate for the elevated plasma levels, U/P (urine/plasma) urate was lower in dydy mice. With RNA supplement, plasma and urinary urate were increased in both dydy and Dydy mice; again U/P urate was lower in dydy mice. It appears that the dydy mice to a certain extent are comparable to some gouty subjects, whose hyperuricemia is not accompanied by a corresponding increase in urinary uric acid. There was no difference in converting uric acid to allantoin either on basal diet alone or with RNA supplement. Oxonic acid effectively, though transiently, blocked the uricase activity in both dydy and Dydy mice resulting in hyperuricemia and hyperuricosuria with decreased allantoin. Uric acid content was increased markedly in the kidney without histological evidence of urate deposition, apparently related to the unsustained effect of oxonic acid, which was rapidly excreted.

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