Excretion of creatine, creatinine, and 4-amino-5-imidazolecarboxamide (AIC) was studied in genetically determined muscular dystrophy in the human and mouse. The AIC excretion was normal in both affected humans and mice as compared with groups of comparably aged controls. The creatine-to-creatinine ratio for human muscular dystrophics was more than four times as great as for their unaffected siblings. Both normal and dystrophic mice showed a "creatinuria" as compared to humans. The creatine-to-creatinine ratio for dystrophic mice was significantly higher than the controls, but the difference was apparent only in the first 2 months of life.
The hind leg muscle of normal mice and mice with hereditary muscular dystrophy was taken for individual analyses of the creatine-phosphorylating enzyme, creatine kinase. Creatine kinase activity was always found to be higher in the muscle of normal mice than in that of dystrophic mice, and the values in each group decreased with increasing age of the mice. The difference was greatest in mice of 2 weeks of age, and in the light of these findings some suggestions are made about the pathogenesis of muscular dystrophy.
Serum creatine phosphokinase activity has been found to be lower in dystrophic mice of strain 129 than in normal controls of this strain. One group of controls had very low levels of creatine phosphokinase activity, but it was not possible to repeat this finding by alterations in environmental conditions. It is concluded that serum creatine phosphokinase activity is normally lower in dystrophic than in unaffected mice of strain 129.
The hind leg muscle of normal mice and mice with hereditary muscular dystrophy was taken for individual analyses of the creatine-phosphorylating enzyme, creatine kinase. Creatine kinase activity was always found to be higher in the muscle of normal mice than in that of dystrophic mice, and the values in each group decreased with increasing age of the mice. The difference was greatest in mice of 2 weeks of age, and in the light of these findings some suggestions are made about the pathogenesis of muscular dystrophy.
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