Abstract
Normal and dystrophic mice were injected intravenously with uridine-2-C14 at various stages of the disease. Radioactivity in the acid-soluble fraction of most of the tissues studied was unchanged or not significantly different in dystrophic animals. In vivo incorporation of uridine-2-C14 into RNA increased in dystrophic muscle as compared to normal muscle at 30 days, remained the same at 60 days, and was reduced at 90 days. Similar results were also observed on the in vitro incorporation of uridine-2-C14 catalyzed by homogenates of normal and dystrophic muscle. Dystrophic brain and pancreas showed a decrease in the incorporation at each stage investigated as compared to controls. No change in the incorporation was noted in dystrophic and normal liver, kidney, spleen, and heart. The decrease in uridine 2-C14 incorporation in dystrophic muscle at 90 days could be due to an increased RNA content. Such a phenomenon was explained as due to infiltration of dystrophic muscle by invading macrophages. The metabolism of RNA is not decreased in the dystrophic muscle in preliminary stages of the disease as compared to the control.