Abstract
The movements of 14C-labeled glycine and α-aminoisobutyric acid (AIB) into and out of skeletal muscle slices from control and vitamin E-deficient rabbits were studied. Vitamin E deficiency increased 14C-amino acid accumulation at 60 minutes of incubation without having any demonstrable effect either on the early phase of entry (zero to 30 minutes) or on the efflux of 14C-amino acids. Inhibition of 14C-glycine incorporation into protein by puromycin had no effect either on the early phase of entry or on the accumulation of 14C-glycine by control or vitamin E-deficient muscle. The early phase of 14C-glycine entry followed first-order kinetics; its rate constant in sec-1 was 5.5 × 10-4. Whereas steady-state distribution ratios of 14C-amino acids were reached by control muscle in about 30 minutes, dystrophic muscle continued to accumulate the 14C-amino acids for 60 minutes or more. Small differences in influx, efflux, or both, can result in significant differences in net accumulation with extended time. Thus, we suggest that vitamin E-deficient muscle has one or more compartments capable of increasing the accumulation of 14C-glycine and 14C-AIB due to a change either in influx or efflux which is too small to demonstrate. These compartments may be located in regenerating muscle cells, or in other cell types more abundant in the dystrophic muscle.
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