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Vitamin E Deficiency and the Accumulation of Amino Acids in Skeletal Muscle^1,2,

Departments of Biochemistry, Pathology and Medicine, University of Arkansas School of Medicine, Little Rock, Arkansas

The movements of ¹⁴C-labeled glycine and -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 x 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.

² Part of these data were included in a preliminary report at the 52nd Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, 1968.

³ Present address: Department of Biological Chemistry, The University of Michigan, Ann Arbor, Michigan 48104.

⁴ Present address: Bundesforschungsanstalt für Lebensmittelfrischhaltung, Karlsruhe, Germany.

⁵ Present address: Division of Biochemistry, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D. C. 20012.

Manuscript received 20 January 1969.