Abstract
Confirming previous observations 1 on nutritionally dystrophic rabbits and rats, Houchin 2 recently reported the oxygen consumption of dystrophic hamster muscle to be much above that of normal muscle. It was also demonstrated that within 27 hours after administration of α-tocopherol acetate to the dystrophic hamster, the Qo2 of the muscle was reduced toward normal value without significant regeneration of normal muscle status as indicated by a persistent high chloride content.
These observations naturally suggested that α-tocopherol may play a role in the normal processes of muscle metabolism. The data in this paper establish the fact that α-tocopherol phosphate† acts in vitro on muscle cells from vitamin E-deficient animals to lower the excessive oxygen consumption toward the. normal.
Vitamin E-deficient rabbits, hamsters, and adolescent rats were studied. The oxygen consumption of muscle slices was determined in the usual manner in the Warburg apparatus. The control medium was a modified Locke-Ringer's solution; to prepare the experimental medium 5 mg α-tocopherol phosphate were dissolved in a few drops of water and made up to 100 cc with the Locke-Ringer's solution. The solution was well shaken immediately before the required amount was measured out. The results are expressed as Qo2 (cubic millimeters of oxygen per milligram dry weight per hour).
As seen in Table I the oxygen consumption of muscle from E-deficient rabbits and hamsters in the medium containing α-tocopherol phosphate was 41.3% and 35.7% lower than that of slices from the same muscle in the unsupplemented medium. The oxygen consumption was thus considerably reduced toward that of normal animals.
The oxygen consumption of the muscle of control animals was not altered beyond experimental error by the medium containing α-tocopherol phosphate. When the Qo2 had already been lowered by previous administration of α-tocopherol to dystrophic rabbits, the addition of a-tocopherol phosphate to the medium caused no significant change.
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