706 XI. VITAMINS E (tocopherols) 



reduction in adenosine triphosphate (ATP), and with an augmentation of 

 adenosine triphosphatase. ^^^ Rumery and co-workers ^^^ observed a 

 marked loss of actomyosin in the muscles of weanling rats in "late-lacta- 

 tion" paralysis, with a concomitant increase in the proportion of insoluble 

 protein, and with a simultaneous loss of protein nitrogen and of non-protein 

 nitrogen as paralysis developed. This occurred between the ages of 

 eighteen and twenty-five days. When spontaneous recovery ensued, 

 these abnormalities were corrected by the time the rats were thirty days 

 old, even though a deficiency sometimes persisted. Essentially parallel 

 changes have been noted in the hamster suffering from muscular dystrophy, 

 as well as during its repair when a-tocopherol was administered.^*^ These 

 changes were followed in great detail histologically, by West and 

 Mason. 1*1 ~^*' One is led to the conclusion that a-tocopherol in some way, 

 either directly or indirectly, exerts a control over the protein synthesis in 

 the muscle cell. Milman and her co-workers^** observed that, in vitamin 

 E-deficient hamsters, serum protein was increased (presumably as a result 

 of the protein lost from the muscles) , and that the rate of release of amino 

 nitrogen was curtailed in tissue slices. 



(e) Allantoin. Allantoin, which is the normal end-product of purine 

 metabohsm in animals lower in the scale than man and monkey, also 

 appears to be under the control of a-tocopherol. Thus, Young and 

 Dinningi** proved that the excretion of allantoin increased in rabbits on a 

 vitamin E-deficient diet prior to the onset of the muscular dystrophy. An 

 increased excretion of allantoin was found to occur concomitantly with 

 an augmented concentration of nucleic acids in the skeletal muscles. 

 These data were interpreted as evidence that the increased elimination of 

 allantoin was the result of an accelerated turnover rate of tissue nucleic 

 acids,'** rather than of a loss of nucleic acids from the muscle. Subse- 

 quently, Dinning et a/.i*^'*^ proved this hypothesis by the use of C'*- 

 labeled sodium formate, which was administered to rats and rabbits which 



"0 R. E. Rumery, S. I. Mauer, and K. E. Mason, ./. Exptl. Zool, 129, 495-503 (1955). 



1^1 W. T. West and K. E. Mason, Muscle Lesions in Vitamin E-Deficient Hamsters and 

 Their Response to Antidystrophic Compounds. Abst. Report Third Intern. Congr. on 

 Vitamin E, Venice, 1955, Vol. I, p. 21. 



152 W. T. West and K. E. Mason, Am. J. Physical Med., 34, 223-239 (1955). 



1" K. E. Mason and W. T. West, Anat. Rec, 118, 327-328 (1954). 



IS'* A. E. Milman, D. N. Silides, and A. T. Milhorat, Proc. Soc. Exptl. Biol. Med., 83, 

 637-638 (1953). 



"6 J. M. Young and J. S. Dinning, J. Biol. Chem., 193, 743-747 (1951). 



15* J. S. Dinning, Vitamin E and Nucleic Acid Metabolism, Abst. Report Third Intern. 

 Congr. on Vitamin E, Venice, 1955, Vol. I, p. 50. 



1" J. S. Dinning, /. Biol. Chem., 212, 735-739 (1955); J. S. Dinning, J. T. Sime, and 

 P. L. Day, Ibid., 217, 205-211 (1955). 



