tocophp:rols in various metabolic processes 785 



eonoentration of tocopherol phosphate prodiioed inhibition. Tooopheryl 

 phosphate has both a specific action and a secondary effect involving the 

 removal of calcium. ^^' Other enzyme systems which have been shown to 

 be inhibited by vitamin E phosphate include trypsin, ^^- liver acid phos- 

 phatase/^^ hyaluronidase,^^"* liver esterase, ^^"^ lipoxidase^^^'-'*^^ (only 

 temporarily) and a malic oxidase system employing cytochrome c and 

 cholinesterase.^''^ On the other hand, Jacobi et al.^^'^ reported that the a- 

 tocopheryl phosphate has little or no effect upon a malic oxidase-methylene 

 l>lue system, a lactic oxidase-methylene blue system, D-amino acid oxidase, 

 uricase, an adenosinetriphosphatase system containing calcium, and liver 

 acid phosphatase. Catalase activity was somewhat increased. Accord- 

 ing to Rabin ovitz and Boyer,^^^ the observed effects of D-a-tocopheryl 

 phosphate on the several enzyme systems, in which the enzyme systems 

 were inhibited, may be the result of its properties as an anion with a large 

 non -polar group; these effects are not necessarily related to its activity 

 as a vitamin. 



n. Miscellaneous Factors Related to the Role of Tocopherol. Since 

 vitamin E improves the efficiency of utilization of protein, it is reasonable 

 to postulate that the symptoms of protein deficiency would be accentuated 

 on a vitamin E-free diet, and vice versa. Moore"^ was the first to show 

 that rats reared on low-protein and low-vitamin E diets differed from those 

 which received adequate vitamin E. When vitamin E was absent, there 

 was a shorter survival time, a decreased efficiency in protein utilization at 

 certain levels of protein intake, the occurrence of hepatic lesions, and a 

 depigmentation of the incisors. Holman^-^ found that after dogs had been 

 fed for tAvo months on low-protein, loAv-vitamin E diets, they developed a 

 pronounced necrotizing arteritis when subjected to induced renal in- 

 sufficiency. This condition could be covniteracted by vitamin E. 



When regimens adeciuate in protein but low in vitamin E were fed to 

 rats, it was found that the onset of muscular dystrophy could be hastened 

 by the hepatoxic agent, triorthocresyl phosphate. ^^^ Thompson'*"^ re- 

 ported a similar result on the rabbit, while Draper et alr^- noted an ac- 



382 K. L. Zierler, D. Grob, and J. L. Lilienthal, Jr., Am. J. Physiol, 153, 127-132 

 (1948). 



'" H. P. Jacobi, J. W. Chappell, and S. Morgulis, Federation Proc., 6, 163 (1947). 



39* W. H. Miller and A. M. Dessert, Ann. New York Acad. Sci., 52, 167-179 (1949). 



39^a C. Van der Meer and H. T. M. Nieuwerkerk, Biochim. et Biophys. Acta, 7, 263-271 

 (1951). 



3« R. T. Holman, Arch. Biochem., 15, 403-413 (1947). 



39« H. O. Kunkel, Arch. Biochem., SO, 306-316 (1951). 



3" H. P. Jacobi, J W. Chappell, and S. Morgulis, Arch. Biochem., 27, 22-28 (1950). 



398 M. Rabinovitz and P. D. Beyer, ./. Biol. Chem., 183, 111-121 (1950). 



