468 IX. CAROTPiNOIDS AND VITAMINS A 



while the alcohol is associated with the most soluble fraction (albumin). 

 It was also demonstrated that vitamin A alcohol in pig blood is linked with 

 the more soluble protein fraction. Lovern et al.^^^ called attention to the 

 fact that, even in the case of fishes, the liver vitamin A is in part associated 

 with protein. Vitamin A aldehyde (retinene) was found by Rajagopal 

 and Datta^'*'^ to combine with protein. The vitamin A aldehyde content 

 of the protein-retinene complex was 0.003%; in the case of the vitamin 

 A-protein complex, 120 to 200 LIT. of vitamin A was associated with 6 to 

 8 g. of protein.'^" 



(6) The Presence of Vitamin A Alcohol and of Vitamin A Esters. Vita- 

 min A in the plasma occurs both in the form of the free alcohol and as the 

 ester. Vitamin A alcohol is the predominant form in the fasting individ- 

 ual. ^^^ However, when vitamin A is administered orally, the ester form 

 alone is increased, irrespective of whether the vitamin A is given as the al- 

 cohol or as the ester. ^-''•'^^■^'*^ Hoch also noted some increase in the vita- 

 min A alcohol in the plasma as a result of the mobihzation of endogenous 

 vitamin A, for example, following parturition, or the ingestion of etha- 

 nol 3'*^ '^49 



The view is widespread that no definite relationship exists between the 

 level of vitamin A in the blood and that in the liver.^^^'^^""^^^ Thus, Lewis 

 et al. ^^° suggest that the plasma tends to resist any changes in the vitamin 

 A concentration, in spite of wide variations in the proportion of vitamin A 

 present in the liver. However, Glover and co-workers^^*'^^^ interpreted 

 their data as an indication that the level of vitamin A alcohol in the plasma 

 is proportional to that of the free vitamin A in the liver, although they 

 recognize that the level of plasma vitamin A does not correspond to that of 

 the total hepatic stores of vitamin A, which are largely in the form of the 

 ester. Ganguly and Iviinsky^" reached conclusions opposite to those of 



3« J. A. Lovern, J. R. Edisbury, and R. A. Morton, Nature, I40, 276 (1937). 



3« K. Rajagopal and P. K. Datta, Nature, 170, 370-371 (1952). 



3*8 H. Hoch, Nature, 158, 59 (1946). 



3" H. Hoch and R. Hoch, Brit. J. Exptl. Pathol, 27, 316-328 (1946). 



350 J. M. Lewis, O. Bodansky, K. G. Falk, and G. McGuire, ./. Nutrition, 23, 351-363 

 (1942). 



351 J. M. Lewis, O. Bodansky, K. G. Falk, and G. McGuire, Proc. Soc. Exptl. Biol. 

 A/ed., 46, 248-250(1941). 



352 H. W. Josephs, Bull. John.s Hopkins Univ., 71, 253-264 (1942). 



3" p. B. Horton, W. A. Murrill, and A. C. Curtis, /. Clin. Invest., 20, 387-393 (1941). 



354 S. Brenner, M. C. H. Brookes, and L. J. Roberts, J. Nutrition, 23, 459-471 (1942). 



355 J. Glover, T. W. Goodwin, and R. A. Morton, Biochem. J., 40, Ivii (1946); 4U 

 97-100 (1947). 



356 J. Glover, T. W. Goodwin, and R. A. Morton, Biochem. J., 41, 97-100 (1947). 

 35' J. Ganguly and N. I. Krinsky, Biochem. J., 54, 177-181 (1953). 



