DIGESTION, ETC. OF CAROTENOIDS IN THE G.I. TRACT 297 



tene U, 13% 290 ; 7-carotene set (all-trans, 42%) 292 ; neo-7-carotene P, 

 19% 291 ; mixture of neo-7-carotenes, 16% 291 ; pro-7-carotene, 41% 292 ; 

 cryptoxanthin set (all-trans, 57%) 321 ; neocryptoxanthin A, 42% 322 ; 

 and neocryptoxanthin U, 27%. 323 The provitamin activity of the pro-7- 

 carotene is slightly higher in the chick than in the rat. 324 Kemmerer and 

 Fraps 320 found that the carotene isolated from the gastrointestinal tract 

 of rats four to six hours after the feeding of neo-jS-carotene U had been 

 changed to the aR-trans form and to neo-/3-carotene. 



(2) The Stability of (5-Carotene in the Intestine 



Carotene has repeatedly been found to be less effective as a source of 

 vitamin A when fed in pure solvents than when administered in crude oils. 

 For example, /3-carotene was reported to have no potency as a source of 

 vitamin A when fed in ethyl oleate. 325 Drummond et al. S2G attributed the 

 lack of vitamin A potency under such conditions to an oxidation of the 

 carotene. After the demonstration by Mattill 327 of the protective effect 

 of polyphenols in preventing the autoxidation of lard, Olcovich and Mat- 

 till 328 were able to demonstrate that hydroquinone exerts a stabilizing in- 

 fluence on /3-carotene in ethyl oleate or ethyl laurate, and prevents its 

 oxidation. A number of workers 329-332 then turned to hydroquinone as 

 an agent for preventing oxidative destruction of the carotene. Moore 333 

 in 1940, and Davies and Moore 334 in 1941, were also among the first to 

 recognize the sparing effect of tocopherol on /3-carotene and vitamin A. 

 Carotene was also shown to be destroyed in the gastrointestinal tract 

 when fed with methyl linoleate or methyl linolenate. 225 Tomarelli and 



321 L. Zechmeister, Bull. soc. chim. biol, 31, 956-964 (1949). 



822 H. J. Deuel, Jr., E. R. Meserve, A. Sandoval, and L. Zechmeister, Arch. Biochem., 

 10, 491-496(1946). 



323 H. J. Deuel, Jr., S. M. Greenberg, E. Straub, T. Fukui, A. Chatterjee, and L. Zech- 

 meister, Arch. Biochem., 23, 239-241 (1949). 



324 S. M. Greenberg, C. E. Calbert, J. H. Pinckard, H. J. Deuel, Jr., and L. Zech- 

 meister, Arch. Biochem., 24, 31-39 (1949). 



326 W. Duliere, R. A. Morton, and J. C. Drummond, J. Soc. Chem. Ind., 48, 316-321T 

 (1929). 



326 J. C. Drummond, B. Ahmad, and R. A. Morton, /. Soc. Chem. Ind., 49, 291-296T 

 (1930). 



327 H. A. Mattill, J. Biol. Chem., 90, 141-151 (1931). 



328 H. S. Olcovich and H. A. Mattill, J. Biol. Chem., 91, 105-117 (1931). 



329 C. A. Baumann and H. Steenbock, /. Biol. Chem., 101, 561-572 (1933). 



330 F. G. McDonald, J. Biol. Chem., 103, 455-460 (1933). 



331 R. G. Turner and E. R. Loew, /. Infectious Diseases, 52, 102-120 (1933). 



332 F. J. Dyer, K. M. Kev, and K. H. Coward, Biochem. J., 28, 875-881 (1934). 



333 T. Moore, Biochem. J., 34, 1321-1328 (1940). 



334 A. W. Davies and T. Moore, Nature, 147, 794-796 (1941). 



