CHOLINE 



sulphide was isolated from the livers, it would appear that the lipo- 

 tropic action of sulphocholine is due to its incorporation into liver 

 phospholipids in place of choline. Dimethyl thetin and dimethyl 

 propiothetin were also lipotropic. 



Although only the above compounds have a lipotropic effect in 

 the absence of methionine and the presence of homocystine, both mono- 

 and dimethylaminoethanol prevented perosis in chicks fed a basal diet 

 deficient in choline and methionine whilst dimethylaminoethanol, but 

 not the mono-derivative, increased the growth rate, though much less 

 effectively than choline.^ Both compounds stimulated growth to the 

 same extent as choline when methionine was added. Using cholineless 

 mutants of Neurospora crassa, Jukes et al}^ and N. H. Horowitz ^^ 

 showed that aminoethanol was converted into choline in three steps, 

 and feeding experiments with mono- and dimethylaminoethanol con- 

 taining deuterio-methyl groups proved that these compounds were 

 preciusors of choline in animals. ^^ 



The low growth-promoting activity of dimethylaminoethanol is 

 believed to be due to the inability of the animal to utilise the methyl 

 groups present in the molecule, indicating that when choline takes 

 part in transmethylation reactions, it releases only one methyl group, 

 giving rise to dimethylaminoethanol which " would thus assume a 

 pivotal position as both the immediate precursor and the principal 

 demethylation product of choline ". 



Although the triethyl analogue of choline had a slight lipotropic 

 action in rats, it was toxic to mice and the toxicity was neutralised 

 by an equal amount of choline. It also blocked the contraction of 

 isolated frog muscle by choline, but not by acetylcholine, and it was 

 therefore suggested that the compound interfered with the formation 

 of acetylcholine from choline. ^^ 



References to Section 14 



1. A. W. Meyer and V. du Vigneaud, /, Biol. Chem., 1942, 143, 373. 



2. T. H. Jukes, /. Nutrition, 1941, 21, SuppL, 13. 



3. J. M. Patterson and E. W. McHenry, /. Biol. Chem., 1942, 145, 



207. 



4. C. S. McArthur, Science, 1946, 104, 222. 



5. H. J. Almquist and T. H. Jukes, Proc. Soc. Exp. Biol. Med., 1942, 



51, 243. 



6. A. D. Welch, /. Biol. Chem., 1941, 137, 173 ; A. D. Welch and 



R. L. Landan, ibid., 1942, 144, 581. 



7. H. J. Almquist and C. R. Grau, /. Nutrition, 1944, 27, 263. 



8. T. H. Jukes and A. D. Welch, /. Biol. Chem., 1943, 146, 19. 

 8a. G. A. Maw and V. du Vigneaud, ibid., 1948, 176, 1029, 1037. 



9. T. H. Jukes and J. J. Oleson, ibid., 1945, 157, 419 ; T. H. Jukes, 



J. J. Oleson and A. C. Dombush, /. Nutrition, 1945, 30, 219. 



604 



