METABOLISM 



rapidly excreted pantothenic acid in which the nitrogen atom was 

 replaced by the N^^-isotope when this was administered parentally.^* 

 The fact that W^ was absent from a nimnber of tissues showed that 

 pantothenic acid was not metabolised by mice in a manner analogous 

 to the amino acids. Urinary pantothenic acid excretion in rats was 

 higher on a diet containing 64 % of casein than on one containing 



Dogs with a bladder fistula excreted 7-2 fig. of pantothenic acid in 

 two hours, and there was no increased excretion two hours after oral 

 administration of i mg. of pantothenic acid per kg. of bodyweight. 

 After an oral dose of 4 mg. per kg., however, 0-9 to 5-0 % was excreted 

 in two hours.® Following the intravenous injection of i and 4 mg. per 

 kg., 22 to 31 % and 41 to 57 % respectively of the dose was excreted, 

 the excretion being maximal after forty and twenty minutes, respec- 

 tively. More pantothenic acid was excreted following an oral dose 

 than after subcutaneous injection. With unlimited access to food, 

 dogs excreted up to 50 % of the dietary pantothenic acid in the faeces 

 but no increase in the faecal excretion occurred after intravenous 

 administration of calcium pantothenate.^^ 



It is not known what degradation products of pantothenic acid 

 are fonned in vivo, but it is known ^^ that pantolactone is not one of 

 the substances formed in man. The excretion of pantolactone was 

 the same whether it was given orally or intravenously, suggesting that 

 intestinal bacteria did not attack the lactone ring. The excretion of 

 pantoic acid, on the other hand, was slightly less after oral than after 

 intravenous administration, suggesting that it was partially decom- 

 posed by the intestinal flora. 



The amount of pantothenic acid excreted in the faeces was slightly 

 greater after oral administration of pantolactone, possibly owing to 

 modified metabolism of the intestinal bacteria. 



References to Section 10 



1. S. R. Stanbery, E. E. Snell and T. D. Spies, /. Biol. Chem., 1940, 



135. 353. 



2. M. J. Pelczar and J. R. Porter, Proc. Soc. Exp. Biol. Med., 1941, 



47, 3. 



3. H. Mcllwain and F. Hawking, Lancet, 1943, 1, 449. 



4. P. B. Pearson, V. H. Melass and R. M. Sherwood, /. Nutrition, 



1946, 32, 187. 



5. T. D. Spies, S. R. Stanbery. R. J. Williams, T. H. Jukes and S. H. 



Babcock, /. Amer. Med. Assoc, 1940, 115, 523. 



6. R. H. Silber and K. Unna, /. Biol. Chem., 1942, 142, 623. 



7. L. D. Wright, ibid., 445. 



8. L. D. Wright, ibid., 1943, 147, 261. 



375 



