XIII. REQUIREMENTS AND FACTORS 585 



tryptophan administration^^- ^^'^^ and prevents the normal increase of pyri- 

 dine nucleotides in red blood cells following tryptophan.^^ In most instances 

 these defects were overcome promptly after pyridoxine therapy. Since 

 pyridoxine deficienc}^ is known to result in abnormal tryptophan metabo- 

 lism ^""^^ it was logical to believe that pyridoxine deficiency might also 

 interfere with the synthesis of nicotinic acid from trj^ptophan. 



However, several reports^^"^® appeared indicating that the liver of pyri- 

 doxine-deficient rats could still transform tryptophan to nicotinic acid 

 derivatives. Furthermore, deficiencies of thiamine or riboflavin or simple 

 reduction in caloric intake also appeared to result in a reduced excretion 

 of urinary nicotinic acid derivatives after tryptophan. ^^ Spector^^ found no 

 interference with the tryptophan to nicotinic acid conversion in force-fed 

 pyridoxine-deficient rats. Heimberg et al.^'^ obtained evidence that the in- 

 volvement of pyridoxine in nicotinic acid synthesis was not a direct meta- 

 bolic effect. These seemingly contradictory reports may be explained by a 

 recent investigation by Kring and associates,^* who also found that pyri- 

 doxine deficiency did not inhibit the formation of liver pyridine nucleotides 

 from tryptophan. However, if they intensified the deficiency state by using 

 the antagonist desoxypyridoxine, they could demonstrate such an inter- 

 ference. However, even this severe deficiency did not interfere with the 

 formation of liver pyridine nucleotides from nicotinic acid. 



So far as is known, this interesting interrelationship between pyridoxine 

 and tryptophan has no practical significance in altering the nicotinic acid 

 requirements of either animals or man. 



(3) Folic Acid. Krehl and associates'^' i°° found that folic acid improved 



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