Relation of tryptophan and niacin to pyridine nucleotides of tissue.

In a previous report (1) from this laboratory it was observed that a tryptophan deficiency in the rat brought about a decrease in activity of several liver enzyme systems. In particular the endogenous respiration of liver tissue was markedly decreased during a tryptophan deficiency. In a similar study of a methionine deficiency (2) it was noted that liver endogenous respiration was not significantly altered. Therefore, it appeared that the effect of the tryptophan upon liver endogenous respiration was unique to that amino acid. Because of the well known transformation of tryptophan to niacin in animals (3, 4) and since niacin is believed to be the precursor of the liver pyridine nucleotides (DPN and TPN),’ it was possible that the decrease in liver endogenous respiration induced by a tryptophan deficiency was due to a loss of liver pyridine nucleotides. In the presence of adequate dietary niacin, however, this possibility appeared to be somewhat remote since dietary niacin had been assumed to be capable of maintaining liver pyridme nucleotide content at a normal level even if tryptophan was absent from the ration. The level of niacin in the ration, however, while believed to be adequate under ordinary conditions, might not have been adequate if tryptophan were omitted entirely from the diet. In the present paper we wish to report some of our findings concerning the interrelationships of tryptophan and niacin in maintaining the pyridine nucleotide content of rat liver. We have investigated the problem both from an analytical and an enzymatic point of view in order to observe the direct involvement of the liver pyridine nucleotides.