The fate of ingested acetyl-L- and D-tryptophan in the human subject.

The metabolism of acetyltryptophan has been studied by various workers. Baldwin and Berg (1) and Rose (2) have reported that acetyl-ntryptophan will not maintain nitrogen balance in the adult human; however, the acetylated L isomer was equal to an equivalent amount of L-tryptophan in this respect. In contrast with these results, Albanese et al. (3) report that, with the exception of a 5 per cent urinary loss, all the orally administered acetyl-m-tryptophan was available to man and that acetylD-tryptophan, when given as the racemic mixture, will support a positive nitrogen balance in human infants (4). They (3, 4) cite, for evidence of acetyl-n-tryptophan utilization, that there was (a) no indigo red production upon the addition of 0.1 N iodine to urine excreted during the succeeding 6 hours, and that (b) acetyl-L-tryptophan caused higher excretion of tryptophan than did acetyl-m-tryptophan. They conclude that “metabolic deacetylation of acetyl-d-iryptophane results in the formation of an indole derivative which, unlike that formed in the metabolism of d-tryptophane, is available to man.” Luck et al. (5) found that, 70 to 83 per cent of intravenously injected acetyl-m-tryptophan was excreted in the urine within 6 hours. As Albanese et al. (4) point out, the method of administration used by the latter group (5) may overwhelm the enzyme systems responsible for the utilization of the acetyl derivatives. With the above information at hand, we decided to administer separately the D and L isomers of acetyltryptophan to adult humans in order to gain more information as to the fate of the derivatives. Our data show that approximately 75 per cent of the ingested acetyl-D-tryptophan was not absorbed and was excreted in the feces.