Influence of iron and ascorbic acid on tryptophan metabolism in man.

South African Bantu patients with a scurvy-type skin, which developed after a prolonged, iron-induced hemosiderosis, were studied with ascorbic acid-1-C14 and the 2 gm tryptophan load test. The metabolism of the two compounds was found to be abnormal in these patients. The data suggested that ascorbic acid was rapidly (iron accelerated) metabolized to monodehydroascorbate, a compound that rapidly reacts with tissue DPNH to form DPN. This mechanism could reduce tissue levels of DPNH such that the feed-back control of tryptophan pyrolase enzyme was depressed. The change in control level of the pyrrolase enzyme permitted large quantities of tryptophan to be converted into the kynurenine pathway products, and a smaller quantity for the serotonin pathway. This mechanism could contribute to the abnormal tryptophan metabolism found in chronic pellagrins with dementia.