Urinary excretion of nicotinic acid and N-methyl-nicotinamide by rats fed tryptophan and diets deficient in various B vitamins.

The inability of vitamin Be-deficient rats and mice to convert dietary tryptophan to nicotinic acid and its metabolites has been observed by several workers (l-4). Further, when vitamin Be supplements were given to rats previously deficient in the vitamin, the animals usually recovered the ability to transform tryptophan into nicotinic acid metabolites, although the response was apparently influenced by the severity of the deficiency of vitamin Bc (24). Animals fed diets adequate in vitamin B6 but differing in quality and quantity of protein or in the type of carbohydrate fed do, however, synthesize large amounts of nicotinic acid metabolites when tryptophan is fed (5-7).l Considerable speculation has arisen as to the site of conversion of tryptophan to nicotinic acid derivatives, particularly as to the r&e of intestinal microorganisms and of synthesis in the tissues of the animal. Recent findings have revealed that at least some of the synthesis of nicotinic acid from tryptophan can occur within the tissues (8) in studies conducted without the complicating effects of intestinal microorganisms. This biochemical transformation has stimulated a great deal of interest, therefore, not only in the effect of dietary factors on the apparent conversion of tryptophan to nicotinic acid, but in the site of synthesis. In the present study, experiments were conducted to determine whet.her rats deficient in vitamins other than vitamin Be were able to convert tryptophan to nicotinic acid. The urinary excretion of nicotinic acid and its methylated derivative