![]() |
|
|
Department of Physiology, Presidency College, Calcutta, India
Nicontinic acid and amide, quinolinic acid and N'-methyl nicotinamide (N'MN) were estimated in the urine of normally-fed and tryptophan-fed rhesus monkeys after they had received chloromycetin palmitate. Chloromycetin reduced the urinary excretion of nicotinic acid and amide, quinolinic acid and N'MN in both normal and tryptophan-fed monkeys.
Nicotinic acid and amide, nicotinuric acid, quinolinic acid and N'MN were estimated in the urine of rhesus monkeys after the administration of pyridoxine hydrochloride in tryptophan-and sulfaguanidine-fed monkeys. The pyridoxine supplement led to an increased excretion of nicotinuric acid, quinolinic acid and N'MN by these animals. It has been suggested that pyridoxine is needed for the conversion of tryptophan to nicotinic acid.
The urinary excretion of metabolites of nicotinic acid was also estimated after the administration of tryptophan in monkeys which were injected intraperitoneally with carbon tetrachloride to damage the liver. The excretion of metabolites of nicotinic acid in the urine of monkeys poisoned with carbon tetrachloride did not vary consistently. Liver, therefore, was not the site of the synthesis of nicotinic acid from tryptophan.
The urinary excretion of metabolites of nicotinic acid was also estimated in normal and scorbutic monkeys after they were fed tryptophan. Ascorbic acid deficiency had no effect on the excretion of these metabolites.