Xanthurenic acid excretion and possible pyridoxine deficiency produced by isonicotinic acid hydrazide and other convulsant hydrazides.

Dogs were injected with L-tryptophane followed by one of four convulsant hydrazides (semicarbazide, thiosemicarbazide, thiocarbohydrazide, and isonicotinic acid hydrazide) or desoxypyridoxine, and their xanthurenic acid excretion determined. Within 15 to 30 minutes after administration all of the convulsant hydrazides tested produced an increase in the excretion of xanthurenic acid. The effects of isonicotinic acid hydrazide are not different from the other convulsant hydrazides. Desoxypyridoxine in equipotent convulsive doses does not produce xanthurenuria acutely. The time course of the development of hydrazide-induced xanthurenuria corresponds to the time of onset of hydrazide seizures in unanesthetized animals. The relative potency of these hydrazides in producing xanthurenuria in dogs is roughly correlated with their potency in producing seizures in mice. On the basis of these findings it appears that the convulsant activity of these hydrazides is related to the production of an acute pyridoxine deficiency. The actions of isonicotinic acid hydrazide on pyridoxine metabolism are not unique to isonicotinic acid hydrazide but occur with the four convulsant hydrazides tested.