Abstract
Isonicotinic acid hydrazide (INH) did not inhibit any of the normal pathways of niacin metabolism investigated in the rat. When added to a B6-deficient ration, INH had a pronounced toxic effect characterized by inhibition of growth, decreased survival time and epileptiform convulsions. The elevated excretion of xanthurenic acid, considered characteristic of the B6-deficient rat, was not apparent in INH-treated animals.