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Effect of Isonicotinic Acid Hydrazide on Niacin and Pyridoxine Metabolism in Rats

Fred S. Rosen

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Abstract

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.

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What this paper is about

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.

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Available abstract

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.

Key concepts: Xanthurenic acid, Niacin, Pyridoxine, Isonicotinic acid, Pyridoxine Deficiency, Metabolism, Hydrazide, Excretion

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Effect of Isonicotinic Acid Hydrazide on Niacin and Pyridoxine Metabolism in Rats — Research Paper | ScholarLens