Richard W. Vilter

THE VITAMIN B6--HYDRAZIDE RELATIONSHIP.

Publisher Summary Isoniazid and other hydrazides can induce vitamin B6 deficiency manifestations, especially convulsions and neuritis. These can be prevented by vitamin B6 administration. The probable mechanism responsible is the formation of a pyridoxal-isonicotinic acid hydrazide (INH) hydrazone. Vitamin B6 may be excreted in this combination or the hydrazone may bind pyridoxal phosphate, preventing it from combining with certain vitamin B6-dependent apoenzymes. Other apoenzymes may have a greater affinity for vitamin B6 phosphate than INH and may not be inhibited at all. Inhibition of pyridoxal kinase may be a very important effect inducing vitamin B6 deficiency. Though very large doses of vitamin B6 may inhibit the effectiveness of INH against the tubercle bacillus, doses of vitamin B6 used in clinical medicine do not seem to interfere with the antituberculous effect of INH in vivo and in vitro.

The effect of pyridoxine deficiency induced by desoxypyridoxine in human subjects upon the excretion of N1-methylnicotinamide after tryptophan administration☆

There is evidence in the literature that the conversion of tryptophan to N1-methylnicotinamide may require pyridoxine (1,2,3). Holt (4) has suggested that a reduction in the amount of N’-methylnicotinamide excreted after a test dose of tryptophan may be used as a test for pyridoxine deficiency. Other evidence has been reported (5,6), however, that pyridoxine is not a factor of primary importance in the conversion and that the apparent relationship between pyridoxine deficiency and poor conversion of tryptophan to N’-methylnicotinamide is due to severe caloric restriction (6) or protein imbalance (7,8). Heimberg, Rosen, Leder, and Perlzweig (9) have shown that the protein level of the diet is of primary importance to the amount of N’-methylnicotinamide excreted, after test doses of tryptophan; the higher the protein level the lower the amount of N1-methylnicotinamide. They found no evidence to support a primary need for pyridoxine in this conversion, though at a 10% casein level, pyridoxine deprivation induced a reduction in the amount of N’-methylnicotinamide excreted. Using desoxypyridoxine, a pyridoxine antagonist, we have produced what appears to be pyridoxine deficiency in human beings (10). Seborrhea-like dermatitis and mucous membrane lesions are induced which respond to pyridoxine but not to other members of the vitamin B com-

Adenylic acid in human nutrition.

Excerpt From our studies of a large series of persons with mixed vitamin deficiency, we reported recently1, 2, 3that the diagnostic manifestations of pellagra, beriberi, riboflavin deficiency, vita...

THE EFFECT OF ROENTGEN-RAY ON THE BLOOD CODEHYDROGENASES I AND II

Excerpt It is a well known fact that therapeutic doses of roentgen-ray frequently give rise to a train of symptoms characterized by nausea, vomiting, abdominal cramps, headache and general malaise....

President Nixon's Budget Proposals and the Medical Colleges

Excerpt As our medical schools were beginning to recover from the manpower drain caused by World War II, the National Institutes of Health, supported by Congressional action, began to award funds f...