scholarly journals Competitive Action of Isonicotinic Acid Hydrazide and Vitamin B6 in the Formation of Indole by E. coli

Nature ◽  
1952 ◽  
Vol 170 (4332) ◽  
pp. 803-803 ◽  
Author(s):  
MASAHIKO YONEDA ◽  
NOBUO KATO ◽  
MITSUHARU OKAJIMA
Keyword(s):  
Vitamin B6 ◽  
Isonicotinic Acid ◽  
Acid Hydrazide ◽  
Isonicotinic Acid Hydrazide ◽  
E Coli ◽  
Competitive Action

The effects of isonicotinic acid hydrazide on the early chick embryo

Development ◽  
1973 ◽  
Vol 29 (1) ◽  
pp. 209-219
Author(s):  
M. A. Castellano ◽  
J. L. Tórtora ◽  
N. I. Germino ◽  
F. Rama ◽  
C. Ohanian
Keyword(s):  
Vitamin B6 ◽  
Acid Metabolism ◽  
Isonicotinic Acid ◽  
Acid Hydrazide ◽  
Considerable Extent ◽  
Isonicotinic Acid Hydrazide ◽  
Control Group ◽  
Preventive Action ◽  
Pyridoxine Hydrochloride ◽  
Developing Nervous System

1. Unincubated White Leghorn fertile eggs were injected with isonicotinic acid hydrazide (INH) through a hole in the shell. A control group was injected with normal saline, a second group with INH plus vitamin B6, and a third group was left unopened. 2. INH, in the doses we used, proved to be lethal for more than 50% of the early chick embryos, and also produced important developmental alterations. 3. Alterations produced by INH were primarily observed at the level of the neural epithelium, particularly at its cephalic portion. The most important ones were a degenerative and necrotic process of the neural epithelium, and a distortion of the normal anatomical relations of the cephalic structures. 4. The embryonic mortality and developmental alterations induced by INH were prevented to a considerable extent by the concurrent injection of pyridoxine hydrochloride and INH. 5. The preventive action of vitamin B6 suggests that toxicity of INH in the chicken embryos is due to the antivitamin-B6 action of INH. Through this mechanism INH would block, specially, the amino acid metabolism. The developing nervous system was the embryonic area most sensitive to such metabolic alterations.

Postneonatal Vitamin B6-Dependent Epilepsy

PEDIATRICS ◽  
1992 ◽  
Vol 90 (2) ◽  
pp. 221-223
Author(s):  
STEVEN B. COKER
Keyword(s):  
Amino Acids ◽  
Vitamin B6 ◽  
Pyridoxal Phosphate ◽  
Isonicotinic Acid ◽  
Acid Hydrazide ◽  
Aminobutyric Acid ◽  
Isonicotinic Acid Hydrazide ◽  
Peripheral Neuritis ◽  
Normal Vitamin ◽  
Vitamin B6 Deficiency

Vitamin B6 acts as coenzyme in decarboxylation and transamination of amino acids. Pyridoxal phosphate is the coenzyme for a glutamic decarboxylase and γ-aminobutyric acid transaminase, enzymes necessary in production and metabolism of brain γ-aminobutyric acid. Vitamin B6 deficiency has been known to produce peripheral neuritis, dermatitis, anemia, and convulsions in infants.1 Administration of isonicotinic acid hydrazide may produce a vitamin B6-responsive neuropathy. Convulsions from vitamin B6 dependency occur despite normal vitamin B6 levels. These seizures, according to pediatric and neurological texts, occur immediately after birth up to 6 months.1-4 In 1985, Goutieres and Aicardi5 described three patients with atypical pyridoxine-dependent seizures with onset at 7 weeks, 5 days, and 4 months.

scholarly journals THE ISOLATION AND PROPERTIES OF THE ISONICOTINIC ACID HYDRAZIDE ANALOGUE OF DIPHOSPHOPYRIDINE NUCLEOTIDE

1954 ◽  
Vol 209 (2) ◽  
pp. 467-484 ◽  
Author(s):  
Leonard J. Zatman ◽  
Nathan O. Kaplan ◽  
Sidney P. Colowick ◽  
Margaret M. Ciotti
Keyword(s):  
Isonicotinic Acid ◽  
Acid Hydrazide ◽  
Isonicotinic Acid Hydrazide
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