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

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.

Nature ◽  
1952 ◽  
Vol 170 (4332) ◽  
pp. 803-803 ◽  
Author(s):  
MASAHIKO YONEDA ◽  
NOBUO KATO ◽  
MITSUHARU OKAJIMA

1972 ◽  
Vol 50 (12) ◽  
pp. 1217-1218 ◽  
Author(s):  
J. D. Wood ◽  
S. J. Peesker ◽  
J. I. M. Urton

The administration of isonicotinic acid hydrazide (2.2 mmol/kg) plus pyridoxine (4.4 mmol/kg) to chicks 14–18 h prior to exposure to hyperbaric oxygen provided excellent protection against the onset of oxygen-induced seizures in the birds.


1973 ◽  
Vol 51 (12) ◽  
pp. 959-965 ◽  
Author(s):  
J. D. Wood ◽  
S. J. Peesker

The administration of isonicotinic acid hydrazide and pyridoxine to chicks prior to their being exposed to oxygen at high pressure brought about a delay in the onset of the hyperbaric-oxygen-induced seizures in the birds. The hydrazide was the active anticonvulsant component of the drug mixture but pyridoxine was necessary to prevent seizures induced by the hydrazide itself shortly after its administration. The anticonvulsant action of the drug mixture developed relatively slowly but lasted for several hours and correlated well with concomitant changes in the concentration of γ-aminobutyric acid (GABA) in the brain. No similar correlation was observed between the anticonvulsant action and the activity of either glutamic acid decarboxylase or GABA-α-oxoglutarate aminotransferase.


PEDIATRICS ◽  
1992 ◽  
Vol 90 (2) ◽  
pp. 221-223
Author(s):  
STEVEN B. COKER

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.


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

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