Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.6.1.19 (
GABA transaminase
)
808
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The intramuscular administration of 4,5,6,7-tetrahydroisoxazolo [4,5-c] pyridin-3-ol (THPO) delayed the onset of
isonicotinic acid
hydrazide-induced seizures in very young chicks but not in adult mice, the difference being due to the state of development of the blood-brain-barrier which controls access of the drug to the brain tissue. THPO was also effective in preventing seizures induced in epileptic chicks by intermittent photic stimulation. The anticonvulsant action after combined administration of THPO and gabaculine, an inhibitor of
GABA-alpha-oxoglutarate aminotransferase
activity, was no greater than the anticonvulsant action of gabaculine alone.
...
PMID:Anticonvulsant activity of the glial-selective GABA uptake inhibitor, THPO. 684 84
When
gamma-aminobutyric acid aminotransferase
(
GABA-T
) activity was measured in vitro in rat brain, neither isoniazid (INH) nor for of its known metabolites (
isonicotinic acid
, acetylisoniazid, acetylhydrazine, diacetylhydrazine) inhibited the enzyme in concentrations (5 mM) far higher than those likely to be achieved when INH is administered to man. In contrast, hydrazine (5 micrometers) caused a 50% inhibition of
GABA-T
without inhibiting glutamic acid decarboxylase (GAD). Rats were injected daily for 109 days with hydrazine (0.08 or 0.16 mmol/kg/day), after which amino acid contents and enzyme activities were measured in their brains. Both hydrazine doses caused significant elevations of whole brain GABA content and reductions of
GABA-T
activity, but did not affect GAD activity. Chronic administration of hydrazine at these doses did not reduce weight gain or alter rat behavior, nor did it produce any irreversible pathologic changes in liver or alterations in hepatic aryl hydrocarbon hydroxylase activity. However, hydrazine treatment caused changes in the contents of many brain amino acids besides GABA, and markedly increased concentrations of ornithine, tyrosine, and alpha-aminoadipic acid in rat plasma. Inhibition of
GABA-T
activity and the other biochemical alterations observed in patients given high doses of INH probably result from hydrazine formed in the metabolic degradation of INH. Thus administration of hydrazine might be a more direct means of elevating brain GABA content in patients where this seems indicated, and might not entail a greater risk of adverse effects.
...
PMID:Elevation of brain GABA content by chronic low-dosage administration of hydrazine, a metabolite of isoniazid. 725 11
The effect of several antivitamin B6 on gamma-aminobutyric acid (GABA) metabolism was studied in the rat retina. The rat electroretinogram (ERG) was also recorded after administration of these drugs. Aminooxyacetic acid (AOAA) and hydrazine administration increased the GABA content and inhibited the GABA degrading enzyme,
GABA transaminase
in retina. In addition, there drugs elongated the peak latency of the oscillatory potential in the rat ERG. In contrast, 4-deoxypyridoxine (DOP) or
isonicotinic acid
hydrazide (INAH) administration decreased the GABA content and inhibited the GABA synthesizing enzyme, glutamic acid decarboxylase in retina, and administration of these drugs together with AOAA lessened the degrees of elevation of GABA content and of the elongation of the peak latency produced as compared with AOAA alone, though neither of the former drugs had a significant effect on ERG. The retinal GABA seems to play an important role in relation to the oscillatory potential of ERG.
...
PMID:The effect of antivitamin B6 administration on gamma-aminobutyric acid metabolism in retina and electroretinogram. 741 Dec 49
