Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.19 (GABA transaminase)
 808 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of enzymes involved in the tricarboxylic acid cycle was studied in Nocardia erythropolis IBFM B-293. It was found to be low and hardly change, with some exceptions, in the course of growth in the presence of various carbon sources. Acetate induced enzymes of the glyoxylate cycle which was here an important mechanism of oxalacetate synthesis. The absence of alpha-ketoglutarate dehydrogenase in the case of all studied substrates and the absence of 4-aminobutyrate aminotransferase, the key enzyme of the compensating 4-aminobutyrate shunt, suggest that the tricarboxylic acid cycle is decoupled. Therefore, this cycle does not operate as a mechanism generating energy in N. erythropolis, but fulfills mainly biosynthetic functions.
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PMID:[Characteristics of the tricarboxylic acid cycle in Nocardia erythropolis]. 42 7

A state of the gamma-aminobutyric acid (GABA) system (glutamate, glutamate decarboxylase, GABA, GABA-alpha-ketoglutarate aminotransferase) and the coupled reactions (alpha-ketoglutarate dehydrogenase complex, aspartate- and alanine aminotransferases) was studied in three brain structures (cerebellum, brain cortex and truncus cerebri) after multiple administration of pyridoxal-5'-phosphate (PALP) and its Shiff base with GABA (5 injections at doses 10.0 and 15.0 mg/kg of body mass, respectively). Non-coenzymatic effects of PALP were found to prevail within 1 hr after its last administration: inhibition of PALP-dependent aminotransferases and activation of the alpha-keto-glutarate oxidative decarboxylation were observed. The opposite effects were detected after addition of PALP to brain homogenates in vitro. Administration of the PALP-GABA complex exhibited qualitatively similar to those of PALP effects on the reactions studied in brain. The data obtained suggest that parenteral administration of the coenzyme preparation caused a number of metabolic effects, which are sometimes far from unambigously predicted theoretical considerations. The similarity of PALP and PALP-GABA effects appears to demonstrate ready biotransformation of the Shiff base with liberation of PALP and GABA.
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PMID:[Changes in the brain GABA system after repeated injections of pyridoxal-5'-phosphate and its Schiff base with GABA]. 274 11

Metabolism of the glutamate group of amino acids--glutamic acid, gamma-amino-butyric acid, glutamine, aspartic acid and alanine--was studied in the brain of rat as a function of age. The levels of glutamic acid, glutamine and aspartic acid decreased while those of gamma-aminobutyric acid, and alanine increased with age. The results on the activity of the twelve enzymes involved in the metabolism showed that five of them (glutamate dehydrogenase, glutamine synthase, gamma-aminobutyric acid transaminase, succinic semialdehyde dehydrogenase and NAD+-isocitrate dehydrogenase) decreased, while four of them (glutaminase, glutamotransferase, glutamic acid decarboxylase, and alpha-ketoglutarate dehydrogenase) increased. The other three enzymes (aspartate aminotransferase, alanine aminotransferase and NADP+-isocitrate dehydrogenase) did not show any significant change in activity. An age-related increase was seen in alpha-ketoglutarate and ammonia, the intermediates involved in the metabolism of these amino acids. The changes in the level of these amino acids are discussed in relation to the altered energy metabolism during aging.
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PMID:Metabolism of the glutamate group of amino acids in rat brain as a function of age. 614 62

The composition and properties of the tricarboxylic acid cycle of the microaerophilic human pathogen Helicobacter pylori were investigated in situ and in cell extracts using [1H]- and [13C]-NMR spectroscopy and spectrophotometry. NMR spectroscopy assays enabled highly specific measurements of some enzyme activities, previously not possible using spectrophotometry, in in situ studies with H. pylori, thus providing the first accurate picture of the complete tricarboxylic acid cycle of the bacterium. The presence, cellular location and kinetic parameters of citrate synthase, aconitase, isocitrate dehydrogenase, alpha-ketoglutarate oxidase, fumarate reductase, fumarase, malate dehydrogenase, and malate synthase activities in H. pylori are described. The absence of other enzyme activities of the cycle, including alpha-ketoglutarate dehydrogenase, succinyl-CoA synthetase, and succinate dehydrogenase also are shown. The H. pylori tricarboxylic acid cycle appears to be a noncyclic, branched pathway, characteristic of anaerobic metabolism, directed towards the production of succinate in the reductive dicarboxylic acid branch and alpha-ketoglutarate in the oxidative tricarboxylic acid branch. Both branches were metabolically linked by the presence of alpha-ketoglutarate oxidase activity. Under the growth conditions employed, H. pylori did not possess an operational glyoxylate bypass, owing to the absence of isocitrate lyase activity; nor a gamma-aminobutyrate shunt, owing to the absence of both gamma-aminobutyrate transaminase and succinic semialdehyde dehydrogenase activities. The catalytic and regulatory properties of the H. pylori tricarboxylic acid cycle enzymes are discussed by comparing their amino acid sequences with those of other, more extensively studied enzymes.
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PMID:The tricarboxylic acid cycle of Helicobacter pylori. 1009 6

Valproate, one of the major antiepileptic drugs used today, has besides its wide use in both generalized and partial epilepsies, several new approved indications including the treatment of bipolar disorders, neuropathic pain, and as a migraine prophylaxis. This wide spectrum of activities is reflected by several different mechanisms of action, which are discussed in this review. With regard to the antiepileptic effect of VPA, a special emphasis is put on the effect on the GABAergic system and the effect on enzymes like succinate semialdehyde dehydrogenase (SSA-DH), GABA transaminase (GABA-T), and alpha-ketoglutarate dehydrogenase, related to the tricarboxylic acid (TCA) cycle and thereby cerebral metabolism. In vitro studies have shown that VPA is a potent inhibitor of SSA-DH. In brain homogenates, GABA-T is inhibited at high concentrations only. Besides affecting the GABA-shunt, VPA might also inhibit the TCA cycle at the alpha-ketoglutarate dehydrogenase step. The effect of VPA on excitatory neurotransmission and on excitatory membranes are mechanisms likely to be responsible for the 'mood-stabilizing' effect as well as in the treatment of migraine. GABA-mediated responses may be involved in neuropathic pain. But still there are many aspects of the mechanisms of action of VPA that remain unknown.
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PMID:Mechanisms of action of valproate: a commentatory. 1081 95

The mechanism of action of the antiepileptic drug lamotrigine has previously been investigated only in acute experiments and is thought to involve inhibition of voltage-dependent sodium channels. However, lamotrigine is effective against more forms of epilepsies than other antiepileptic drugs that also inhibit sodium channels. We investigated whether chronic lamotrigine treatment may affect cerebral amino acid levels. Rats received lamotrigine, 10 mg/kg/day, for 90 days. The hippocampal level of GABA increased 25%, and the activities of glutamate decarboxylase and succinic semialdehyde/GABA transaminase increased 12 and 21% (p< 0.05), respectively, indicating increased GABA turnover. The uptake of GABA and glutamate into proteoliposomes remained unaltered. The level of taurine increased 27% in the hippocampus and 16% in the frontal and parietal cortices. The activities of hexokinase and alpha-ketoglutarate dehydrogenase, remained at control values. Serum lamotrigine was 41.7+/-1.5 microM (mean+/-S.E.M.), which is within the range seen in epileptic patients. Acute experiments with 5, 20 or 100 mg lamotrigine/kg, caused no changes in brain amino acid levels. The results suggest that chronic lamotrigine treatment increases GABAergic activity in the hippocampus. The cerebral increase in taurine, which has neuromodulatory properties, may contribute to the antiepileptic effect of lamotrigine.
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PMID:Chronic lamotrigine treatment increases rat hippocampal GABA shunt activity and elevates cerebral taurine levels. 1116 4