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At least 631 records · Page 35Linked to original sources
PubMed1977

Chromosomal location of soluble glutamic-pyruvic transaminase-1 (Gpt-1) in the mouse.

Three alleles at the Gpt-1 (glutamic-pyruvic transaminase-1) locus in the mouse, as identified by electrophoresis on cellulose acetate, and their distribution among inbred mouse strains and wild stocks are described. The Gpt-1 locus was shown to control the soluble form of the enzyme. Three-point linkage analysis established th location of Gpt-1 on chromosome 15 between uw and bt. In addition, a new staining procedure is described that allows the visualization of GPT activity on gels by the deposition of formazan. This is an improvement over previous methods that produced bands of nonfluorescence against a fluorescent background.

Alanine Transaminase↗
PubMed1983

Physiological effects of an allozyme polymorphism: glutamate-pyruvate transaminase and response to hyperosmotic stress in the copepod Tigriopus californicus.

In order to regulate cell volume during hyperosmotic stress, the intertidal copepod Tigriopus californicus, like other aquatic crustaceans, rapidly accumulates high levels of intracellular alanine, proline, and glycine. Glutamate-pyruvate transaminase (GPT; EC 2.6.1.2), which catalyzes the final step of alanine synthesis, is genetically polymorphic in T. californicus populations at Santa Cruz, California. Spectrophotometric studies of homogenates derived from a homozygous isofemale line of each of the two common GPT alleles indicated that the GPTF allozyme has a significantly higher specific activity than the GPTS allozyme. Under conditions of hyperosmotic stress, individual adult copepods of GPTF and GPTF/S genotypes accumulated alanine, but not glycine or proline, more rapidly than GPTS homozygotes. When young larvae were subjected to the same hyperosmotic conditions, GPTS larvae suffered a significantly higher mortality than GPTF or GPTF/S larvae. These results suggest that the biochemical differences among GPT allozymes result in specific physiological variation among GPT genotypes and that this physiological variation is manifested in differential genotypic survivorships under some naturally occurring environmental conditions.

Alanine Transaminase↗
PubMed1993

Linkage between complement components 6 and 7 and glutamic pyruvate transaminase in the marsupial Monodelphis domestica.

The sixth and seventh components of complement were found to be polymorphic and tightly linked in the laboratory opossum (Monodelphis domestica), as they are in eutherian mammals. In addition, strong evidence for linkage of the C6-C7 haplotype to the gene for glutamic pyruvate transaminase (GPT) was obtained for females but not for males. This result, combined with previous observations, established as a generality that recombination is severely reduced in females of this species by comparison with males. It also establishes synteny of C6-C7 and GPT in a marsupial species, as exists in mice. Because these loci are not syntenic in humans, the results imply that this synteny is ancestral to the separation of marsupials and eutherians and that it was broken relatively recently in the mammalian lineage leading to human beings. The newly described C6 and C7 polymorphisms provide additional power for developing a linkage map for M. domestica and for localizing genes that confer susceptibility to diseases for which this species is used as a model.

Alanine Transaminase↗
PubMed1984

The involvement of GABA-transaminase in the blood-brain barrier to radiolabelled GABA.

The involvement of GABA-transaminase (GABA-T) in the blood-brain barrier to GABA was investigated using a sensitive radiotracer technique which allows measurement of tracer permeation as a cerebrovascular permeability-area product, PA. In Sprague-Dawley rats subjected to peripheral GABA-T inhibition and occlusion of hepatic circulation, chromatographic (TLC) analysis together with lyophylized plasma samples showed the radioactivity measured in brain parenchyma was derived from the permeation of unchanged [3H]GABA and not its blood-borne metabolites. Permeation (PA) of i.v. injected [3H]GABA was poor in all brain regions examined. Pretreatment of these rats with various compounds known to inhibit endothelial GABA-T activity did not cause any increased permeation of [3H]GABA into the brain. These results suggest that the poor permeation of GABA into the rat brain is unrelated to the activity of GABA-T at endothelial sites.

4-Aminobutyrate Transaminase↗
PubMed1986

Stereoselective uptake of the GABA-transaminase inhibitors gamma-vinyl GABA and gamma-acetylenic GABA into neurons and astrocytes.

The cellular uptake of the GABA-transaminase inhibitors gamma-vinyl GABA (GVG) and gamma-acetylenic GABA (GAG) was studied in cultured neurons and astrocytes. By the use of the individual enantiomers R- and S-GVG and R- and S-GAG it could be shown that in both cell types only the S-enantiomers could be actively transported. Comparing neurons and astrocytes only neurons exhibited a high affinity uptake system for S-GVG (Km 78.2 +/- 20.3 microM; Vmax 0.71 +/- 0.06 nmol.min-1.mg-1 cell protein). In case of S-GAG it could not be established with certainty whether the neuronal uptake was of the high affinity type. Both GVG and GAG were studied as inhibitors of GABA uptake into neurons and astrocytes. S-GVG and S-GAG were found to be weak inhibitors of GABA uptake suggesting that S-GVG is not transported by the GABA carrier in neurons. The finding of a much more efficient uptake of S-GVG into neurons than into astrocytes is in line with the previous observation that neuronal GABA-T is more sensitive than astrocytic GABA-T to S-GVG.

4-Aminobutyrate Transaminase↗
PubMed1984

Enzyme activities of monoamine oxidase, catechol-O-methyltransferase and gamma-aminobutyric acid transaminase in primary astroglial cultures and adult rat brain from different brain regions.

The activities of monoamine oxidase (MAO), catechol-O-methyltransferase (COMT) and gamma-aminobutyric acid transaminase (GABA-T) were measured in primary cultures from newborn rat cultivated from 6 different brain regions. These primary cultures contained mostly astroglial cells, evaluated by the presence of the glial fibrillary acidic protein (GFAp, alpha-albumin) and the S-100 protein. The enzyme activities in the corresponding brain area from adult rat were also quantified. MAO activities were on the same level in 14-day old cultures and in adult rat brain homogenates, with significantly lower values in brain stem as compared to the other brain regions examined. COMT activities were on a higher level in the cultures than in adult rat brain homogenates. Astroglial cells from hippocampus were found to have the highest and those from brain stem the lowest COMT-activities. GABA-T activities were lower in the cultures than in adult rat homogenates. No significant differences were seen in the various astroglial cultures. Accumulation of [3H]dopamine and [3H]gamma-aminobutyric acid (GABA) visualized by autoradiography showed only a slight uptake of dopamine in comparison with the uptake of GABA. It is concluded that astroglial cells in culture have enzymatic properties similar to those of astroglial cells in different brain regions of adult rat brain. Studies are in progress to evaluate if the regional heterogeneity observed among cultivated astroglial cells is affected by in vivo differentiation until cultivation and/or time in culture.

4-Aminobutyrate Transaminase↗
PubMed1987

Effects of the gamma-aminobutyrate transaminase inhibitors gabaculine and gamma-vinyl GABA on gamma-aminobutyric acid release from slices of rat cerebral cortex.

The release of [3H]gamma-aminobutyric acid (GABA) from pre-loaded slices of rat cerebral cortex was investigated in the presence and absence of the GABA-transaminase inhibitors gabaculine and gamma-vinyl GABA. In the experiments carried out without an inhibitor, an ion-exchange column chromatographic technique was used to separate [3H]GABA from tritiated metabolites released with it into the superfusate. The presence of gabaculine (5 microM) substantially reduced the Ca2+-dependence of the release of [3H]GABA evoked by a 4 min 30 mM K+ pulse, whereas this was not appreciably reduced by the presence of gamma-vinyl GABA (2 mM or 10 mM). Nevertheless, the characteristics of [3H]GABA release were not identical in the presence and absence of either inhibitor.

4-Aminobutyrate Transaminase↗
PubMed1985

GABA-transaminase and glutamic acid decarboxylase changes in the brain of rats treated with pyrithiamine.

Pyrithiamine, a thiamine phosphokinase inhibitor, was fed to rats on a thiamine-deficient diet, producing weight loss, ataxia and loss of righting reflex in 10 days. Some rats were then sacrificed; others were returned to a normal diet, to be sacrificed only when their weight had returned to pre-experimental levels. Rats were sacrificed for assay of glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) activities in homogenates of eight brain regions or were perfused for gamma-aminobutyric acid transaminase (GABA-T) histochemistry. GAD activity was significantly reduced in symptomatic rats in the thalamus greater than cerebellum greater than midbrain greater than pons/medulla. GABA-T staining was similarly reduced, with greatest losses in the thalamus greater than inferior colliculus greater than pons greater than medulla. ChAT activity was not significantly altered in any brain area. Following return to a normal diet. GAD activity was significantly recovered in all areas except the thalamus. GABA-T staining recovered, at least partially, in all areas affected.

4-Aminobutyrate Transaminase↗
PubMed1991

GABA-transaminase activity in rat and human brain: regional, age and sex-related differences.

The activity of 4-aminobutyrate:2-oxoglutarate transaminase (GABA-T) has been investigated in the rat and human brain. Both rat and human brain GABA-T retained its full activity for at least 2 months and with a loss of less than 10% after 6 months when frozen at -20 degrees C as tissue parts. There was a loss of activity of mouse brain GABA-T of about 15% per 24 hours postmortem. In the rat brain, GABA-T activity varied from low values in cortex and hippocampus to high in brain stem and cerebellum. There was a significant increase of GABA-T activity with age from 1 to 6 weeks and a significant reduction of the activity with age thereafter. Male rats had significant higher activity than female rats. In the human brain, GABA-T activities were measured in twelve regions of autopsied brains from 10 adult control subjects. No difference was found between the activities in the left and right sides. There is considerable variation in enzyme activity across the brain, with low activities in e.g. pons and medulla oblongata and high activities in e.g. caudatus, substantia nigra and hypothalamus. The activity of the enzyme is significantly different both between brain regions and between individuals.

4-Aminobutyrate Transaminase↗
PubMed1987

Intrahepatic cholestasis of pregnancy with marked elevation of transaminases in a black American.

A case of intrahepatic cholestasis of pregnancy (ICP) in a black American is presented. This is the first case reported in a black. Marked elevation of transaminases with mild biochemical evidence of cholestasis was initially suggestive of viral hepatitis. A clinical course characterized by pruritus with minimal constitutional symptoms, rapid resolution of biochemical abnormalities after delivery, and negative hepatitis A and B serologies was consistent with the diagnosis of ICP. Review of the classic features of ICP with emphasis on some unusual aspects of the disorder is included.

Adult↗
PubMed1980

Pancreatic juice gamma-glutamyltransferase, alanine transaminase, and alkaline phosphatase in pancreatic disease.

Pancreatic juice gamma-glutamyltransferase (GGT, EC 2.3.2.2) has been proposed as a marker of pancreatic disease. We have collected pancreatic juice endoscopically from 24 control patients and 43 patients with a variety of hepatic, pancreatic, and biliary disorders. Pancreatic juice GGT, alanine transaminase (ALT, EC 2.6.1.2), and alkaline phosphatase (ALP, EC 3.1.3.1) were measured and found to be present in all samples. GGT was significantly higher in patients with pancreatic cancer (range 21-1175 IU/liter, P less than 0.005) compared with controls (range 2-52 IU/liter). Of 17 patients with pancreatic juice GGT concentrations greater than 52 IU/liter, eleven had definite pancreatic disease (seven pancreatic cancer, four chronic pancreatitis) and, in the remaining six, pancreatitis was possible although not proven. Pancreatic juice ALT and ALP provided no useful diagnostic criteria. GGT in pancreatic juice seems to be a nonspecific marker of pancreatic disease and merits further study.

Alanine Transaminase↗
PubMed1977

Lactate dehydrogenase and transaminase activities in the cerebrospinal fluid of protein-energy malnourished children.

The present study is aiming to assess whether there are variations in the activities of the enzymes glutamic-oxalacetic transaminase (GOT) and lactate dehydrogenase (LDH) in the cerebrospinal fluid (CSF) of children suffering from protein-energy malnutrition (PEM). In this respect, serum and CSF activities of GOT and LDH were assayed in thirteen cases suffering from kwashiorkor and ten normal cases serving as controls. Increased activities of both enzymes in sera and CSF of PEM children compared with normals were observed. The significance of these variations was discussed.

Child↗
PubMed1995

Abnormal serum transaminases following therapeutic doses of acetaminophen in the absence of known risk factors.

J.M., a healthy, 25-year-old male, volunteered for a study involving warfarin and acetaminophen. Acetaminophen 1 g four times a day was started for 21 days. Liver function tests taken at regular intervals for the first 12 days were unremarkable. On day 18, however, aspartate aminotransferase (AST) was 527 IU/liter and alanine aminotransferase (ALT) was 166 IU/liter. Acetaminophen was discontinued and serum transaminase levels returned to baseline levels two weeks later (AST = 26, ALT = 20). Analysis of J.M.'s urine samples over the first 18 days showed excretion patterns of glucuronide, sulfate, and glutathione derived cysteine and mercapturic acid conjugates were similar to the other subjects in the study. Acetaminophen causes hepatotoxicity in overdose or malnourished or alcoholic patients, none of which applied to our subject. Differences in metabolic activation and capacity for glutathione synthesis can predispose individuals given therapeutic doses of acetaminophen to adverse effects. Failure to detoxify a highly reactive metabolite, formed by P-450 metabolism, via glutathione conjugation is responsible for the development of acute hepatic necrosis. Accumulation of the toxic metabolite due to depleted glutathione stores may have occurred with prolonged high dosing in our subject and been responsible for his abnormal rise in liver enzymes.

Acetaminophen↗
PubMed1996

The rate of turnover of cortical GABA from [1-13C]glucose is reduced in rats treated with the GABA-transaminase inhibitor vigabatrin (gamma-vinyl GABA).

Brain GABA levels rise and plateau following prolonged administration of the irreversible GABA-transaminase inhibitor vigabatrin (gamma-vinylGABA). Recently it has been shown that increased GABA levels reduces GAD67 protein, one of two major isoforms of glutamic acid decarboxylase (GAD). The effects of GABA elevation on GABA synthesis were assessed in vivo using 1H and 13C-edited NMR spectroscopy. Rates of turnover of cortical glutamate and GABA from intravenously administered [1-13C]glucose were measured in alpha-chloralose anesthetized rats 24 hours after receiving vigabatrin (500 mg/kg, i.p.) and in non-treated controls. GABA concentration was increased 2-fold at 24 hours (from 1.3 +/- 0.4 to 2.7 +/- 0.9 mumol/g) and GABA-T activity was inhibited by 60%. Tricarboxylic acid cycle flux was not affected by vigabatrin treatment compared to non-treated rats (0.47 +/- 0.19 versus 0.52 +/- 0.18 mumol/g, respectively). GABA-C2 fractional enrichment (FE) measured in acid extracts rose more slowly in vigabatrin-treated compared to non-treated rats, reaching > 90% of the glutamate FE after 3 hours. In contrast, GABA FE > or = glutamate FE in non-treated rats. A metabolic model consisting of a single glutamate pool failed to account for the rapid labeling of GABA from glutamate. Metabolic modelling analysis based on two (non-communicating) glutamate pools revealed a approximately 70% decrease in the rate of GABA synthesis following vigabatrin-treatment, from 0.14 (non-treated) to 0.04 mumol/g/min (vigabatrin-treated). These findings, in conjunction with the previously reported differential effects of elevated GABA on the GAD isoforms, suggests that GAD67 may account for a major fraction of cortical GABA synthesis in the alpha-chloralose anesthetized rat brain in vivo.

4-Aminobutyrate Transaminase↗
PubMed1998

Measuring human brain GABA in vivo: effects of GABA-transaminase inhibition with vigabatrin.

Gamma-aminobutyric acid (GABA) plays a pivotal role in suppressing the origin and spread of seizure activity. Low occipital lobe GABA was associated with poor seizure control in patients with complex partial seizures. Vigabatrin irreversibly inhibits GABA-transaminase, raising brain and cerebrospinal fluid (CSF) GABA concentrations. The effect of vigabatrin on occipital lobe GABA concentrations was measured by in vivo nuclear magnetic-resonance spectroscopy. Using a single oral dose of vigabatrin, the rate of GABA synthesis in human brain was estimated at 17% of the Krebs cycle rate. As the daily dose of vigabatrin was increased to up to 3 g, the fractional elevation of brain GABA was similar to CSF increase. Doubling the daily dose from 3 to 6 g failed to increase brain GABA further. Increased GABA concentrations appear to reduce GABA synthesis in humans as it does in animals. With traditional antiepileptic drugs, remission of the seizure disorder was associated with normal GABA levels. With vigabatrin, elevated CSF and brain GABA was associated with improved seizure control. Vigabatrin enhances the vesicular and nonvesicular release of GABA. The release of GABA during seizures may be mediated in part by transporter reversal that may serve as an important protective mechanism. During a seizure, this mechanism may be critical in stopping the seizure or preventing its spread.

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

Developmental modulation of cysteine conjugate beta-lyase/glutamine transaminase K/kynurenine aminotransferase mRNA in rat brain.

Cysteine conjugate beta-lyase/glutamine transaminase K/kynurenine aminotransferase (CS-lyase/GTK/KAT) is a tri-functional enzyme found in several organs, including the brain. Kynurenine aminotransferase is important in tryptophan metabolism in the CNS, producing kynurenic acid, a NMDA receptor antagonist and neuroprotective. Tryptophan not metabolised via kynurenine aminotransferase may form quinolinic acid, a NMDA receptor agonist and neurotoxin. Kynurenic acid co-treatment blocks quinolinic acid induced lesions in the CNS in rat. In many conditions exhibiting neurodegeneration (i.e. Huntington's, Parkinsonism, Down's syndrome) quinolinic acid and/or kynurenic acid concentrations are altered, suggesting the ratio of these chemicals may be important in neurodegeneration. We have investigated the developmental modulation of CS-lyase/GTK/KAT mRNA in rat brain. CS-lyase/GTK/KAT mRNA was measured in 14, 21, 28, 35, 42 day post-natal and adult rats. While many regions demonstrated a steady increase to adult levels, two other profiles were seen. Five regions rapidly reached adult levels of the mRNA, while two peaked above the adult level before falling back. This provides evidence that expression of the CS-lyase/GTK/KAT gene is physiologically modulated, and provides the basis for further investigation into the mechanism of control. Artificial modulation could possibly be used to alter levels of the neuroprotectant kynurenic acid in neurodegeneration.

Animals↗