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At least 757 records · Page 42Linked to original sources
PubMed2006

Fatty liver and transaminase changes with adjuvant tamoxifen therapy.

We investigated the time it took to develop fatty liver and changes in serum aspartate aminotransferase and alanine aminotransferase levels in patients with breast cancer treated with adjuvant tamoxifen. Liver sonography to detect fatty liver and measurement of serum aspartate and alanine aminotransferase levels were performed regularly for patients with early breast cancer. The results were compared in groups of patients with and without adjuvant tamoxifen as well as those on chemotherapy. Eighty-two of 156 patients treated with tamoxifen developed fatty liver, compared with eight of 62 patients not taking it. Fatty liver appeared as early as 3 months after beginning tamoxifen and was detected within 2 years in most cases. It persisted for 48 months after discontinuing tamoxifen in 17 of the 82 patients who developed it. The incidence of fatty liver in patients receiving both chemotherapy and tamoxifen was the same as that in patients receiving tamoxifen alone. While 115 patients had elevations of aspartate aminotransferase, alanine aminotransferase or both, the magnitude of the elevation was clinically significant in only 32 patients. Patients on both chemotherapy and tamoxifen had a higher incidence of elevated transaminases than those on tamoxifen alone. Adjuvant tamoxifen increases the incidence of fatty liver, but has only a minimal effect on aspartate aminotransferase and alanine aminotransferase. Fatty liver may appear as early as 3 months after beginning tamoxifen and may persist for more than 4 years after discontinuing it. Therefore, long-term follow-up is warranted. Chemotherapy is not clearly associated with fatty liver, but may cause a greater degree of hepatocellular damage than does tamoxifen.

Alanine Transaminase↗
PubMed2006

The effect of antioxidant supplementation on hepatitis C viral load, transaminases and oxidative status: a randomized trial among chronic hepatitis C virus-infected patients.

OBJECTIVE: To assess the effect of antioxidant supplementation on hepatitis C viral load, transaminases and oxidative status. METHODS: We performed a randomized, placebo-controlled, double-blind trial to assess the effect of antioxidant supplementation on serum alanine aminotransferase, plasma hepatitis C viral load as well as oxidative and antioxidant markers in patients with hepatitis C virus infection. The participants received a daily dose of ascorbic acid (500 mg), D-alpha-tocopherol (945 IU) and selenium (200 microg) or placebo tablets for 6 months. RESULTS: Twenty-three patients were included. During supplementation, the antioxidant group had significantly higher levels of plasma ascorbic acid and alpha-tocopherol than the placebo group and the activity of erythrocyte glutathione peroxidase had significantly increased from baseline to month 6. No differences were observed in serum alanine aminotransferase and log10-transformed plasma hepatitis C virus-RNA between the groups or changes from the baseline at any time. No consistent differences between groups or changes from the baseline with respect to erythrocyte activities of antioxidative enzymes (glutathione reductase, superoxide dismutase and catalase) or plasma levels of oxidative markers (malondialdehyde and 2-amino-adipic semialdehyde) were found. CONCLUSION: Supplementation with vitamin C, E and selenium increased the antioxidant status, but had no effects on alanine aminotransferase, viral load or oxidative markers.

Adult↗
PubMed2005

Daily interferon monotherapy for chronic hepatitis C in patients with normal or near-normal serum alanine transaminase levels: a comparison of two protocols.

OBJECTIVES: Up to 30% of the 5 million patients with chronic hepatitis C in the United States have normal serum alanine transaminase (ALT) levels. These individuals have not been treated aggressively, and reported response rates have been low. No study has targeted patients treated in a community practice setting. METHODS: Consecutive patients with chronic hepatitis C with normal or near-normal serum ALT levels seen over a 2-year period in a community gastroenterology-hepatology practice were randomly assigned to receive either 3 MU or 6 MU daily interferon (IFN)-alpha-2a monotherapy for 12 months. RESULTS: Sixteen patients (8 in each treatment arm) qualified for study. End-of-treatment response was 87.5% with 6 MU IFN daily and 75% with 3 MU IFN daily, whereas sustained virologic response was 62.5% and 50%, respectively. Genotype 1 patients had an improved outcome with the higher 6 MU dose. CONCLUSIONS: Daily IFN monotherapy achieves high response rates in patients with chronic hepatitis C with normal or near-normal ALT. Present-day pegylated interferon regimes can be expected to be as effective.

Adult↗
PubMed1999

A putative branched-chain-amino-acid transaminase gene required for HC-toxin biosynthesis and pathogenicity in Cochliobolus carbonum.

The cyclic tetrapeptide HC-toxin is required for pathogenicity of the filamentous fungus Cochliobolus carbonum on maize. HC-toxin production is controlled by a complex locus, TOX2. The isolation and characterization of a new gene of the TOX2 locus, TOXF, is reported. It is shown that TOXF is specifically required for HC-toxin production and pathogenicity. It is present as two or three copies in all HC-toxin-producing (Tox2+) isolates and is absent in toxin-non-producing strains. The deduced amino acid sequence of TOXF has moderate homology to many known or putative branched-chain-amino-acid transaminases from various species. A strain of C. carbonum with all copies of TOXF disrupted grew normally but lost HC-toxin production and pathogenicity. It is proposed that TOXF has a biosynthetic role in HC-toxin synthesis, perhaps to aminate a precursor of Aeo (2-amino-9,10-epoxi-8-oxodecanoic acid).

Amino Acid Sequence↗
PubMed2002

The branched-chain amino acid transaminase gene family in Arabidopsis encodes plastid and mitochondrial proteins.

Branched-chain amino acid transaminases (BCATs) play a crucial role in the metabolism of leucine, isoleucine, and valine. They catalyze the last step of the synthesis and/or the initial step of the degradation of this class of amino acids. In Arabidopsis, seven putative BCAT genes are identified by their similarity to their counterparts from other organisms. We have now cloned the respective cDNA sequences of six of these genes. The deduced amino acid sequences show between 47.5% and 84.1% identity to each other and about 30% to the homologous enzymes from yeast (Saccharomyces cerevisiae) and mammals. In addition, many amino acids in crucial positions as determined by crystallographic analyses of BCATs from Escherichia coli and human (Homo sapiens) are conserved in the AtBCATs. Complementation of a yeast Deltabat1/Deltabat2 double knockout strain revealed that five AtBCATs can function as BCATs in vivo. Transient expression of BCAT:green fluorescent protein fusion proteins in tobacco (Nicotiana tabacum) protoplasts shows that three isoenzymes are imported into chloroplasts (AtBCAT-2, -3, and -5), whereas a single enzyme is directed into mitochondria (AtBCAT-1).

Amino Acid Sequence↗
PubMed1991

On the inhibition of glutamic acid decarboxylase and gamma-aminobutyric acid transaminase by sodium cyanide.

The effects of sodium cyanide (NaCN) on the gamma-aminobutyric acid metabolizing enzymes glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) were studied in vitro. With no pyridoxal-5-phosphate added, GAD was non-competitively inhibited by NaCN, with an IC50 of 280 microM. GAD was also inhibited when exposed to an equimolar amount of NaCN and pyridoxal-5-phosphate. NaCN inhibited GABA-T. The inhibition kinetics suggests that NaCN may react with more than one of the substrates and products present during the reaction, i.e. pyridoxal-5-phosphate, alpha-ketoglutarate and/or succinic semialdehyde. The presence of pyridoxal-5-phosphate in the reaction mixture completely protected GABA-T from inhibition by NaCN. The gamma-aminobutyric acid synthesizing enzyme, GAD may thus be inhibited in vivo by NaCN or by a reaction product of NaCN and pyridoxal-5-phosphate. The gamma-aminobutyric acid catabolizing enzyme, GABA-T is not as vulnerable to inhibition by NaCN, since the cyanide-pyridoxal-5-phosphate complex is ineffective as inhibitor.

4-Aminobutyrate Transaminase↗
PubMed1989

The effect of vigabatrin on brain and platelet GABA-transaminase activities.

1. The inhibition profiles of GABA-transaminase (GABA-T) in rat brain and platelet have been compared following a single intraperitoneal dose of vigabatrin. The inhibition profiles exhibit similarities. The inhibition produced by the drug is dose-dependent and, in the dose range used in man, the dose-response curves are comparable. The pharmaco-dynamic effects of the drug (inhibition of central and peripheral GABA-T) remain after the drug has been eliminated from plasma. It is suggested that the measurement of rat platelet GABA-T may be used as a non-invasive assessment of the efficacy of GABA-T inhibitors in the rat CNS. 2. Human blood platelet GABA-T was significantly inhibited by the administration of a single oral dose of vigabatrin. Chronic administration also produces a significant inhibition of platelet GABA-T. As with rats, the pharmacodynamic effects on the platelet enzyme remained after the drug had been eliminated from plasma. If the situation in man is assumed to parallel that found in the rat then measurement of platelet GABA-T inhibition could prove to be a useful indicator of central inhibition.

4-Aminobutyrate Transaminase↗
PubMed1980

Glutamic pyruvate transaminase phenotypes in polycythaemia rubra vera.

Glutamate pyruvate transaminase (GPT) has been studied in the red cells of 46 patients with a confirmed diagnosis of polycythaemia rubra vera (PRV). The red cells of many of the patients showed low levels of enzyme activity. This activity could be restored by in vitro incubation with pyridoxal phosphate suggesting that the effect was due to low levels of B6 rather than to a primary abnormality of the GPT. Patients with the lowest levels of GPT activity were likely to have clonal chromosomal abnormalities in the bone marrow cells, particularly 20q-. Among 43 patients in whom the GPT phenotypes could be determined by an electrophoretic method there was a marked deficiency of heterozygotes. This disturbance in phenotypic expression may be related to the clonal nature of the disease in PRV, the clone showing lack of response to homeostatic controls and irregularities of gene expression.

Alanine Transaminase↗
PubMed1975

Highly purified glutamine transaminase from rat brain. Physical and kinetic properties.

Glutamine transaminase from rat brain was purified to a high degree. The isolated enzyme appeared to be homogeneous by electrophoresis on polyacrylamide gel. The molecular weight was found to be approximately 98 000; the enzyme is probably composed of two subunits. The absorbance maximum at 410 nm and the inhibition by carbonyl reagents are strong indications for the presence of pyridoxal phosphate. The enzyme showed maximal activity at pH 9.0 to 9.2. Of the amino acids tested, none could replace glutamine in the transamination reaction. Glyoxylate and phenylpyruvate was found to be the best amino acceptors. The Km values for glutamine and glyoxylate were 0.6 and 1.5 mM, respectively.

Animals↗
PubMed1976

Glutamine transaminase from brain tissue. Further studies on kinetic properties and specificity of the enzyme.

Glutamine transaminase, highly purified from rat brain, was studied. In the first series of experiments, the kinetics of the transamination reaction between 2-oxoglutaramate and phenylalanine were examined in order to determine the type of reaction mechanism. This proved to be of the ping-pont type, as can be expected for a transamination. The specificity of the enzyme for various amino acids and 2-oxo acids was then studied in detail. The most active substrates were glutamine, methionine and ethionine as amino-group donors, and phenylpyruvate, glyoxalate and 2-oxo-4-methiobutyrate as amino-group acceptors. For these and several other substrates, the kinetic constants, V and Km, were determined.

Amino Acids↗
PubMed1989

Glutamate:4,5-dioxovaleric acid transaminase from Euglena gracilis. Kinetic studies.

The kinetic properties of the enzyme L-glutamate:4,5-dioxovaleric acid aminotransferase (Glu:DOVA transaminase) from Euglena gracilis have been studied. 5-Aminolevulinic acid formation was linear with time for at least 45 min at 37 degrees C and L-glutamate was the most effective amino-group donor. Lineweaver-Burk double-reciprocal plots suggested a ping-pong reaction mechanism, with Km values for L-glutamate and DOVA of 1.92 mM and 0.48 mM respectively. Competitive parabolic substrate inhibition by DOVA at concentrations greater than 3.5-4.5 mM was observed. Glyoxylate (4-10 mM) was found to be a competitive inhibitor with respect to DOVA, whereas at low concentrations (0-4 mM) noncompetitive plots were obtained. An analysis of the possible enzyme forms involved, was carried out. In more crude preparations most of the enzyme is found to be in the form of an enzyme-glutamate complex.

Animals↗
PubMed1997

Antibodies to hepatitis C virus and elevated transaminase levels in a town of hyperendemicity in Iwate, Japan.

In an annual survey for liver function tests in persons aged > 35 years in Iwate Prefecture, Japan, a town was identified where high levels of alanine aminotransferase abounded. Of 5152 inhabitants aged > 35 years in this town, antibodies to hepatitis C virus (HCV) determined by enzyme-linked immunosorbent assay with HCV core peptides were detected in 798 (15.5%) people, hepatitis B surface antigen was detected in 47 (0.9%) people and antibodies to hepatitis B surface antigen and/or hepatitis B core antigen unaccompanied by surface antigenaemia were detected in 1748 (33.9%) people. Antibodies to HCV core peptides correlated closely with the antibodies detected by passive haemagglutination with recombinant HCV proteins of the second generation. Antibodies to HCV core peptides were particularly common in one of the nine districts of the town (district 8), where 276 (45.3%) of 609 inhabitants tested positive; there were no differences in the frequency of serological markers of hepatitis B virus (HBV) infection among residents in the nine districts. Of the 798 individuals with antibodies to HCV core peptides, 257 (32.2%) were found to have elevated transaminase levels. A history of transfusion was associated with a high frequency of antibodies to HCV core peptides, except in district 8 where such antibodies were equally frequent in residents irrespective of transfusions. These results indicate an epidemiology of HCV distinct from that of HBV in this town and a very local spread of HCV, as well as a high frequency of hepatic injuries in individuals with antibodies to HCV.

Adult↗
PubMed1984

Distribution of glycine, gamma-aminobutyric acid, glutamate decarboxylase, and gamma-aminobutyric acid transaminase in rabbit and mudpuppy retinas.

The distributions of glycine, gamma-aminobutyric acid (GABA), glutamate decarboxylase (EC 4.1.1.15), and GABA transaminase (EC 2.6.1.19) were determined in rabbit and mudpuppy retinas. In both species, peak levels of the amino acids and the enzymes occurred in the inner plexiform layer. Glutamate decarboxylase was almost entirely confined to the inner plexiform layer. Determinations were also made of the GABA content of 107 individual putative amacrine cell somas from mudpuppy retina. About 30% of those somas were found to have high endogenous GABA levels.

4-Aminobutyrate Transaminase↗
PubMed1984

Enzymes of cerebral GABA metabolism and synaptosomal GABA uptake in acute liver failure in the rabbit: evidence for decreased cerebral GABA-transaminase activity.

Measurements of the activities of the two key enzymes in cerebral GABA metabolism--glutamate decarboxylase (GAD) and GABA-transaminase (GABA-T)--were performed in normal rabbits and in rabbits with hepatic encephalopathy due to galactosamine-induced liver failure. Furthermore the uptake of GABA by synaptosomes was studied. Hepatic encephalopathy was associated with a marked decrease in the activity of GABA-T. This decrease in activity was already apparent in galactosamine-treated rabbits before the onset of hepatic encephalopathy. Sera and serum ultrafiltrates of rabbits with hepatic encephalopathy but not of normal rabbits or of rabbits with uremic encephalopathy were shown to inhibit GABA-T activity in vitro. Cerebral GAD activity and synaptosomal GABA uptake in rabbits with hepatic encephalopathy and in untreated animals were not different. These later findings indicate that hepatic encephalopathy is not associated with alterations of presynaptic GABA nerve terminals in the central nervous system. The demonstration of a decrease in cortical GABA-T activity provides indirect evidence for decreased GABA turnover in the brains of rabbits with hepatic encephalopathy and thus is compatible with augmented GABA-ergic inhibitory neurotransmission contributing to the neural inhibition of hepatic encephalopathy.

4-Aminobutyrate Transaminase↗
PubMed1985

A monoclonal antibody to rabbit brain GABA transaminase.

A monoclonal antibody of class IgG (subclass IgG1) has been prepared to rabbit brain GABA transaminase (GABA-T). This antibody reveals a single band of molecular weight 52,000 on a nitrocellulose filter blotted with purified GABA-T. On a filter blotted with unfractionated rabbit brain supernatant a major band of molecular weight 58,000 is revealed. An immunoaffinity column was prepared by coupling proteins from ascites fluid containing anti-rabbit GABA-T antibody to Bio-Rad Affi-Gel 15. This column bound purified GABA-T and extracted from unfractionated rabbit brain supernatant a protein of molecular weight 58,000, which was almost homogeneous and which had GABA-T enzyme activity. Using immunoaffinity chromatography, therefore, a high degree of purification of GABA-T may be achieved in a single step. Further, this technique may preserve an authentic form of the enzyme that is lost during the conventional purification procedure. The antibody inhibits GABA-T enzyme activity, up to a maximum of 35%.

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

Relationship between platelet and brain GABA transaminase inhibition by single and multiple doses of vigabatrin in rats.

Vigabatrin (gamma-vinyl-GABA, GVG) is an inhibitor of brain GABA transaminase (GABA-T) that also inhibits platelet GABA-T in rats and humans. We have compared the effects of single and multiple doses of GVG on both enzymes in 19 groups of 10 adult male Wistar rats, treated with increasing GVG doses (0-1,600 mg/kg/day) for 1, 8, and 28 days. The platelet GABA-T was more sensitive to the inhibitory effects of GVG than the brain enzyme was especially with low dosages of GVG. After 8 days of treatment, higher GVG plasma levels and a higher inhibition of both enzymes were shown. However, after 28 days, lower GVG plasma levels and similar inhibition of both enzymes compared to the eighth day were found. Correlations between platelet and brain GABA-T for individual rats were statistically significant after 1 day (r = 0.40, p less than 0.01) but not after 8 and 28 days of treatment because of the total inhibition of platelet GABA-T and only partial inhibition of brain GABA-T. We concluded the following: (a) platelet GABA-T is more inhibited than brain GABA-T when low doses of GVG are used and (b) multiple doses reach a higher inhibition of both enzymes than single doses, which could be explained by an increase in GVG concentrations.

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

Gamma-vinyl GABA (vigabatrin): relationship between dosage, plasma concentrations, platelet GABA-transaminase inhibition, and seizure reduction in epileptic children.

The relationship between vigabatrin gamma-vinyl GABA (GVG, vigabatrin) daily dosage or steady-state plasma concentrations (CSS), platelet GABA-transaminase (GABA-T) inhibition, and seizure reduction were studied in 16 children with refractory epilepsy. After 2 months of observation and 1 month of single-blind add-on placebo, a fixed GVG dosage was added for 2 months. The dosage was then adjusted in two 2-month periods each, based on the patient's clinical response. In the fixed-dose period, GVG dosages of 56.8 mg/kg/day and CSS of 8.1 mg/L reduced GABA-T activity from 13.9 to 5.1 pmol/min/mg protein (p less than 0.001) and that of seizures from 51.4 to 22.3 seizures per month (p less than 0.01). Seizure reduction was correlated with dosage (r = 0.83, p less than 0.001), but not with CSS or with platelet GABA-T inhibition. After the GVG dose-adjustment periods, in which dosages of 84.4 mg/kg/day and CSS of 10.6 mg/L were reached, only a slight reduction was observed in both GABA-T activity (from 5.1 to 4.9 pmol/min/mg protein) and seizures (from 22.3 to 18.1 seizures per month). In GVG-responsive patients (excluding placebo-sensitive and GVG-resistant patients), a greater reduction of seizures was achieved (from 17.0 to 7.1 seizures per month, p less than 0.05), which was not accompanied by greater inhibition of GABA-T. GVG treatment in children should be started with a dosage of 50 mg/kg/day, increased to 75 or even 100 mg/kg/day when a partial response is observed. If seizures do not improve or if they become worse, the patient should be considered resistant and GVG should be discontinued.

4-Aminobutyrate Transaminase↗
PubMed2006

The effect of increased branched-chain amino acid transaminase activity in yeast on the production of higher alcohols and on the flavour profiles of wine and distillates.

In Saccharomyces cerevisiae, branched-chain amino acid transaminases (BCAATases) are encoded by the BAT1 and BAT2 genes. BCAATases catalyse the transfer of amino groups between those amino acids and alpha-keto-acids. alpha-Keto-acids are precursors for the biosynthesis of higher alcohols, which significantly influence the aroma and flavour of yeast-derived fermentation products. The objective of this study was to investigate the influence of BAT-gene expression on general yeast physiology, on aroma and flavour compound formation and on the sensory characteristics of wines and distillates. For this purpose, the genes were overexpressed and deleted in a laboratory strain, BY4742, and overexpressed in an industrial wine yeast strain, VIN13. The data show that, with the exception of a slow growth phenotype observed for the BAT1 deletion strain, the fermentation behaviour of the strains was unaffected by the modifications. The chemical and sensory analysis of fermentation products revealed a strong correction between BAT gene expression and the formation of many aroma compounds. The data suggest that the adjustment of BAT gene expression could play an important role in assisting winemakers in their endeavour to produce wines with specific flavour profiles.

Alcohols↗