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At least 271 records · Page 15Linked to original sources
PubMed1982

Roles of cysteine sulfinate and transaminase on in vitro dark reversion of urocanase in Pseudomonas putida.

Urocanase is inactivated in intact cells of Pseudomonas putida and photoactivated by brief exposure of the cells to the UV radiation in sunlight. The dark reversion (inactivation) in vitro is explained by the formation of a sulfite-NAD adduct. Our objective was to investigate the dark reversion in vivo. Various compounds were added to P. putida cells, and the reversion was measured, after sonication, by comparison of the activity before and after UV irradiation. Sulfite, cysteine sulfinate, and hypotaurine enhanced the reversion of urocanase in resting cells. The reversion was time and concentration dependent. Sulfite modified the purified enzyme, but cysteine sulfinate and hypotaurine could not, indicating that those two substances had to be metabolized to support the reversion. Both of those compounds yielded sulfite when they were incubated with cells. Transaminases form sulfite from cysteine sulfinate. P. putida extract contained a transaminase whose activity involved as alpha-keto acid and either cysteine sulfinate or hypotaurine for (i) production of sulfite, (ii) disappearance of substrates, (iii) formation of corresponding amino acids, and (iv) urocanase reversion. Porcine crystalline transaminase caused reversion of highly purified P. putida urocanase with cysteine sulfinate and alpha-ketoglutarate. We conclude that in P. putida cysteine sulfinate or hypotaurine is catabolized in vivo by a transaminase reaction to sulfite, which modifies urocanase to a form that can be photoactivated. We suggest that this photoregulatory process is natural because it occurs in cells with the aid of sunlight and cellular metabolism.

Alanine↗
PubMed1990

Molecular analysis of two genes of the Escherichia coli gab cluster: nucleotide sequence of the glutamate:succinic semialdehyde transaminase gene (gabT) and characterization of the succinic semialdehyde dehydrogenase gene (gabD).

We have characterized two genes of the Escherichia coli K-12 gab cluster, which encodes the enzymes of the 4-aminobutyrate degradation pathway. The nucleotide sequence of gabT, coding for glutamate:succinic semialdehyde transaminase (EC 2.6.1.19), alternatively known as 4-aminobutyrate transaminase, was determined. The structural gene consists of 1,281 nucleotides specifying a protein of 426 amino acids with a molecular mass of 45.76 kDa. The protein shows significant homologies to the ornithine transaminases from Saccharomyces cerevisiae and from rat and human mitochondria. Three functionally and structurally important amino acid residues of the transaminase were identified by sequence comparison studies, and evolutionary relationships of the aminotransferases are discussed. The gabD gene, encoding succinic semialdehyde dehydrogenase (EC 1.2.1.16), was cloned and shown to be located adjacent to the 5' end of gabT. Expression studies with subfragments of the initially cloned DNA region revealed a maximal size of 1.7 kb for gabD. Both genes are cotranscribed from a promoter located upstream of gabD.

4-Aminobutyrate Transaminase↗
PubMed1991

Etiology and pathogenesis of marked elevation of serum transaminase in patients with acute gallstone disease.

From 1980 through 1988, biliary surgery was performed in 197 patients with acute gallstone disease and concomitant elevation of serum glutamic oxalacetic transaminase (SGOT) or serum glutamic pyruvic transaminase (SGPT) of over 300 Karmen units. In 137 patients, anatomic inspection and liver biopsy were performed during the acute stage of the disease. Impacted and floating bile duct stones were found in 69 (50%) and in 43 (32%) of the 137 patients, respectively. The main liver histology was necrosis of liver cells. After surgery, high serum transaminase fell rapidly with immediate recovery in 99% of the patients. In the remaining 60 patients, their signs and symptoms settled soon after initial conservative treatment and surgery was performed after an average time of 21 days. At laparotomy, impacted bile duct stones were found in 2 (3%) and liver histology revealed regeneration of liver cells. These findings suggest that marked elevation of serum transaminase in patients with acute gallstone disease might be due to an acute inflammatory liver cell injury caused by impacted bile duct stones or migrating stones, which would be transient and reversible after early resolution of the bile duct obstruction.

Acute Disease↗
PubMed2004

Elevated liver enzymes following open Roux-en-Y gastric bypass for morbid obesity - does timing of liver retraction affect the rise in the levels of transaminases?

BACKGROUND: Liver retraction in open Roux-en-Y gastric bypass (RYGBP) for morbid obesity may cause an elevation in liver transaminase levels postoperatively. This study attempts to ascertain whether timing of placement of the liver retractor would have any effect on the degree of derangement of the liver function tests. METHODS: 12 patients undergoing open RYGBP were prospectively randomized into 2 groups. One group had the liver retractor applied early on in the operation, and had the gastric pouch constructed first, followed by construction of the jejunojejunostomy and Roux-en-Y gastrojejunostomy. The second group had the jejunojejunostomy performed first, followed by placement of the liver retractor to allow construction of the gastric pouch and Roux-en-Y gastro-jejunostomy. Liver function tests were monitored postoperatively in both groups, and these were then statistically analyzed with respect to the duration of liver retraction. RESULTS: Delayed liver retraction resulted in statistically significantly smaller increases in aspartate transaminase (AST) and alanine transaminase (ALT) compared with early liver retraction. AST levels returned to normal values within 1 week in both groups of patients. ALT levels returned to normal values within 1 week in the delayed liver retraction group, whereas levels took >1 week to return to normal in the early liver retraction group. CONCLUSIONS: Liver retraction causes abnormal transaminase levels following open RYGBP. Delayed liver retraction results in less rise in the AST and ALT levels compared with early liver retraction. Surgeons should construct the Roux-en-Y limb and jejunoje junostomy first, before proceeding with construction of the gastric pouch and gastrojejunostomy, thereby decreasing the duration of liver retraction and consequent relative liver ischemia.

Gastric Bypass↗
PubMed1983

Aspartate- and tyrosine transaminase activities in the organs of the rat during its breeding cycle.

The aspartate- and tyrosine transaminase activities of liver kidney, brain, hind leg striated muscle, skin, adipose tissue, small intestine and stomach of pregnant, lactating and post-lactating rats were determined. The ratios of activities between both enzymes were uniform in the different tissues studied, with minimal values for liver and adipose tissue. The patterns and activity ratios found during the breeding cycle of the rat agreed with tyrosine transaminase being an independent entity of aspartate transaminase in liver and adipose tissue, coexisting to some degree in most other tissues and being probably only an artifact (according to recent findings in the literature) in brain, muscle and intestine. The different patterns of change found during this period in most organs suggest different hormonal regulation and help support the possibility of an independent rôle for tyrosine transaminase in them.

Adipose Tissue↗
PubMed1999

Waist circumference and body mass index as predictors of elevated alanine transaminase in Danes aged 30 to 50 years.

INTRODUCTION: We examined whether waist circumference and waist-to-hip circumference ratio were a better predictor for elevated alanine transaminase level than body mass index. METHODOLOGY: In a cross-sectional survey we examined body mass index, waist circumference, waist-to-hip ratio, alcohol consumption, and alanine transaminase level in a random sample of 903 men and women aged 30 to 50 years from The Ebeltoft Health Promotion Project in Denmark. RESULTS: Body mass index, waist circumference and waist-to-hip ratio explained an approximate 12% variation in alanine transaminase in men and 4% in women, whereas waist-to-hip circumference ratio explained a 2% variation in women. The risk of elevated alanine transaminase level in men, calculated as odds ratio, with a body mass index (kg/m2) above 30, or a waist circumference above 102 cm, or a waist-to-hip circumference ratio above 0.9 was 9.3 (95% confidence interval [CI], 3.6-24.1), 5.6 (95% CI, 2.5-12.5) and 2.7 (95% CI, 1.3-5.3) respectively, but there was no elevated risk among women. CONCLUSIONS: Waist circumference and body mass index were both predictors in men. Waist-to-hip ratio was also a predictor in men, but not as strong a predictor as waist circumference and body mass index. No association was found in women. This difference is probably explained by differences in the accumulation of intra-abdominal adipose tissue among men and women with the same degree of obesity.

Adult↗
PubMed1999

Studies on the influence of the copper content in the drinking water on the newborn copper burden and transaminases activity.

INTRODUCTION: Clinical parameters for the early diagnosis of a potential development of childhood cirrhosis are not available. A cross-section study was performed to investigate whether the serum copper content and the activities of the newborn's glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) may be associated with the copper contents of the drinking water and/or the maternal serum and thus could serve as early indicator of an elevated health hazard. MATERIAL AND METHODS: The serum concentration of copper was analyzed in samples of 141 mother-newborn pairs. Additionally, in umbilical cord serum the activities of the transaminases GOT and GPT were determined. Low molecular bound or free copper was quantified in 30 randomly chosen serum filtrates. According to questionnaire data, in 62 of the 141 households the drinking water installations consisted of copper. In these cases, the element was analyzed in drinking water. RESULTS: The copper content of the drinking water was found ranging between 0.02 and 2.5 mg Cu/l (median 0.22 mg Cu/l), the maternal serum copper content ranged from 770-3720 micrograms Cu/l (median 2275 micrograms Cu/l), the neonatal serum from 220 to 1930 micrograms Cu/l (median 500 micrograms Cu/l), respectively. GOT (6-33 U/l); median 14 U/l) and GPT (3-21 U/l; median 6 U/l) activities could be judged as reference range data. In the statistical analysis, an association between the copper content of the drinking water and the maternal or neonatal serum copper content could not be found. Pearson regression analysis revealed slight, yet significant correlations of the neonatal GOT and GPT activities with the maternal serum copper content (GPT: r2 = 0.06; p < 0.05; GOT: r2 = 0.05; p < 0.05; each n = 139). In addition, the copper content of the mother's serum filtrates was correlated with the newborns' serum filtrates (Spearman: r = 0.61; p < 0.001; n = 30). CONCLUSIONS: The prenatal copper exposure of the infant could be mainly determined by low molecular or free serum maternal copper, which seems to be able to penetrate the placental barrier easily. The association between maternal serum copper content and neonatal transaminases activity can be judged as clinically not relevant and might be a physiologic response.

Adult↗
PubMed2004

4-methylthio 2-oxobutanoate transaminase: a specific target for antiproliferative agents.

We have previously shown that the addition of 4-methylthio-2-oxobutanoate (MTOB) to cultures of methionine dependent neoplastic cells which lack endogenous MTOB restores their capacity to grow in the absence of exogenous methionine. Transition state inhibitors of the MTOB transaminase,responsible for the transamination of MTOB to methionine, had also been designed and selected for their capacity to inhibit the proliferation of methionine dependent neoplastic cells but not that of normal cells in culture. We now show that the transition state analogue : L-methionine ethyl esterpyridoxal(MEEP) with a structure corresponding to the oxo acid receptor covalently linked to pyridoxamine and the amine donor analogue: D-aspartate beta hydroxamate (D-AH) are efficient inhibitors of MTOB transaminase. [3H] MEEP uptake into transformed HeLa cells is similar to that in normal MRC5 cells, yet growth inhibition is seem in the transformed but not in the normal cells.MEEP irreversibly inhibits the activity of this enzyme when added to HeLa cells in culture but not that of the purified rat liver enzyme, probably due to pyridoxal phosphate already bound in the active site. On the contrary, D-AH is a noncompetitive reversible inhibitor of the purified rat liver enzyme in vitro and also inhibits intracellular HeLa MTOB transaminase. Furthermore, in HeLa cells both inhibitors induce DNA strand breaks typical of apoptotic cell death. These results provide evidence that MTOB transaminase is a potential target for antiproliferative agents which could selectively affect methionine-dependent neoplastic cells. The transition state intermediale : MEEP as an amine acceptor analogue was found to be 20 fold more effective than D-AH as the amine donor analogue in inducing apoptosis.

Animals↗
PubMed2005

Mildly elevated liver transaminase levels in the asymptomatic patient.

Mild elevations in liver chemistry tests such as alanine transaminase and aspartate transaminase can reveal serious underlying conditions or have transient and benign etiologies. Potential causes of liver transaminase elevations include viral hepatitis, alcohol use, medication use, steatosis or steatohepatitis, and cirrhosis. The history should be thorough, with special attention given to the use of medications, vitamins, herbs, drugs, and alcohol; family history; and any history of blood-product transfusions. Other common health conditions, such as diabetes, heart disease, and thyroid disease, can cause or augment liver transaminase elevations. The recent American Gastroenterological Association guideline regarding the evaluation and management of abnormal liver chemistry tests proposes a practical, algorithmic approach when the history and physical examination do not reveal the cause. In addition to liver chemistries, an initial serologic evaluation includes a prothrombin time; albumin; complete blood count with platelets; hepatitis A, B, and C serologies; and iron studies. Depending on the etiology, management strategies may include cessation of alcohol use, attention to medications, control of diabetes, and modification of lifestyle factors such as obesity. If elevations persist after an appropriate period of observation, further testing may include ultrasonography and other serum studies. In some cases, biopsy may be indicated.

Alanine Transaminase↗
PubMed1990

Elevated liver transaminase levels in children with blunt abdominal trauma: a predictor of liver injury.

The medical records of 43 hemodynamically stable children with elevated serum transaminase levels (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) who underwent abdominal computed tomographic (CT) scan for blunt abdominal trauma were reviewed. Nineteen patients (44.2%) had AST levels greater than 450 IU/L and ALT levels greater than 250 IU/L, and 17 of these 19 patients had hepatic injury identified on abdominal CT scan. Of the 43 patients, 25 (58.1%) had AST and ALT levels of less than 450 IU/L and 250 IU/L, respectively, and none of these patients had evidence of hepatic injury on CT scan. Elevated serum transaminase levels (AST greater than 450 IU/L and ALT greater than 250 IU/L) identified all of the patients with hepatic injury visible on abdominal CT scan. The sensitivity and specificity of elevated serum transaminase levels were 100% and 92.3%, respectively, for predicting hepatic injury. It is recommended that hemodynamically stable pediatric patients with blunt abdominal trauma and AST levels greater than 450 IU/L and/or ALT levels greater than 250 IU/L undergo abdominal CT scan to determine the presence and extent of hepatic injury. Children with serum transaminase levels below these values are at decreased risk of liver injury.

Abdominal Injuries↗
PubMed1985

Changes in the transaminase activities in the middle and posterior silk-gland tissues of eri-silkworm, Philosamia ricini, in relation to spinning process.

The middle silk gland tissue of eri-silkworm exhibits a higher glutamate-oxaloacetate transaminase activity (about twice) than that of the glutamate-pyruvate transaminase, while the posterior silk gland tissue exhibits a higher (three to four times) glutamate-pyruvate transaminase activity than that of the glutamate-oxaloacetate transaminase.

Alanine Transaminase↗
PubMed1980

Changes in free amino acid nitrogen concentration and transaminases in lead treated rats.

Intraperitoneal administration of lead acetate for a period of 4 days in albino rats caused an increase of free amino acid nitrogen level in plasma, liver and kidney. There was diminution of glycogen content in both liver and kidney. The activities of plasma alanine-glutamic transaminase and aspartic-glutamic transaminase were increased with reduction in the activities of alanine-glutamic transaminase and aspartic-glutamic transaminases in liver and kidney.

Alanine Transaminase↗
PubMed1995

Glutamine transaminase K is not a major cysteine S-conjugate beta-lyase of rat kidney mitochondria: evidence that a high-molecular weight enzyme fulfills this role.

Glutamine transaminase K (homodimer; M(r) of monomer approximately 45,000) is a major cysteine S-conjugate beta-lyase of rat kidney cytosol. Several cysteine S-conjugates are known to cause kidney damage. Mitochondria are especially sensitive, and glutamine transaminase K activity is present in the mitochondrial fraction of rat kidneys. Therefore, it is possible that the mitochondrial form of glutamine transaminase K is a cysteine S-conjugate beta-lyase of the rat kidney and that this activity contributes to the mitochondrial damage. However, the literature contains conflicting data on this point. We obtained highly purified mitochondrial glutamine transaminase K and showed that it possesses little cysteine S-conjugate beta-lysae activity with S-(1,2-dichlorovinyl)-L-cysteine and S-(1,1,2,2-tetrafluoroethyl)-L-cysteine as substrates. Recently, a high-molecular-weight cysteine S-conjugate beta-lyase (M(r) approximately 330,000) was shown to be present in the cytosol of rat kidney homogenates and partially purified. We present evidence that suggests that a similar high-molecular-weight enzyme is present in rat kidney mitochondria and that this protein may be a major cysteine S-conjugate beta-lyase of these organelles.

Animals↗
PubMed1995

[Transaminases and histological activity in chronic hepatitis C].

The purpose of our study was to verify the correlation between biochemical and histological inflammatory activity in chronic hepatitis C. The histological activity index (HAI) of 42 patients with chronic hepatitis C was correlated with their transaminase activity. There was indeed a significant correlation between histological activity and the AST (r = 0.54, p = 0.0002) and ALT level (r = 0.36, p = 0.018) respectively. Due to considerable scatter of the results, transaminase activity did not allow reliable assessment of inflammatory activity in individual cases. In the majority, markedly elevated transaminase activity was associated with marked histological inflammatory activity, whereas normal or slightly elevated transaminase activity was found in all stages of inflammatory activity. To assess inflammatory activity in chronic hepatitis C, a liberal indication for liver biopsy should therefore be adopted.

Adult↗
PubMed1994

[The effect of chronic acidosis on the activity of renal glutamate decarboxylase and GABA-transaminase].

Chronic acidosis evoked by a 7-day application of ammonium chloride in concentration of 2% increased the activity of glutamate decarboxylase (GAD) in renal homogenates of rats to approximately 160%. The enzyme activators, chlorides and adenosine triphosphate influenced in varying measures the GAD activity in renal homogenates of both controlled and acidotic animals. Whilst ATP was gradually loosing the activating effect, chlorides preserved it. The renal GAD is firmly bound on insoluble structures. The increase in GAD activity due to acidosis was accompanied by increasing permanence of this bind. After the substitution of ammonium chloride by drinking water, the return of the increased GAD activity to previous normal values lasted 7 days, whilst apparent normalization of the weight of experimental animals reoccurred on the first day. Subfractionation of the crude renal mitochondrial fraction by use of enzyme markers localized GAD in mitochondria. In renal homogenates the activities of GABA-transaminases were assessed. GABA-alpha-ketoglutarate transaminase was 5x more active than GABA-pyruvate transaminase. Acidosis resulted in augmentation of both transaminases--the first to 130%, the second to 160%. (Tab. 5, Fig. 3, Ref. 25.)

4-Aminobutyrate Transaminase↗
PubMed1983

In vitro and in vivo effects on brain GABA metabolism of (S)-4-amino-5-fluoropentanoic acid, a mechanism-based inactivator of gamma-aminobutyric acid transaminase.

The effects of intraperitoneal administration of (S)-4-amino-5-fluoropentanoic acid, a mechanism-based covalent inactivator of gamma-aminobutyric acid transaminase (GABA-T), on whole brain GABA metabolism in mice were investigated. A dose-dependent and time-dependent irreversible inactivation of GABA-T was observed with a concomitant increase in whole brain GABA levels. The compound exhibited no in vitro nor in vivo time-dependent inhibition of glutamate decarboxylase (GAD), alanine transaminase, or aspartate transaminase (Asp-T). It was, however, a potent competitive reversible inhibitor of GAD and a weak competitive inhibitor of Asp-T. The chloro analogue, (S)-4-amino-5-chloropentanoic acid, was ineffective.

4-Aminobutyrate Transaminase↗
PubMed1984

High-performance liquid chromatographic analysis of analogous amino and oxo acids for the determination of amino acid oxidase and transaminase activities.

An analytical method, based on reversed-phase high-performance liquid chromatography, for the determination of analogous amino and oxo acids, has been developed. The assay may be employed to monitor amino acid oxidase and transaminase activities. Simultaneous quantitative determination of substrate and product is readily achieved. In particular, the amino acid oxidase activity within whole microbial cells immobilized by entrapment in Ca2+-alginate has been studied. The assay of transaminases has been exemplified with glutamic-pyruvic transaminase.

Alanine Transaminase↗
PubMed1985

Interaction of soluble pig heart glutamate-aspartate transaminase with various beta,gamma-unsaturated amino acids.

beta-Ethylidene-DL-aspartate (beta EA) and beta-methylene-DL-glutamate (beta MG) were synthesized and tested as potential suicide inhibitors of soluble pig heart glutamate-aspartate transaminase (sGAT). beta MG was found to be a) a substrate with a very low turnover number relative to glutamate and b) a competitive inhibitor with respect to aspartate (albeit with a large binding constant). At high concentrations beta MG inactivated the enzyme but only very slowly. beta EA was also found to be a substrate with a very low turnover number; it did not inactivate the enzyme (1 hr, 25 degrees C) even at a high concentration. However, beta EA was found to bind to the enzyme with an affinity comparable to that of aspartate and glutamate. beta-Methylene-DL-aspartate (beta MA) has been shown to rapidly inactivate glutamate-aspartate transaminase. Therefore, it appears that glutamate-aspartate transaminase can bind analogues of aspartate with alkene groups in the beta position. The conjugated carbonyl groups of beta MA and beta EA will enhance Michael addition in comparison with that expected for vinylglycine. On the other hand, the presence of the methyl groups should reduce the electrophilicity of the double bond of beta EA compared to beta MA. This deactivation and/or steric hindrance to Michael attack may account for the inability of beta EA to inactivate sGAT. Therefore, it may be possible to design selective suicide inhibitors of glutamate-aspartate++ transaminase with the following structure: HO2CC(= CHX)CH(CO2H)NH2, where X is an electron-withdrawing group. Ideally, X would increase the reactivity of the double bond while affording a minimum of steric hindrance to susceptible enzyme-bound bases.

Amino Acids↗