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

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Query: EC:1.4.1.2 (glutamate dehydrogenase)
4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A flow-injection analysis biosensor system was developed for the amperometric assay of creatinine based on coupled reactions of three immobilized enzymes, using an oxygen electrode as the detection device. The ammonia produced by creatinine deiminase-catalyzed hydrolysis of creatinine was further converted into L-glutamate with two sequentially aligned enzyme reactors: glutamate dehydrogenase and glutamate oxidase. Endogenous ammonia was simultaneously compensated with a double peak recording system, where the flow was split after sample injection and rejoined before the glutamate dehydrogenase reactor. The system gave linear calibration in a range of 0.1-2.0 mM for creatinine and the first peak of ammonia, and 0.1-3.0 mM for the second peak of ammonia. One run was completed within two minutes. The system can be readily applied to the assay of creatinine in urine and showed good correlation with that from the currently used Jaffe method.
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PMID:Amperometric assay of creatinine in urine by flow injection analysis based on conjugated reactions of immobilized enzymes. Simultaneous compensation of endogenous ammonia. 147 77

Two or three different kinds of immobilized enzymes can be aligned in a minireactor so that sequential enzymatic reactions are carried out from upstream to downstream during flow-injection analysis. A lactate oxidase-catalase reactor, used as precolumn for removing pre-existing lactate in serum before the lactose dehydrogenase (LDH) reactions, was useful for the determination of serum LDH activity, which did not require any blank correction. A sequential glutamate dehydrogenase-glutamate oxidase reactor was also useful for a novel chemiluminometric determination of ammonia. On the other hand, a co-immobilized creatininase-creatinase-sarcosine oxidase reactor, in spite of containing creatininase which catalyses the reversible reaction, was the most efficient for the determination of serum creatinine.
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PMID:Use of various types of column reactors for flow-injection analysis. 151 46

One hundred and one young-adult female Sprague-Dawley rats were acclimatized to metabolic cages for 2 days. After that time 24-hour urine was collected at a constant cooling temperature of 0-4 degrees C. After gel filtration the enzyme activities were determined, and the resulting values were used to calculate 24-hour excretions. The following reference ranges (2.5 and 97.5 percentiles) were determined (in mU/24 h): lactate dehydrogenase 43-181; phosphohexoseisomerase 45-1445; glutathione-S-transferase 1-299; alkaline phosphatase 27-1239; leucine arylamidase 72-377; gamma-glutamyltransferase 1334-9188; arylsulphatase A 59-309; beta-galactosidase 76-305; beta-glucuronidase 20-2756; beta-N-acetyl-D-glucosaminidase 66-491; glutamate dehydrogenase 7-711. There was a significant (though not very high) correlation with diuresis for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase, and for glutamate dehydrogenase, lactate dehydrogenase, phosphohexoseisomerase and alkaline phosphatase. The relation to creatinine excretion was markedly close for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase (r = 0.71-0.83), as well as for alkaline phosphatase, leucine arylamidase and gamma-glutamyltransferase. There was a relatively high correlation between the excretion of beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase among themselves (r = 0.63-0.81) as well as between leucine arylamidase and gamma-glutamyltransferase (r = 0.75).
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PMID:Excretion of urinary enzymes in female Sprague-Dawley rats in relation to cellular compartment, creatinine excretion and diuresis. 179 3

In the last few years there has been increasing evidence that adult respiratory distress syndrome is only part of a much more complex syndrome called multiorgan failure (MOF). Since renal and lung failure have become rare because of our increased understanding of the pathomechanisms involved and the treatment changes, liver dysfunction has been noted more often. In a clinical trial with 38 patients with severe trauma, we investigated liver function using ordinary parameters like the transaminases, bilirubin, etc. To define one group with MOF and one without we used the Goris MOF Score. In both groups glutamate dehydrogenase (GLDH) was increased initially up to 14 U/l, indicating hypoxia of the liver cells right after trauma. From day 6 on, a second increase up to 12 U/l of GLDH in the MOF group was evidence of liver cell dysfunction. The glutamine oxalacetic transaminase (GOT) level remained normal in both groups after an initial increase of up to 60 U/l in both groups. As 30% of serum GOT is released by muscle cells, the initial peak values could be due to direct muscle trauma, because an initial increase was noted even in the creatinine kinase. A decrease in clotting factor V down to 30% on day 8 in the MOF group indicated that the metabolic synthesis activity of the liver was lower. Bilirubin increased in the MOF group from day 5 on up to 240 mumol/l on the day 14. As this increase was not parallel to the gamma glutamyl transferase (Gamma BT) level, the reason for the bilirubin increase may be dysfunction of the liver cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Liver failure as part of multiple organ failure following polytrauma]. 195 76

Ammonia in food samples was determined by its reaction in an immobilised enzyme reactor containing glutamate dehydrogenase (GIDH) in a flow injection system, by measuring the decrease in the absorbance of ultraviolet radiation by reduced nicotinamide adenine dinucleotide (NADH). There was a linear relationship (r = 0.9995) between peak height and ammonia concentration over the range 0.05-0.6 mM. The detection limit was 0.005 mM for an injection volume of 19 microliters. Sampling frequency was 60 h-1 and the precision was better than 1.09% for 11 successive assays. The interference effect of urea and ascorbic acid at concentrations greater than 100 mg per 100 g of product should be taken into account. The interference caused by glycine, creatinine and amino acids is negligible. Only a 20% loss in the activity of the GIDH column was observed after 500 determinations during a 3-month period.
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PMID:Enzymic determination of ammonia in food by flow injection. 209 94

This study provides explanation for conflicting evidence in the literature relating to changes in mitochondrial function and metabolic parameters during chemically induced diabetes. Diabetes of 3 days' duration (early ketosis) did not alter heart, kidney, or liver mitochondrial respiratory rates with glutamate or succinate even though serum glucose and triglycerides were elevated. Diabetes of 5 weeks' duration did not alter kidney or liver mitochondrial function in the fed adult rat although weight gain was depressed. The amount of kidney mitochondrial protein isolated per gram of tissue was increased by 30% in the diabetic. This increase was reversed by insulin treatment as were the other biochemical modalities measured. Superimposition of a 24-hr fast resulted in enhanced gluconeogenesis as measured by an animal weight loss of 17% within 24 hr (liver weight loss, 21%) and an elevation of serum urea nitrogen by 180% compared to fasted control. Respiratory rates of diabetic kidney mitochondria with glutamate were unaffected in the fasted animal whereas diabetic liver mitochondrial respiratory rates during succinate oxidation were reduced by 43%. Respiratory control was unchanged in the fasted diabetic rat. All the observed changes were reversed by insulin. Variation in the serum and liver metabolic indices (urea nitrogen, creatinine, glycerol, free fatty acids, free amino acids, triglycerides, and glucose) and liver mitochondrial responses to 7 weeks of chemically induced diabetes was affected by the rat strain, Sprague-Dawley versus Sherman, and rat weight, 72 g versus 222 g. Liver mitochondrial respirations in fed Sherman rats were not depressed by diabetes. Both rat strains had elevated liver free fatty acids and glutamate dehydrogenase activity in the diabetic state. Serum leucine, isoleucine, and valine were more elevated and serum lysine and arginine were more depressed in the diabetic Sprague-Dawley rat than in the Sherman rat. Conjectures on these results are presented in the text.
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PMID:Metabolic and mitochondrial disturbances in streptozotocin-treated Sprague-Dawley and Sherman rats. 293 62

Using fully mechanized analytical equipment, interference by haemolysis in the determination of 26 clinical chemical parameters was determined quantitatively by adding haemolysate to serum. Haemoglobin concentrations up to 6.6 g/l caused essentially no interference in the following determinations: albumin (immuno-nephelometric), alpha-amylase, calcium, chloride, cholesterol, cholinesterase, creatinine, iron, glucose, glutamate dehydrogenase, uric acid, urea, sodium, inorganic phosphate, total protein, transferrin and triglycerides. In the presence of haemoglobin, erroneously high values were found for: lactate dehydrogenase (haemoglobin higher than 0.2 g/l), aspartate aminotransferase, potassium and acid phosphate (haemoglobin higher than 1.5 g/l), creatine kinase (haemoglobin higher than 2.5 g/l) and alanine aminotransferase (haemoglobin higher than 3.4 g/l). Erroneously low values were found for bilirubin (haemoglobin higher than 0.8 g/l), alkaline phosphatase and albumin (by electrophoresis) (haemoglobin higher than 1.5 g/l) and gamma-glutamyltransferase (haemoglobin higher than 3.0 g/l).
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PMID:Haemolysis as an interference factor in clinical chemistry. 371 97

The effect of 3-mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase [GTP:oxaloacetate carboxy-lyase (transphosphorylating), EC 4.1.1.32], was tested on NH3 formation via the purine nucleotide cycle and glutamate dehydrogenase (EC 1.4.1.2). NH3 excretion in rats increased 70-fold after 48 h of NH4Cl feeding, from 12.2 +/- 4.5 to 862 +/- 190 mumol/mg of creatinine. At 4 h after a single intraperitoneal injection of 3-mercaptopicolinate into NH4Cl-fed rats, NH3 excretion was inhibited by 93%. Kidneys of NH4Cl-fed plus 3-mercaptopicolinate-treated rats, compared with those of NH4Cl-fed rats, showed a 3.5-fold increase in the content of IMP, 5-fold increase in adenylosuccinate, 4-fold increase in aspartate, and a 30% increase in AMP. 3-Mercaptopicolinate completely inhibited NH3 and glucose formation from glutamate in tubules from acidotic rats and NH3 formation from aspartate in kidney perfusion experiments. When transamination in tubules was prevented by 2-amino-4-methoxy-trans-but-3-enoic acid, formation of glucose, but not of NH3, from glutamate was inhibited. 3-Mercaptopicolinate completely inhibited NH3 formation from aspartate in the presence of the aminotransferase inhibitor in kidney tubules. The data show that NH3 can be formed via glutamate dehydrogenase and the purine nucleotide cycle at significant and approximately equal rates. 3-Mercaptopicolinate has no direct effect on NH3 formation via glutamate dehydrogenase, but inhibits that via the purine nucleotide cycle. We conclude that gluconeogenesis is not regulatory for NH3 formation in kidney.
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PMID:The relationship between glutamate deamination and gluconeogenesis in kidney. 613 15

Alcoholism is a common disease; it is found in 10% to 15% of all patients admitted to general hospitals. There is no single characteristic finding, but on the other hand, changes as compared with normal values have been reported in the literature for more than 30 frequently assayed clinical chemical and haematological parameters. In the project reported here all 24 clinical chemical parameters and all 8 haematological parameters frequently assayed were studied in each of 82 hospitalized men with a confirmed diagnosis of alcoholism. The diagnosis of alcoholism was made on the basis of the Munich Alcoholism Test (MALT) together with the following standardized assessments and examinations: past history, an alcohol questionnaire, general physical examination and neurological examination. All forms were filled in completely. All steps in the clinical laboratory investigations were standardized, and all were subject to ongoing reliability control. The clinical problem is usually not to differentiate alcohol abusers or alcoholics from healthy persons but rather to identify the alcoholics among a population of patients with a variety of illnesses. For this reason 70 patients from two hospitals who were clearly neither alcohol abusers nor alcoholics were studied in exactly the same manner as the alcoholics. In this combined group of 152 hospitalized patients significant differences were found in the distribution of the values for the alcoholics and the non-alcoholics for the following clinical chemical and haematological parameters: at the 0.1% level gamma-glutamyltransferase, aspartate aminotransferase, urea, creatinine and mean corpuscular volume (MCV), and at the 1% level glutamate dehydrogenase, alanine aminotransferase and alkaline phosphatase. From these eight parameters those combinations of between two and six parameters were selected that discriminated best between the alcoholics and the non-alcoholics. Using conventional decision limits the following was found: For the alcoholics two or more of the results for the following five parameters were outside the decision limits given in parentheses: gamma-glutamyltransferase (greater than or equal to 28 U/l), aspartate aminotransferase (greater than or equal to 18 U/l), alanine aminotransferase (greater than or equal to 22 U/l), MCV (greater than or equal to 96 fl), creatinine (less than or equal to 66.3 mumol/l). The diagnostic sensitivity (alcoholics) is 85%, the diagnostic specificity (non-alcoholics) is 64%.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Detection and exclusion of alcoholism in men on the basis of clinical laboratory findings. 614 78

The course of plasma catalytic activities of total creatine kinase, creatine kinase isoenzyme MB, total, cytoplasmatic and mitochondrial aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, glutamate dehydrogenase and concentrations of myoglobin, urea, acidic alpha 1-glycoprotein and creatinine were followed in 33 patients suffering from acute myocardial infarction. All patients were randomized in a double-blind, prospective study. One group (18 patients) was infused with streptokinase 1.5 X 10(6) units/90 minutes; the control group received routine continuous i.v. heparin treatment (1000 units/h). Ten hours after completion of the study protocol, treatment of both groups of patients was continued with heparin, 1000 units/h and Aspisol, 1 g/day2). Streptokinase treatment induced earlier wash-out and therefore earlier peak levels of several enzymes: total creatine kinase (11 hours), creatine kinase isoenzyme MB (6 hours), total and cytoplasmatic aspartate aminotransferase (6 hours) and lactate dehydrogenase (9 hours). Total creatine kinase peak catalytic activity and myoglobin peak concentration were higher in the group receiving thrombolytic therapy. A significantly different course of catalytic activity between both treatment groups was found for total creatine kinase and creatine kinase isoenzyme MB, total and cytosolic aspartate aminotransferase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. The course of mitochondrial aspartate aminotransferase catalytic activity was different only 12 hours after the beginning of treatment. The shift of several catalytic activities to an earlier peak level in plasma may indicate reperfusion of ischaemic myocardium due to thrombolytic therapy.
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PMID:Systemic short-term fibrinolysis with high-dose streptokinase in acute myocardial infarction: time course of biochemical parameters. 639 65


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