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)

The morphologic changes in the liver were investigated along with those in the activity of the specific liver enzymes in the blood plasma of rats in the case of the severe form of acute radiation disease. The rats were treated with 670 Rad at the rate of 90 Rad/min. The studies were carried out on the 1st, 8th , 15th, 22nd, and 30th day following irradiation. It was found that under the conditions of the experiment the activity of the cytoplasmic enzymes sorbitoldehydrogenase , cholinesterase, and leucinaminopeptidase strongly rose on the 1st day after treatment (the activity of sorbitoldehydrogenase increased 11 times). The activity of acid phosphatase and glutamate dehydrogenase also increased strongly, whereupon there was deterioration of the mitochondrial and lysosomal structures. Seen were well expressed processes of fatty and parenchymal dystrophy. The studies on the changes in the activity of these enzymes can be used as an adjunct, resp., an auxiliary test to the haematologic indices in the evaluation of the severity of radiation disease.
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PMID:[Enzymatic and morphological study of the liver in acute radiation sickness]. 673 Mar 19

1. The acute oral LD50 and chronic LC50 toxicity values for ethylene dibromide (EDB) were estimated for japanese quail. 2. Single sub-acute oral and intraperitoneal doses of EDB (1/2 LD50) and chronic oral doses of EDB (1/3 LC50) were administered to quail in order to characterise the sub-lethal effects of EDB residues. 3. At 24 h after sub-acute dosing, relative liver weight, plasma aspartate aminotransferase (AT) [EC 2.6.1.1] and L-iditol (sorbitol) dehydrogenase (SDH) [EC 1.1.1.14] were elevated and decreases were found in hepatic total lipid, total protein, AT and glutamic dehydrogenase (NAD (P)+) (GDH) and plasma cholinesterase (ChE) [EC 3.1.1.8] and total lipid. 4. Following chronic administration, elevations in relative liver weight, plasma ChE and total lipid, haemoglobin and haematocrit were found and hepatic AT, GDH and total lipid were decreased. 5. The changes in hepatic and plasma enzymes and constituents are discussed in relation to possible biphasic effects resulting from EDB exposure.
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PMID:A study on the toxicity and the biochemical effects of ethylene dibromide in the Japanese quail. 702 16

Activities of 14 enzymes were determined in psoas muscle, smooth muscle, diaphragm, heart, brain, liver, kidney, spleen, pancreas, salivary glands, zygomatic gland, intestinal mucosa, subcellular fractions, and plasma of the dog. In pups, plasma activity of most enzymes was high, except iditol dehydrogenase (ID), glutamate dehydrogenase (GLD), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and D-fructose-1,6-diphosphate aldolase (ALS). Alkaline phosphatase (ALP), ALS, cholinesterase (CHS), creatine kinase (CK), alpha-hydroxybutyrate dehydrogenase (HBD), lactate dehydrogenase (LD), and malate dehydrogenase (MD) decreased significantly (P less than 0.01) with increasing age, but in dogs greater than 7 months, all enzymes except CK, HBD, and ALT revealed reasonably constant plasma values. Enzymes ALT, GLD, CHS, and ID are specific for liver, CK and ALS for muscle, HBD to some degree for myocardium, and alpha-amylase for pancreas. The ALP and gamma-glutamyltransferase were located in microsomes, GLD in mitochondria, MD and AST in mitochondria and cytoplasm, and isocitric dehydrogenase, LD, and the other enzymes only in cytoplasm.
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PMID:Enzyme activities in the dog: tissue analyses, plasma values, and intracellular distribution. 703 2

Acute cholestatic hepatitis developed in two patients, a 58-year-old man and a 54-year-old woman, who had been treated for hypercholesterolaemia with the cholesterol-synthesis inhibitor lovastatin for 3 years and 2 months, respectively. Both of them at first complained only of tiredness and loss of appetite, but then developed jaundice with colourless stool and dark urine. Alkaline phosphatase concentration rose up to maximally 1227 and 569 U/l, gamma-GT to 403 and 410 U/l, respectively. The transaminases and glutamate dehydrogenase were also elevated, while serum cholinesterase had fallen to 2346 and 2418 U/l, respectively. Histological examination of liver biopsies 6 months and 4 weeks, respectively, after onset of jaundice also suggested drug-toxic liver damage. There was no evidence for other causes. After lovastatin had been discontinued the various cholestasis parameters regressed only slowly.
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PMID:[Lovastatin-induced acute cholestatic hepatitis]. 786 82

Previous studies have shown the pathogenic effects of grains cultivated in the endemic areas of Keshan disease and selenium is effective in the prevention of this disease. In this study, liver damages induced by feeding grains from an endemic area (endemic diet), and the effects of selenium and alpha-tocopherol supplement were examined. After 3 months on the endemic diet, the amounts of serum enzymes were significantly increased when compared to controls (animals receiving diet from a non-endemic area). Liver enzymes (alkaline phosphatase and choline esterase) were also found to be altered in the serum, further suggesting liver damages in animals on an endemic diet. Supplement of the endemic diet with selenium or alpha-tocopherol reversed the changes in serum enzymes. Increase in lipid peroxidation in the liver of animals on the endemic diet was observed when compared to that in control animals. Selenium and alpha-tocopherol supplements prevented the increase in lipid peroxidation in the liver by the endemic diet. Semi-quantitative histochemical analysis of glutamate dehydrogenase and succinate dehydrogenase in liver tissue showed that the livers of animals on an endemic diet were more sensitive to ischemic damages in vitro. Supplementation of the endemic diet with either selenium or alpha-tocopherol reduced the sensitivity to ischemic damages. The results suggest that increased lipid peroxidation in the liver of rats on an endemic diet may be responsible for liver damages and elevation of serum enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of selenium and alpha-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in rats. 796 93

A complex of enzymatic tests, characterizing the liver function and cellular cytolysis in patients with acute myocardial infarction of various severities (without complications and with various types of complications and outcomes) was used in examinations over the first week of the disease. Significant changes in five of the seven tested enzymes were found: aspartate aminotransferase, glutamate dehydrogenase, sorbitol dehydrogenase, cholinesterase, alanine aminotransferase, the degree and incidence of changes in their activities being the lowest in the patients with acute myocardial infarction without complications, higher in those with this condition with isolated complications, still higher in those with combined complications and a favorable outcome, and the highest in those with combined complications and a lethal outcome. Secondary hepatopathy in patients with acute myocardial infarction augments as the complications develop, particularly in arrhythmia, disordered conductivity, and combined complications. Measurements of glutamate dehydrogenase and sorbitol dehydrogenase are recommended starting from the first day of the disease, of cholinesterase from the third day of the disease for a dynamic monitoring of the liver status in order to timely detect and correct hepatopathy and assess the status of patients with complicated acute myocardial infarction.
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PMID:[Enzyme diagnosis of liver dysfunction in acute myocardial infarct and its complications]. 800 Jul 90

The aim of this study was to investigate the regulation of various proteins of the GHIGF axis during progression of liver failure and to search for potential prognostic markers of functional hepatic reserve. Serum levels of growth hormone (GH) and high affinity growth hormone binding protein (GHBP), insulin-like growth factor I (IGF-I) and IGF binding proteins (IGFBP) -1, -2 and -3 were determined in patients with liver cirrhosis. A continuous decline in the concentrations of IGF-I, IGFBP-3 and serum GH-binding activity (GHBP) was observed during progression of cirrhosis and the data correlated significantly with choline esterase, total serum protein and the Child score. In addition, GHBP showed a significant correlation with the enzymatic activity of glutamate dehydrogenase or transaminases and seems so to be influenced by the degree of liver cell damage. In contrast, IGFBP-1 and IGFBP-2 levels were significantly elevated in preterminal disease suggesting an upregulatory mechanism is still effective in this situation. Only when liver function had markedly deteriorated, the serum levels of these two parameters decreased again, possibly due to an impaired synthesis. The excellent correlation between the serum levels of IGF-I (r = -0.64, p < 0.001) or IGFBP-3 (r = -0.67, p < 0.001) and the Child score index suggests that they reflect the hepatic functions just as conventional indicators. For an appropriate interpretation of the liver function the measurement of the growth related peptides can be a valuable tool to estimate pathological alteration in the functional hepatic reserve or in the glucose homeostasis.
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PMID:Regulation of growth hormone (GH), insulin-like growth factor (IGF)I, IGF binding proteins -1, -2, -3 and GH binding protein during progression of liver cirrhosis. 853 56

Alpha 1-Antitrypsin deficiency predisposes to pulmonary emphysema, liver cirrhosis and hepatocellular carcinoma. Anecdotal evidence and a large autopsy study suggest that severe lung and liver disease rarely coexist in the same subject, but this has not been studied in patients. Therefore we investigated 27 patients with severe alpha 1-deficiency (Pi ZZ) and pulmonary emphysema for signs of liver disease and impaired hepatic function. A subgroup of 7 patients underwent quantitative liver function tests. On physical examination or ultrasonography, cirrhosis or tumor was not suspected in any patient. Conventional liver function tests were completely normal in 17 patients. Elevated serum activities of gamma-glutamyltranspeptidase and/or aminotransferases were seen in 10 patients. In some, the elevation was only marginal and in none more than twice normal. The serum bilirubin concentration and activity of alkaline phosphatase were increased in 1 patient. Serum protein, albumin, fibrinogen, antithrombin III, alpha 1-fetoprotein concentrations, serum activities of cholinesterase and glutamate dehydrogenase, activated partial thromboplastin time and prothrombin time were normal in all patients. The indocyanine green half-life was abnormal only in 1 of 6 patients, suggesting that hepatic blood flow was not impaired in the study group. However, the lidocaine half-life and galactose elimination capacity, parameters of hepatic metabolization, were impaired in 4 and 6 of 7 patients, respectively. We conclude that liver disease or impaired liver function is not a clinically relevant problem in most patients with pulmonary emphysema due to alpha 1-antitrypsin deficiency. But results of quantitative liver function tests, although performed in only a small group of patients, suggest that hepatic metabolization might be impaired even in those patients who present with pulmonary disease.
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PMID:Liver function in patients with pulmonary emphysema due to severe alpha-1-antitrypsin deficiency (Pi ZZ). 873 89

Peculiarities of the CNS response to chronic treatment with L-DOPA were revealed by quantitative cytochemical methods in August (stress-sensitive) and Wistar (emotionally resistant) rats. In August rats L-DOPA administration caused aminopeptidase activity increase in sensomotor cortex layer 3 and nucleus accumbens, glutamate dehydrogenase activity growth in nucleus accumbens as well as the elevation of monoaminoxidase (MAO) activity in nucleus caudatus and nucleus accumbens (serotonin as substrate) and in nucleus caudatus and hippocampus (tryptamine as substrate), while acetyl cholinesterase activity did not change at all. At the same time in Wistar rats only glutamate dehydrogenase activity increase was observed in nucleus caudatus and nucleus accumbens.
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PMID:[Comparative cytochemical study of the central nervous system in Wistar and August rats in dopamine system hyperfunction]. 960 63

The hepatic ischemia-reperfusion syndrome was investigated in 28 patients undergoing elective partial liver resection with intraoperative occlusion of hepatic inflow (Pringle maneuver) using the technique of liver vein catheterization. Hepatic venous oxygen saturation (ShvO2) was monitored continuously up to 24 hours after surgery. Aspartate aminotransferase, glutamate dehydrogenase, gamma-glutamyl transpeptidase, pseudocholinesterase, alpha-glutathione S-transferase, reduced and oxidized glutathione, procalcitonine, and interleukin-6 were serially measured both before and after Pringle maneuver during the resection and postoperatively in arterial and/or hepatic venous blood. ShvO2 measurement demonstrated that peri- and postoperative management was suitable to maintain an optimal hepatic oxygen supply. As expected, we were able to demonstrate a typical enzyme pattern of postischemic liver injury. There was a distinct decrease of reduced glutathione levels both in arterial and hepatic venous plasma after LR accompanied by a strong increase in oxidized glutathione concentration during the phase of reperfusion. We observed increases in procalcitonin and interleukin-6 levels both in arterial and hepatic venous blood after declamping. Our data support the view that liver resection in man under conditions of inflow occlusion resulted in ischemic lesion of the liver (loss of glutathione synthesizing capacity with disturbance of protection against oxidative stress) and an additional impairment during reperfusion (liberation of reactive oxygen species, local and systemic inflammation reaction with cytokine production). Additionally, we found some evidence for the assumption that the liver has an export function for reduced glutathione into plasma in man.
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PMID:Hepatic ischemia-reperfusion syndrome after partial liver resection (LR): hepatic venous oxygen saturation, enzyme pattern, reduced and oxidized glutathione, procalcitonin and interleukin-6. 1287 55


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