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 hypothesis that mictochondrial damage is a significant factor in the pathogenesis of alcoholic liver disease (ALD) was investigated by enzymic analysis of mitochondrial fractions isolated from needle biopsy specimens from control patients, patients with fatty liver due to chronic alcoholism, and from patients with other forms of liver disease. Enzymes associated with the inner and outer mitochondrial membranes showed normal levels in ALD. Enzymes associated with the mitochondrial matrix, glutamate dehydrogenase, malate dehydrogenase and aspartate aminotransferase showed significantly raised levels in ALD, but the levels in patients with non-alcoholic liver disease was normal. In addition, analysis of the mitochondria by sucrose density gradient centrifugation revealed no differences between control tissue and liver from patients with alcoholic liver disease. These results do not indicate that there is significant mitochondrial damage in ALD. The raised mitochondrial matrix enzymes may represent an adaptive response to the ethanol load.
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PMID:Mitochondrial enzyme activities in liver biopsies from patients with alcoholic liver disease. 65 61

In liver and serum, AST activity is dependent on two isoenzymes, which are mitochondrial and cytosolic in nature. In an attempt to explain the well-known increase of serum mitochondrial AST-to-total AST ratio in chronic alcoholism (which is due to a specific increase of the mitochondrial isoenzyme), we analyzed: (a) liver and serum AST, ALT and glutamate dehydrogenase activities in 23 active drinkers with minimal liver changes, 11 alcoholic patients with cirrhosis who had stopped drinking, 18 nonalcoholic patients with viral chronic hepatitis and 11 subjects with normal livers; and (b) the expression of messenger RNAs for AST isoenzymes in the corresponding liver samples. Enzymatic activities were decreased in the liver irrespective of the origin of the liver disease. In patients with viral chronic hepatitis (or in those with alcoholic cirrhosis when abstinent), variations in liver proteins and messenger RNAs paralleled significant decreases in mitochondrial AST, ALT and glutamate dehydrogenase and a nonsignificant decrease of cytosolic AST. In alcoholic patients with minimal liver changes, the significant decrease of hepatic cytosolic AST, ALT and glutamate dehydrogenase activities contrasted with a close-to-normal liver mitochondrial AST activity; the increased amounts of mitochondrial AST messenger RNA give evidence for a pretranslational mechanism of regulation, indicating a possible increase in the total production of mitochondrial AST in the liver. The decrease of hepatic cytosolic AST activity was statistically significant only in alcoholic patients without cirrhosis who had a normal cytosolic AST mRNA level, thus suggesting a contributory role of translational or posttranslational regulation. In conclusion, regulation of AST isozymes during liver disease is complex, including differential, pretranslational and translational or posttranslational mechanisms.
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PMID:Hepatic activity and mRNA expression of aspartate aminotransferase isoenzymes in alcoholic and nonalcoholic liver disease. 191 63

Usefulness of several biochemical markers for the monitoring of chronic alcoholism were studied. Among generally used markers, only gamma-GTP showed a significant difference between alcoholic and non-alcoholic liver diseases. Serum glutamate dehydrogenase (GDH) activity was significantly high in alcoholic liver disease. When the ratios of GDH to ornithine carbamyl transferase (OCT) were calculated, differences between alcoholic and non-alcoholic liver diseases became clearer without overlapping of any value. Serum desialo-transferrin was found in about 60% of the alcoholics, and disappeared by abstinence. Microheterogeneity of serum protein was also found in other glycoproteins. Serum prealbumin level was significantly high in alcoholics without severe liver disease. Acetaldehyde dehydrogenase (ALDH) activity of erythrocytes was significantly low in alcoholics, and gradually increased after abstinence. These results indicate that microheterogeneity of glycoproteins, serum prealbumin level and erythrocyte ALDH activity are good markers of alcohol abuse, and serum GDH/OCT ratio is the most sensitive marker of alcoholic liver injury. Serum gamma-GTP activity is a good marker of both conditions.
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PMID:Biochemical markers of chronic alcoholism. 286 79

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

Because a previous study among 385 psychiatric admissions had shown each of three rapid interviews to be far superior to each of nine laboratory tests in screening for excessive drinking and alcoholism, the separation of patients with these drinking patterns from normal drinkers was reexamined by the more sophisticated technique of discriminant analysis. It was thus possible to determine where there was overlap in the information provided by some tests in contrast to "new information" provided by others and whether the arbitrary cut-off points of the normal ranges of the laboratory tests were contributing to their poor sensitivity. Discriminant analysis again confirmed the good performance of the rapid interviews, particularly the Brief Michigan Alcoholism Screening Test and the Reich interview, but it also identified glutamate dehydrogenase (GDH) as the best of the laboratory tests and of comparable efficacy to the rapid interview for the group of excessive drinkers. By comparison, gamma-glutamyl transpeptidase and mean corpuscular volume performed poorly. Using the whole range of results rather than a single cut-off point for discriminant analysis did not alter the relative performance of the screening tests. The optimum combination of tests was that of the Reich interview and the GDH, achieving 100% sensitivity for excessive drinking and alcoholism without any decline in the specificity or predictive value of a positive test result.
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PMID:A discriminant-function analysis of screening tests for excessive drinking and alcoholism. 614 44

Serum glutamate dehydrogenase concentration was assessed as a marker of the degree of hepatocyte necrosis found at liver biopsy in 95 patients suspected of having alcoholic liver disease. Although the serum concentration was raised in 54 patients, no relation between it and the severity of hepatocyte necrosis could be established. Glutamate dehydrogenase was therefore not confirmed to be a useful indicator of hepatocyte necrosis in patients with chronic alcoholism.
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PMID:Serum glutamate dehydrogenase as a marker of hepatocyte necrosis in alcoholic liver disease. 679 35

The time course of plasma glutamate dehydrogenase (GDH) elevation was studied in 42 male alcoholics admitted for alcohol detoxification or for the treatment of medical complications of alcoholism and in 2 volunteers consuming 2 g/kg/day of ethanol under metabolic ward conditions. GDH values were usually highest during or immediately after cessation of drinking; thereafter, they fell rapidly toward the normal range. Early GDH values correlated well with liver histology in 37 patients who subsequently underwent diagnostic liver biopsy.
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PMID:Plasma glutamate dehydrogenase: clinical application in patients with alcoholic liver disease. 700 46

Serum glutamate dehydrogenase (EC 1.4.1.3.) activity was measured in 73 hospital patients who had a history of chronic alcohol abuse and who all had a liver biopsy performed. High levels of serum GDH activity occurred in those patients with recent excess alcohol consumption independently of the underlying liver histology, and did not discriminate between those patients with and those without alcoholic hepatitis.
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PMID:Serum glutamate dehydrogenase is not a reliable marker of liver cell necrosis in alcoholics. 706 13

Usage of alcohol during the period of therapeutic remission of chronic alcoholism without complete restoration of its symptoms indicates failure of therapeutic remission (FTR). A method was suggested to detect FTR by enzymic activity of gamma-glutamyltranspeptidase, aspartate transaminase, alanintransaminase and glutamate dehydrogenase. FTR is stated at differential threshold of the above enzymes 32, 25, 26 and 6.5 u/l, respectively. Validity of the method was confirmed at examination of 110 chronic alcoholics and 61 healthy persons. Early FTR detection prevents occurrence of true recurrence of chronic alcoholism.
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PMID:[The follow-up of therapeutic remission in alcoholics]. 748 35

The serum activity of alanine aminotransferase, aspartate aminotransferase, glutamate dehydrogenase, gamma-glutamyl transferase and creatinine kinase was studied in 81 patients with chronic alcoholism and 31 patients with alcoholic psychoses. Eighty-one healthy apparently non-drinkers served as a control group. It is concluded that when acute alcoholic psychoses develop, patients with chronic alcoholism display a simultaneous increase in the activity of enzymes releasing from damaged muscular and hepatic tissues. This makes the application of a number of the diagnostic criteria developed in classical clinical enzymology impossible. The phenomenon of concurrent increases in the activity of creatine kinase, aspartate aminotransferase and glutamate dehydrogenase by 4 times or more has been proposed to be used as a criteria for identifying alcoholic psychosis in alcoholics.
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PMID:[The characteristics of the changes in the blood enzyme activity of patients with acute alcoholic psychoses]. 815 28


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