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 activities of nine enzymes in liver specimens obtained from four children who had died from Reye's syndrome were compared to the corresponding activities of a control group of four children who had died from unrelated causes. At the 95% significance level, the alterations could be classified into three groups. Five activities [lactate dehydrogenase, alanine aminotransferase, glucose 6-phosphatase, cytochrome oxidase, and malate dehydrogenase (mitochondrial plus cytosolic)] showed no change. Three enzymes [glutamate dehydrogenase, isocitrate dehydrogenase (NADP), and monoamine oxidase] were decreased. One activity (glucose 6-phosphate dehydrogenase) was increased. The malate dehydrogenase isozymes were resolved by electrophoresis, and the two bands were stained and measured. The ratio of cytosolic:mitochondrial enzyme was significantly greater in Reye's syndrome than in the control group. These results lend further support to the view that in Reye's syndrome the impairment of hepatic function is largely confined to the mitochondria. The lowered activity of monoamine oxidase means that the abnormalities extend to the outer mitochondrial membrane. Imbalances of the cytosolic:mitochondrial enzyme activities were evaluated in needle biopsy specimens from four other children under conditions where neurologic abnormalities were less severe. Two patients had elevated ratios of both glutamate:lactate dehydrogenase and cytosolic:mitochondrial malate dehydrogenase activities, and a third had only an abnormal malate dehydrogenase ratio. In contrast to these Reye's syndrome patients, a fourth case admitted with a provisional diagnosis of Reye's syndrome showed no abnormality in either ratio in stage IV coma.
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PMID:Comparison of cytosolic and mitochondrial hepatic enzyme alterations in Reye's syndrome. 745 35

Defects in cytochrome oxidase (CO; complex 4) have recently been demonstrated in blood platelets and in brain tissue from patients with Alzheimer's disease (AD) with possible etiological implications. Because of pathogenetic similarities with AD, we have measured the activities of several mitochondrially localised enzymes in the blood platelets of individuals afflicted with trisomy-21 (Down's syndrome). The activities of monoamine oxidase, cytochrome oxidase, isocitrate dehydrogenase, and glutamate dehydrogenase were assayed in washed platelets from sixty caucasian, male and female control individuals (ages 18-60) and ten, young Down's Syndrome patients (ages 9-21). Significant reductions in the activities of monoamine oxidase, cytochrome oxidase, and isocitrate dehydrogenase were found. In all cases the average activities in Down's syndrome individuals were approximately two-thirds those of controls (DS/Controls = 0.68, 0.67, 0.64 respectively). The activity of the fourth enzyme studied, glutamate dehydrogenase, was found to be similar to controls. Results suggest that these reductions are a consequence of a generalised mitochondrial disturbance which may lie behind some pathogenetic aspect(s) of the disease.
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PMID:Mitochondrial enzyme deficiencies in Down's syndrome. 774 61

In the course of a long-term L-DOPA administration (14 days) and 2 weeks after its cessation the activities of some protein enzymes (aminopeptidase, acid phosphatase), neuromediator (MAO, ACE) and oxidative (glutamate dehydrogenase, glucose-6-phosphate dehydrogenase) metabolism were studied by quantitative cytochemical methods in brain motor structures (sensorimotor cortex, caudate nucleus) and in structures not directly related to motor functions (hippocampus) of rats with high and low motor activity. After L-DOPA (madapar) cessation significant changes were revealed in the formation of motor system of the brain, primarily in the group of rats with low motor activity. It is suggested that a decrease in MAO activity after madapar cessation may be responsible for dyskinesia arising after cessation of L-DOPA preparations treatment.
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PMID:[Pathochemical changes in the motor structures of the brain under the influence of the administration of L-DOPA preparations and their withdrawal (experimental research)]. 790 Apr 46

Blood ammonia content and enzymes involved in ammonia metabolism, namely glutamine synthetase (GS), glutamate dehydrogenase (GDH), monoamine oxidase (MAO), alanine amino-transferase (ALT) and aspartate aminotransferase (AST), were studied in Plasmodium yoelii-infected drug-treated mice tissues. The ammonia content in blood increased with the rise of parasitaemia. Hepatic GS, GDH and MAO showed a marked decrease in enzyme activity during parasitic infection. In contrast, cerebral GS and MAO showed a significant increase during infection. However, the parallel measurement of renal enzymes did not show any noticeable alterations except for ALT and AST. Oral pyrimethamine treatment (10 mg/kg for 4 days) in infected mice (5-10%) returned the altered levels of the above enzymes to almost normal 1 week after the cessation of drug treatment.
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PMID:Studies on ammonia-metabolizing enzymes during Plasmodium yoelii infection and pyrimethamine treatment in mice. 877 35

Quantitative cytochemical methods revealed the decrease of MAO activity (substrate--tryptamine) in the hippocampus of L-dioxytryptamine treated August rats genetically predisposed to emotional stress under the effect of delta sleep inducing peptide (DSIP). Activities of aminopeptidase and glutamate dehydrogenase were decreased in n.accumbens while changes of the activities of these enzymes were not significant in the layers III and V of sensomotor cortex and n.caudatus. In all brain structures Ache and MAO (substrate 5-hydroxytryptamine) activities were not influenced by DSIP.
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PMID:[Changes in the enzyme activity in the brain structures of August rats under the influence of the delta sleep-inducing peptide against a background of prolonged L-dihydroxyphenylalanine administration]. 1070 90

The present study was undertaken to determine whether ATP-MgCl(2) administration in rats could protect hepatic mitochondrial function and improve energy metabolism during hepatic ischemia and subsequent reperfusion. Global hepatic ischemia was produced for 60 min followed by reperfusion. The rats then received 0.5 ml of saline or ATP-MgCl(2) intravenously. In saline-treated ischemic rats, serum alanine-aminotransferase levels peaked at 5 h. The aminotransferase level was significantly reduced in the ATP-MgCl(2) treatment group. The wet weight-to-dry weight ratio of the liver was significantly increased by ischemia/reperfusion. ATP-MgCl(2) treatment minimized the increase in this ratio. The ketone body ratio in blood, which reflects the mitochondrial free NAD(+)/NADH ratio, decreased after ischemia and at 1 h following reperfusion. This decrease was somewhat improved by ATP-MgCl(2) infusion. At 1 and 5 h after reperfusion, mitochondrial monoamine oxidase and glutamate dehydrogenase activities decreased. ATP-MgCl(2) infusion following ischemia restored the lost activities. Hepatic ATP levels in saline-treated rats were found to be 50% lower 5 h following reperfusion; however, treatment with ATP-MgCl(2) resulted in significantly higher ATP levels and energy charge. The accumulation of purine catabolites in ischemic tissues was reduced during reperfusion. ATP-MgCl(2) infusion resulted in accumulation of adenosine in reperfused liver. Mitochondrial lipid peroxidation was elevated in the saline-treated ischemic group, but this elevation was inhibited by ATP-MgCl(2) infusion. The present results lead us to conclude that the amelioration of liver function which occurs with ATP-MgCl(2) infusion following ischemia may be mediated through improvement in ischemia-induced mitochondrial energy metabolism.
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PMID:The beneficial effect of ATP-MgCl(2) on hepatic ischemia/reperfusion-induced mitochondrial dysfunction. 1097 26

Quantitative cytochemical assay showed that single injection of delta sleep-inducing peptide increased monoamine oxidase activity (substrates: serotonin and tryptamine) in the caudate and accumbens nuclei and glutamate dehydrogenase activity in the hippocampus of stress-resistant Wistar rats chronically treated with L-DOPA. Enzyme activities in the sensorimotor cortex did not change. Delta sleep-inducing peptide had no effects on acetylcholine esterase and aminopeptidase activities in the brain of Wistar rats.
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PMID:Neurochemical characteristics of the effects of delta sleep-inducing peptide in Wistar rats with hyperactivity of the dopaminergic system. 1118 19

The morphology of the foregut muscles of five spider families (Theraphosidae, Agelenidae, Araneidae, Lycosidae, Salticidae) was described, and the individual fibre numbers and fibre cross diameters of the muscles were determined. The nomenclature of these muscles was reviewed and modified if necessary. Oxidative enzyme and myosin-ATPase histochemistry revealed eight dilatatory muscles of the foregut to consist of slow (type I) fibres, while fast fibres (type IIB), and intermediate fibres, were only to be found in the two other muscles of the foregut, and in the remaining prosomal muscles (type IIA fibres around the poison gland). The eight sucking muscles proper of the foregut also showed stronger activities of transmitter metabolizing enzymes [monoamine oxidase, glutamate dehydrogenase(NAD)], and comparatively distinct amounts of glycogen and lipids.
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PMID:Observations on the morphology and histochemistry of the foregut muscles of spiders (Arachnida: Araneida). 3013 3

: This study examined the hepatoprotective and anti-inflammatory effects of anthocyanins from Vaccinim myrtillus (bilberry) fruit extract on the acute liver failure caused by carbon tetrachloride-CCl4 (3 mL/kg, i.p.). The preventive treatment of the bilberry extract (200 mg anthocyanins/kg, orally, 7 days) prior to the exposure to the CCl4 resulted in an evident decrease in markers of liver damage (glutamate dehydrogenase, sorbitol dehydrogenase, malate dehydrogenase), and reduced pro-oxidative (conjugated dienes, lipid hydroperoxide, thiobarbituric acid reactive substances, advanced oxidation protein products, NADPH oxidase, hydrogen peroxide, oxidized glutathione), and pro-inflammatory markers (tumor necrosis factor-alpha, interleukin-6, nitrite, myeloperoxidase, inducible nitric oxide synthase, cyclooxygenase-2, CD68, lipocalin-2), and also caused a significant decrease in the dissipation of the liver antioxidative defence capacities (reduced glutathione, glutathione S-transferase, and quinone reductase) in comparison to the results detected in the animals treated with CCl4 exclusively. The administration of the anthocyanins prevented the arginine metabolism's diversion towards the citrulline, decreased the catabolism of polyamines (the activity of putrescine oxidase and spermine oxidase), and significantly reduced the excessive activation and hyperplasia of the Kupffer cells. There was also an absence of necrosis, in regard to the toxic effect of CCl4 alone. The hepatoprotective mechanisms of bilberry extract are based on the inhibition of pro-oxidative mediators, strong anti-inflammatory properties, inducing of hepatic phase II antioxidant enzymes (glutathione S-transferase, quinone reductase) and reduced glutathione, hypoplasia of Kupffer cells, and a decrease in the catabolism of polyamines.
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PMID:Anthocyanins Protect Hepatocytes against CCl4-Induced Acute Liver Injury in Rats by Inhibiting Pro-inflammatory mediators, Polyamine Catabolism, Lipocalin-2, and Excessive Proliferation of Kupffer Cells. 3159 Feb 49


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