Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of phosphate-activated glutaminase was reduced throughout the brain of cases with longstanding illnesses (agonal controls) compared to cases dying suddenly. The reduction was less marked in cortical than sub-cortical areas, with the caudate nucleus occupying an intermediate position. In control brains succinic dehydrogenase and pyruvate dehydrogenase were little affected by the ante-mortem clinical state. Of 9 brain areas studied, only the caudate nucleus showed a reduction of phosphate-activated glutaminase and succinic dehydrogenase in Huntington's disease greater than in agonal controls. The levels of succinic dehydrogenase and pyruvate dehydrogenase were highly correlated in frontal cortex and in caudate nucleus of Huntington's disease and control brains. There was a significant reduction in pyruvate dehydrogenase mean activity and a significant increase in gamma-glutamyl transpeptidase mean activity in Huntington's disease caudate nucleus. The level of pyruvate dehydrogenase significantly decreased and the level of gamma-glutamyl transpeptidase significantly increased with increasing duration of illness, possibly due to a progressive loss of neurons and increase in the density of glia in Huntington's disease caudate nucleus.
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PMID:Distribution of phosphate-activated glutaminase, succinic dehydrogenase, pyruvate dehydrogenase and gamma-glutamyl transpeptidase in post-mortem brain from Huntington's disease and agonal cases. 285 15

Chronic gamma-irradiation during 3.5 and 6 months (at a dose = rate of 46.2 pC/kg X c) of Microtus oeconomus living in conditions of normal and increased (by 50-100 times) gamma-radiation background, and of their progeny (the 1st, 2nd, 3d, and 4th generations) causes in homogenates of cardiac muscle, liver, and brain different changes in activity of succinate dehydrogenase (1.3.99.1, EC), pyruvate dehydrogenase (1.2.4.1, EC), and lactate dehydrogenase (1.1.1.27, EC) associated with the discordance of the processes of tissue respiration and glycolysis. The changes in dehydrogenases activity in Microtus oeconomus subjected to chronic irradiation were nearly the same as those found in their parents.
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PMID:[Effect of chronic gamma irradiation on dehydrogenase activity in the tissues of root voles and their progeny dwelling in a habitat with increased radioactivity]. 355 19

We report the clinical and autopsy findings in a young man of 18 with a chronic progressive disorder comprised of lactic acidosis, mental deterioration, and epileptic seizures which were sometimes accompanied by stroke-like episodes with transient hemiparesis and cortical blindness. He died of congestive heart failure. The autopsy showed lesions of the gray matter of the brain. Both the putamen and parieto-occipital cortex showed loss of neurons and proliferation of macrophages, astrocytes and vessels. There was marked loss of neurons in the inferior olives, and slight reduction of the number of Purkinje cells. Skeletal muscle studies revealed ragged-red fibers and structurally abnormal mitochondria. The heart was enlarged: accumulations of mitochondria occurred in the muscle fibers. The liver exhibited marked fatty degeneration. Biochemical analyses showed normal activities of pyruvate dehydrogenase in thrombocytes, pyruvate carboxylase in lymphocytes, biotinidase in serum as well as succinate dehydrogenase and cytochrome c oxidase. The features of this disorder differ in many respects from cases of mitochondrial encephalomyopathy previously reported and cannot be assigned to any specific disease entity.
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PMID:Mitochondrial encephalomyopathy. A variant with heart failure and liver steatosis. 367 21

The growth response of Listeria monocytogenes strains A4413 and 9037-7 to carbohydrates was determined in a defined medium. Neither pyruvate, acetate, citrate, isocitrate, alpha-ketoglutarate, succinate, fumarate, nor malate supported growth. Furthermore, inclusion of any of these carbohydrates in the growth medium with glucose did not increase the growth of Listeria over that observed on glucose alone. Resting cell suspensions of strain A4413 oxidized pyruvate but not acetate, citrate, isocitrate, alpha-ketoglutarate, succinate, fumarate, or malate. Cell-free extracts of strain A4413 contained active citrate synthase, aconitate hydratase, isocitrate dehydrogenase, malate dehydrogenase, fumarate hydratase, fumarate reductase, pyruvate dehydrogenase system, and oxidases for reduced nicotinamide adenine dinucleotide and reduced nicotinamide adenine dinucleotide phosphate. The alpha-ketoglutarate oxidation system, succinate dehydrogenase, isocitrate lyase, and malate synthase were not detected. Cytochromes were not detected. The data suggest that strain A4413, under these conditions, utilizes a split noncyclic citrate pathway which has an oxidative portion (citrate synthase, aconitate hydratase, and isocitrate dehydrogenase) and a reductive portion (malate dehydrogenase, fumarate hydratase, and fumarate reductase). This pathway is probably important in biosynthesis but not for a net gain in energy.
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PMID:Citrate cycle and related metabolism of Listeria monocytogenes. 499 14

The freshwater murrel, Channa punctatus, was exposed to a sublethal concentration of mercuric chloride (3 micrograms/liter) for 120 days and the following effects were examined: changes in the levels of glucose and lactic acid in blood and of glycogen and lactic acid in liver and muscles; rate of absorption of glucose from the intestine; and changes in the activities of glucose-6-phosphatase (G-6-Pase), hexokinase, lactate dehydrogenase (LDH), pyruvate dehydrogenase (PDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), glutamate dehydrogenase (GDH), L-amino acid oxidase (AO), and xanthine oxidase (XO) in brain, gills, intestine, kidney, liver, and muscles. Mercury-treated fish were hypoglycemic and hypolactemic. The glycogen content of liver and muscles remained unaltered but the muscle lactic acid level decreased significantly. The rate of intestinal absorption of glucose was reduced significantly by exposure to mercury. G-6-Pase activity was decreased in all the tissues. Hexokinase activity also decreased in mercury-exposed fish but it was significant only in intestine, kidney, and liver. The activities of LDH, PDH, SDH, and MDH also were decreased significantly except LDH in brain and MDH in kidney where an insignificant decrease and an insignificant increase, respectively, were recorded. GDH and AO activities were elevated in most of the tissues except GDH in gills, and AO in gills and muscles where a decrease was observed. XO activity in brain, gills, and kidneys was significantly elevated, but no marked alteration was noted in other tissues.
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PMID:Effect of mercuric chloride on some biochemical and physiological parameters of the freshwater murrel, Channa punctatus. 608 7

In autopsied brain tissue from three cases with Leigh disease (subacute necrotizing encephalomyelitis, SNE) and controls, the activity of pyruvate dehydrogenase complex (PDHC) was determined under different conditions. It was found to be at the control level or increased, but not deficient. The activities of succinate dehydrogenase, fumarase, succinate cytochrome c reductase, cytochrome c oxidase, and glutamate dehydrogenase were measured as additional mitochondrial markers and showed no essential differences between SNE and control tissue. The metabolic defect in SNE remains unknown. According to the literature, the defect may be localized to the mitochondrial systems. However, the reported results indicate that it cannot be ascribed to PDHC function. Extensive biochemical studies are necessary for understanding of the pathogenesis in the fatal genetic metabolic disease.
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PMID:Pyruvate dehydrogenase activity is not deficient in the brain of three autopsied cases with Leigh disease (subacute necrotizing encephalomyelopathy, SNE). 643 63

NADH:ubiquinone reductase (complex I) of the mitochondrial inner membrane respiratory chain binds a number of mitochondrial matrix NAD-linked dehydrogenases. These include pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase complex, mitochondrial malate dehydrogenase, and beta-hydroxyacyl-CoA dehydrogenase. No binding was detected between complex I and cytosolic malate dehydrogenase, glutamate dehydrogenase, NAD-isocitrate dehydrogenase, lipoamide dehydrogenase, citrate synthase, or fumarase. The dehydrogenases that bound to complex I did not bind to a preparation of complex II and III, nor did they bind to liposomes. The binding of pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase complex, and mitochondrial malate dehydrogenase to complex I is a saturable process. Based upon the amount of binding observed in these in vitro studies, there is enough inner membrane present in the mitochondria to bind the dehydrogenases in the matrix space. The possible metabolic significance of these interactions is discussed.
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PMID:Complex I binds several mitochondrial NAD-coupled dehydrogenases. 643 16

Alterations in the activities of lactate dehydrogenase, pyruvate dehydrogenase and succinate dehydrogenase in the brian, gills, intestine, kidney, liver and muscles, the levels of glycogen and lactic acid in liver and muscles, and blood glucose have been examined in a fresh-water teleost fish, Channa punctatus after exposure to a sublethal concentration (3 microgram/1) of mercuric chloride for 15, 30 and 60 days. The results revealed that the activities of all the three dehydrogenases were inhibited significantly after 60 days of treatment except for lactate dehydrogenase in brain. Glycogen and lactic acid contents of the liver and muscles and the blood glucose level also decreased significantly after 60 days of exposure. Though gills and muscles showed weak activity of the three dehydrogenases, the percentage of inhibition was more marked in these tissues than in others.
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PMID:Enzymological and biochemical changes produced by mercuric chloride in a teleost fish, Channa punctatus. 646 Mar 48

The apparent paradox of aerobic glycolysis has been investigated in bone and in cartilage. A new cytochemical procedure for hydroxyacyl dehydrogenase (HOAD) activity showed that the maximal activity of this enzyme in both tissues was equivalent to the maximal activity of glyceraldehyde 3-phosphate dehydrogenase (GAPD). The sum of these activities gave a measure of the maximum amount of acetyl-coenzyme A that could be produced. In these tissues, but not in liver which does not exhibit aerobic glycolysis, this summed value exceeded the maximal activity of succinate dehydrogenase (SDH). Consequently, it suggested that where fatty acid oxidation is sufficient to supply all the acetyl-coenzyme A required for the Krebs' cycle, that derived from fatty acid oxidation may inhibit pyruvate dehydrogenase causing accumulation of pyruvate which must be converted to lactate if pentose-shunt activity is to be maintained.
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PMID:Aerobic glycolysis of bone and cartilage: the possible involvement of fatty acid oxidation. 667 23

Chipmunks were chronically exposed to gamma-radiation at an average dose rate of 46 pA/kg. Changes in activity of succinate dehydrogenase (EC 1.3.99.1), pyruvate dehydrogenase (EC 1.2, 4.1) and lactate dehydrogenase (EC 1.1.1.27) were detected in the homogenates of the cardiac muscle, liver and brain at different physiological periods (before, during and after hibernation). The changes observed were related to the impairment of coordination between the processes of tissue respiration and glycolysis.
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PMID:[Level of dehydrogenase activity in chipmunks under normal conditions and during chronic external gamma-irradiation]. 672 68


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