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:2.7.1.1 (hexokinase)
5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that acute coronary occlusion in the dog is often accompanied by increased adrenaline release into the blood. In the present study the consequences of this humoral reaction were studied in anaesthetised healthy mongrel dogs subjected to adrenaline infusion administered at a rate relevant to spontaneous release of this amine in coronary occlusion. Adrenaline was infused in a dose of 1.2 microgram.kg-1.min-1 for 4 h. Dogs receiving saline served as the control. Adrenaline administration led to the decrease in insulin/glucose ratio, to a significant fall in serum triiodothyronine and in blood pH. Free fatty acid levels doubled. Histochemically, a diminution in succinic dehydrogenase and ATPase activity in adrenaline-treated hearts was found. A significant fall in the activity of mitochondrial hexokinase in these hearts was detected spectrophotometrically. Electron microscopic study revealed alterations in the mitochondrial structure. These findings indicate that an excess of adrenaline in ammounts similar to that seen in experimental infarction leads to profound metabolic and hormonal disturbances and exerts a detrimental effect upon myocardium.
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PMID:Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion. 2 14

The metabolic effects on rat cardiac and skeletal muscle of a strenous program of swimming, of cold acclimation and of isoprenaline treatment (0.3 mg/kg daily for 5 five-day weeks) were compared. Exercised and cold-exposed rats gained less body weight than did controls or isoprenaline-treated rats. In all treated groups the heart and the intercapular brown adipose tissue hypertrophied. The size of the adrenals increased only in isoprenaline-treated animals. Cold-acclimation and physical training increased and isoprenaline treatment reduced or did not affect the activities of succinate dehydrogenase, malate dehydrogenase and citrate synthase of cardiac muscle. In the skeletal muscle all treatments resulted in increased activities of these enzymes. Of the anaerobic enzymes analysed, only the activity of hexokinase increased in response to the treatements used. This increase was the same in cardiac as in skeletal muscle, but it was significantly greater with isoprenaline-treatment than with training or with cold-acclimation. The activities of lactate dehydrogenase and phosphofructokinase did not differ significantly. All treatments improved cold resistance, but only swimming exercise and cold acclimation significantly increased tolerance to exercise. It is concluded that prolonged stimulation of adrenergic beta-receptors by catecholamines is responsible for the metabolic changes observed.
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PMID:Comparison of the effects of physical exercise, cold acclimation and repeated injections of isoprenaline on rat muscle enzymes. 12 87

When Cladosporium resinae is provided with n-hexadecane and glucose, n-hexadecane is used preferentially. Studies using [14C]glucose indicated that n-hexadecane did not inhibit glucose uptake but did retard oxidation of glucose to CO2 and assimilation of glucose carbon into trichloroacetic acid-insoluble material. Glucose could be recovered quantitatively from hydrocarbon-grown cells that had been transferred to glucose. Four enzymes that may be involved in glucose metabolism, hexokinase, glucose-6-phosphate dehydrogenase, glucose-phosphate isomerase, and succinate dehydrogenase, were not detected in cells grown on hexadecane but were present in cells grown on glucose. Addition of hexadecane to extracts of glucose-grown cells resulted in immediate loss of activity for each of the four enzymes, but two other enzymes did not directly involved in glucose metabolism, adenosine triphosphatase and alanine-ketoacid aminotransferase, were not inhibited by hexadecane in vitro. Cells grown on hexadecane and transferred to glucose metabolize intracellular hexadecane; after 1 day, activity of hexokinase, glucose-6-phosphate dehydrogenase, glucosephosphate isomerase, and succinate dehydrogenase could be detected and 22% of the intracellular hydrocarbon had been metabolized. Hexadecane-grown cells transferred to glucose plus cycloheximide showed the same level of activity of all the four enzymes as cells transferred to glucose alone. Thus, intracellular n-hexadecane or a metabolite of hexadecane can inthesis of those enzymes is not inhibited.
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PMID:Inhibition of glucose metabolism by n-hexadecane in Cladosporium (Amorphotheca) resinae. 13 54

Enzyme activities were measured in homogenates of left and right ventricles of guinea pigs after 14 and 28 days' exposure to 400 mmHg barometric pressure. All animals developed anorexia and right ventricular hypertrophy. Two control groups of animals were used, one free fed and the other restricted to the amount of food chosen by the hypobaric group. The factorial design of the experiment allowed some distinction between the effects of anorexia, hypertrophy, and hypoxia. Dietary restriction was associated with a decrease in glycogen phosphorylase, hexokinase, and succinate dehydrogenase activity and an increase in the M-subunits of lactate dehydrogenase. Myocardial hypertrophy was associated with an increase in the activity of the enzymes of the glycolytic pathway down as far as phosphoglycerate kinase and an increase in the M-subunits of lactate dehydrogenase. Chronic hypoxia seemed specifically to be associated with an increase in the H-subunits of lactate dehydrogenase and possibly a slight transient increase in succinate dehydrogenase activity. Mixing studies indicated that changes in enzyme activities were likely to be due to changes in enzyme concentrations.
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PMID:Effects of chronic hypoxia and dietary restriction on myocardial enzyme activities. 13 6

A study of post-mortem changes in human central nervous tissue has shown that within 100 h of death, no significant change occurs in the amount of nerve cell DNA and nucleolar RNA nor in some membrane-associated enzymes such as succinate dehydrogenase, NADH and NADPH diaphorase, and cytochrome oxidase. Low molecular weight RNA species, probably transfer and messenger RNA are quickly lost, but there is little alteration in ribosomal RNA content. Cytoplasmic enzymes show variable changes; phosphofructokinase activity is rapidly decreased; hexokinase is unaltered but lactate dehydrogenase, pyruvate kinase and glucose-6-phosphate dehydrogenase initially show increases in activity which subsequently decline. Oxygen uptake diminishes quickly. These findings indicate that mechanical alterations in cell structure, following death, render organelles physiologically ineffective long before any significant changes in certain constituent biochemicals are detected. This report emphasizes the great importance necessary in the selection of appropriately time matched post-mortem tissues if accurate comparative studies of many of the cells constituents are to be made.
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PMID:Post-mortem changes in human central nervous tissue and the effects on quantitation of nucleic acids and enzymes. 14 55

The effects of exposure of glial cells in primary culture and in continuous line (clone NN) to pentobarbital over various periods of time on cellular respiration and activities of enzymes involved in carbohydrate metabolism were studied. The results obtained in glial cells in primary culture were qualitatively identical to those obtained in glial cells in clonal line (NN). Both types of glial cells were shown to develop biochemical tolerance to pentobarbital as defined by an attenuated response to the depressant effects of a challenging dose of pentobarbital on cellular respiration in barbiturate-cultivated cells compared to those grown in drug-free medium. The biochemical tolerance was evident in the presence of glucose and succinate but not malate as substrate. This tolerance to pentobarbital was accompanied by increased activities of hexokinase, glucose-6-phosphate dehydrogenase, succinate dehydrogenase, and glutamate dehydrogenase and by a marked increase in the number of glial cell mitochondria as observed in electron micrographs. The results are interpreted to indicate a compensation of glial cells to the continuous presence of PB by an accelerated glucose uptake and metabolism, an accelerated metabolism of succinate, and an increased mitochondrial activity.
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PMID:Development and mechanism of barbiturate tolerance in glial cell cultures. 15 11

A cross-sectional study was carried out to examine the activities of certain enzymes representing aerobic and anaerobic energy metabolism as well as the biosynthesis of collagen of M. vastus lateralis in 23 male endurance athletes in habitual training, aged 33 to 70 years. 23 sedentary healthy men of corresponding ages were selected for the control group. The mean maximal oxygen uptake of the trained subjects was 53.6 ml-kg--1. min--1 and that of the control subjects 36.3 ml-kg--1. min--1. As compared to the control group the trained subjects had significantly higher values in the muscle malate dehydrogenase, succinate dehydrogenase and prolyl hydroxylase activities, whereas the opposite was true in the activity of lactate dehydrogenase. In hexokinase and creatine phosphokinase no marked differences between the groups were observed. The results showed that endurance training leads to increased activities of oxidative enzymes in the skeletal muscle. The adaptation changes were also observed in old men. The increased activity of prolyl hydroxylase may reflect the general enzymatic adaptation to physical training. A possibility exists that the turnover of muscle collagen in endurance athelets is continuously faster than that in sedentary men of corresponding ages.
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PMID:Enzyme activities in muscle and connective tissue of M. Vastus lateralis in habitually training and sedentary 33 to 70-year-old men. 17 30

A decrease in cytochrome c oxidase activity was observed in kidney tissue within 40 min after the transfusion of incompatible blood; at the same time, the succinate dehydrogenase activity was not altered. Opposite ratios (as compared with normal kidney) of the enzymatic activities were found within 24 hrs after a heterohemotransfusion. An addition of 5 M succinate to the kidney homogenate in vitro or administration of the substance at a dose of 8 mg per 100 g of body weight in vivo caused an activation of free oxidation and a decrease of phosphorylation. The addition of 50 M succinate, combined with hexokinase and NADH2, into the homogenate distinctly increased both the rate of tissue respiration and the coupled phosphorylation.
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PMID:[Mechanism of changes in oxidative phosphorylation in the kidney in nephropathy caused by post-transfusion complications]. 17 70

The 200 Oe magnetic field of power frequency produces an essential effect on metabolism in the tissue of the testicles which are highly sensitive to this factor. A single effect of the field for 24 h results in an increase in the glucose-6-phosphate dehydrogenase activity. 24-28 h after the cessation of the field action it lowers considerably as well as the cytochrome oxidase and hexokinase activities in mitochondria. The lactate dehydrogenase and succinate dehydrogenase activities increased in this case. Restoration of the initial level is marked on the 7th-14th days. Under repeated actions of the stimulation phase the enzymic activities under study (except the lactate dehydrogenase one) are decreased. The mentioned indices restore the initial level on the 14th-28th days. These changes correlates with dynamics of the testosterone level in the testicles and plasm.
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PMID:[Effect of a variable magnetic field on activity of enzymes of carbohydrate metabolism and tissue respiration in testicular tissue]. 21 74

Brusatol, a quassinoid with potent antineoplastic activity against P-388 lymphocytic leukemia cell proliferation, significantly inhibited P-388 cell hexokinase, phosphofructokinase, malic dehydrogenase, and succinic dehydrogenase. Mitochondrial oxidative phosphorylation, basal, and adenosine diphosphate-stimulated respiration, utilizing succinate and alpha-ketoglutarate as the substrate, was suppressed significantly by in vivo treatment with brusatol. However, brusatol treatment had no effect on liver oxidative phosphorylation. Brusatol greatly increased P-388 cyclic AMP levels but had no effect on liver cyclic nucleotides. Similar inhibitory effects on P-388 cell oxidative phosphorylation were found in vitro with brusatol, bruceoside A, and bruceantin. Brusatol had no effect on adenosine triphosphatase activity or on uncoupling of oxidative phosphorylation. Rather, brusatol appeared to increase the concentration of reduced mitochondrial electron-transport cofactors, thereby blocking aerobic respiration. A proposed mechanism of action is discussed.
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PMID:Antitumor agents. XXXV: Effects of brusatol, bruceoside A, and bruceantin on P-388 lymphocytic leukemia cell respiration. 22 89


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