[Ratio of aldolase activity measured with fructosediphosphate and fructosemonophosphate in various organs and tissues of rats].
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Age Factors↗
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[On the correlation fo fructosediphosphate and fructosemonophosphate aldolase activities in rat tissues under toxic conditions and starvation].
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Aldehyde-Lyases↗
An isozyme of erythrocyte pyruvate kinase (PK-Los Angeles) with impaired kinetics corrected by fructose-1, 6-diphosphate.
A mutant isozyme of erythrocyte pyruvate kinase was found in a family of French-Canadian ancestry in association with hemolytic anemia. The isozyme was characterized by normal maximal activity, pH optimum, heat stability, and fructosediphosphate activation constants, but had markedly reduced affinity for the substrate, phosphoenolpyruvate. This kinetic defect was corrected almost entirely in vitro by low concentrations of fructosediphosphate.
Anemia, Hemolytic, Congenital↗
Pyruvate kinase from human skeletal muscle.
A simple method is described for the isolation of crystalline pyruvate kinase from human skeletal muscle. The enzyme was purified by ammonium sulfate fractionation, heat treatment and crystallization. Two crystal forms of pyruvate kinase differing in solubility but not in specific activity were found. The homogenous enzyme preparations in triethanolamine buffer, pH 7.6 reveal at 25 degrees a specific activity of 245 U per mg protein, and of 340 U/mg in potassium phosphate buffer (50 mM). The enzyme is activated by inorganic phosphate and fructosediphosphate to the same extent, and inhibited non competetively by ammonium ion. The molecular weight as measured by gel filtration is 220,000 daltons and the enzyme molecule is composed of 4 subunits.
Chromatography, Gel↗
Comparative intermediary metabolism of vegetative cells and microcysts of Myxococcus xanthus.
Crude extracts of both vegetative cells and glycerol-induced microcysts of Myxococcus xanthus contained the following enzyme activities: phosphofructokinase, phosphoglucoisomerase, fructose-1,6-diphosphatase, fructosediphosphate aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphopyruvate carboxylase, citrate synthase, isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, phosphoglucomutase, and uridine diphosphate glucose pyrophosphorylase. With the exception of isocitrate dehydrogenase, which was present at a fivefold higher concentration in microcysts, all activities in extracts from both types of cells were essentially equal. Hexokinase and pyruvate kinase could not be detected in extracts from either type of cell. Microcysts metabolized acetate at a lower rate than did vegetative cells. Most of this decrease was reflected in a substantial decrease in ability of microcysts to oxidize acetate to CO(2). In addition, microcysts and vegetative cells showed a different distribution of (14)C-label from incorporated acetate.
Acetates↗
[Comparative evaluation of the protective effect of sodium valproate, phenazepam and ionol in stress-induced liver damage in rats].
Ionol, a synthetic antioxidant, limits the stressor liver injury to a greater extent than sodium, valproate and phenazepam, activators of a GABA-ergic link of the stress-limiting organism systems. This injury is exhibited in the organospecific elevated levels of blood enzymes fructosediphosphate aldolase depression of N-demethylase activity of microsomal monooxygenases and a decrease in the amount of cytochromes P-450 and B5.
Animals↗
[Pyrivate kinase deficiency. II. Biochemical studies (author's transl)].
Pyruvate kinase deficiency was studied biochemically in ten homozygous and seven heterozygous individuals who previously had been examined clinically and hematologically (see part I). In crude hemolysates some properties of the deficient enzymes were found to be altered. The pH optimum was shifted towards the alkaline range, and the thermal optimum was found between 17 and 27 degrees Cinstead of between 37 und 47 degrees C. The abnormal enzymes were much less stable than normal pyruvate Kinase (PK), and more susceptible to inhibition by adenosinetriphosphate. The affinity to adenosinediphosphate was normal in all cases whereas the affinity to phosphoenolpyruvate was either normal (two cases/, increased (two cases) or slightly decreased (six cases). Fructosediphosphate activated the abnormal enzymes by a factor of 1.5--18 and simultaneously transformed the sigmoidal affinity curve with phosphoenolpyruvate into the hyperbolic curve known for the normal enzyme. The consumption of glucose and the formation of lactate were higher in PK deficient erythrocytes than in normal cells but lower than in erythrocyte populations with similar reticulocyte counts. The formation of 2,3-diphosphoglycerate was markedly increased, whereas its breakdown was low. A close relation between the degree of reticulocytosis and the impairment of glucose metabolism was found. In patients with high reticulocyte counts, i.e. in the splenectomized patients, the highest concentrations of glucose-6-phosphate, phosphoenolpyruvate, 3-phosphoglycerate and 2,3-diphosphoglycerate as well as a high formation and a low breakdown of 2,3-diphosphoglycerate and a deficit in lactate formation were found. In heterozygotes, small increases of the concentration of glucose-6-phosphate, phosphoenolpyruvate and 3-phosphoglycerate were demonstrated. Our results support the conclusion that PK deficiency is mainly a disorder of the reticulocytes. Their metabolism grossly deteriorates within the venous sinuses of the spleen. Splenectomy improves the clinical course because this critical area of microcirculation with a highly unfavourable metabolic milieu is eliminated.
Anemia, Hemolytic, Congenital↗
[Splitting of fructose diphosphate by muscle and tumor homogenates].
Effect of MgCl2 and ATP on the elevation in lactate, pyruvate and methylglyoxale content was studied on incubation of fructosediphosphate with muscle and tumor homogenates. Muscle homogenate accumulated lactate, pyruvate and methyglyoxale more intensively as compared with tumor homogenate. Pyruvate was formed only in presence of MgCl2 and ATP, although it did not practically affect the elevation of lactate in muscle homogenate. The data obtained suggest that tumor homogenate does not contain the enzymatic system involved in methylglyoxale formation.
Adenosine Triphosphate↗
Effect of high-energy phosphates and free radical scavengers on replant survival in an ischemic extremity model.
In replantation surgery, preoperative and intraoperative ischemia can lead to irreversible changes that prevent reperfusion during the subsequent re-establishment of circulation. These changes are termed the no-reflow phenomenon. Ischemic phase damage was addressed by comparing the dose-response effects of controls vs. five different high-energy phosphate compounds on replanted limb survival. Reperfusion damage was evaluated via comparisons of controls with superoxide dismutase (SOD). Ischemic hindlimbs treated with high-energy phosphates displayed improved survival compared with controls. Limbs treated with SOD demonstrated no change in survival at 4 hours and improved survival at 8 hours. Combining adenosine and SOD had no improved effect on survival. Adenosine was the most effective high-energy phosphate in limiting ischemic damage. The free radical scavenger (SOD) was beneficial only at the later stages of ischemia. In this experimental model, there appears to be a role for both phosphates and free radical scavengers in enhancing ischemic tissue survival.
Adenosine↗
Biochemical characterization of three mutant isozymes of erythrocyte pyruvate kinase: PK-"Gainesville," PK-"San Juan," and PK-"Cape Canaveral".
Pyruvate kinase was partially purified from erythrocytes of three unrelated, nonconsaguineous patients with chronic hemolytic anemia of differing clinical severities. Characterization of the defective PK isozymes by internationally standardized criteria indicated that one (PK-"Gainesville") had severely impaired substrate affinity, another (PK-"San Juan") had markedly reduced residual activity, and the third (PK-"Cape Canaveral") had a combination of milder defects. Each appears representative of subsets emerging from the heterogeneous molecular defects that make up pyruvate kinase deficiency.
Adenosine Triphosphate↗
Pyruvate kinase activity and response to allosteric effectors in rat erythrocytes and reticulocytes fractionated by multiple partitioning in aqueous two-phase systems.
Specific activity of pyruvate kinase decreases as the age of rat erythrocytes increases in fractions obtained by counter-current distribution in dextran-polyethylene glycol biphasic systems; the enzyme is inhibited by ATP and activated by fructose-1,6-bisphosphate at low phosphoenol pyruvate concentrations. Specific activity does not change in fractions from greater than 95 per cent-rich reticulocytes (anaemic rats); the enzyme is inhibited by ATP but not activated by fructose-1,6-bisphosphate. These results can be explained on the basis of different pyruvate kinase isozymes and suggest that decrease in activity is not affecting regulatory properties during erythrocytes aging.
Adenosine Triphosphate↗
Some effects of fructose-1,6-diphosphate on rat myocardial tissue related to a membrane-stabilizing action.
This study aims at elucidating the mechanism of action of extracellular fructose-1,6-diphosphate (FDP). FDP is able to inhibit Ca++ entry into the myocardial tissue with an IC50 value of 11.5 mM and in addition, it is bound by rat heart slices, the binding being activated by Zn and conditions of chemical hypoxia induced by KCN and iodoacetate. The overall effect of extracellular FDP includes an increase of frequency and amplitude of contraction of perfused heart at concentration below 1 mM, and, in general, a stimulation of the oxygen consumption of the tissue. The antihaemolytic effect of FDP suggests its action as a membrane stabilizer. The effects of extracellular FDP on the myocardial cell can be interpreted both on the basis of a limited permeability of the cell membrane to it and as a purely extracellular effect transduced through the cell membrane with a final response consisting of an increase in the intracellular FDP.
Animals↗
Studies of the regulation of renal gluconeogenesis in normal and Pi depleted proximal tubule cells.
Pi depletion of proximal tubule cells isolated from mouse kidney results in a decrease in the cell content of fructose-2,6-bisphosphate and an increase in the rate of gluconeogenesis from pyruvate, malate and succinate. Gluconeogenesis from glycerol is unaffected by Pi depletion. Introduction of fructose-2,6-bisphosphate into the cytosol of ATP-permeabilized cells is accompanied by a fall in gluconeogenesis. The presence of external Ca2+ stimulates gluconeogenesis. When cytosolic Ca2+ is raised to 1.8 microM by permeabilization, the resealed cells still require 2.5 mM Ca2+ in the bathing medium in order to perform gluconeogenesis at the maximum rate. Cells permeabilized in the presence of cAMP show a decreased rate of glucose production. Phorbol ester stimulates gluconeogenesis provided that the phorbol treatment is performed in the absence of Ca2+ ions. It is suggested that Pi depletion may stimulate pyruvate carboxylase activity and facilitate the entry of certain gluconeogenic substrates into mitochondria. It is also proposed that important aspects of the control of renal gluconeogenesis by parathyroid hormone are mediated by protein kinase C.
Animals↗
Fructose-1,6-diphosphate as an in vitro and in vivo anti-alcohol agent in the rat.
Fructose-1, 6-diphosphate (FDP) decreases the effect of ethanol on Ca++ entry and inhibits the ethanol-stimulated phosphate efflux in rat heart slices. FDP also inhibits the ethanol-stimulated [36Cl-]-uptake by rat brain microvesicles and affects the isolated GABA-receptor in a way opposite to that of ethanol. The in vivo effects of FDP include a dose-dependent decrease in ethanol-induced gastric ulcers and a decrease in the serum transaminase levels raised by chronic ethanol administration. Other central actions of ethanol such as diuresis, narcosis, dependence and withdrawal symptoms are also counteracted by FDP.
Animals↗
Effects of vanadate on 6-phosphofructo 2-kinase activity and fructose 2,6-bisphosphate levels in cultured rat hepatocytes.
The presence of vanadate in primary cultures of rat hepatocytes produced a significant increase in the concentration of fructose 2,6-bisphosphate and in the activity of 6-phosphofructo 2-kinase. Compared with insulin, vanadate had a more potent action on the metabolite increase, but a similar effect on the 6-phosphofructo 2-kinase activity. Both the insulin- and the vanadate-dependent enhancements of 6-phosphofructo 2-kinase were inhibited by cycloheximide which specifically blocks protein synthesis on the translational level, suggesting that the increase of the enzyme activity was due to induction rather than to a change in the catalytic activity.
Animals↗
Fructose 1,6-bisphosphate prevents oxidative stress in the isolated and perfused rat heart.
Rat hearts were perfused with the Langendorff technique at constant flux in the presence of the oxidizing agents hydrogen peroxide and diamide. Fructose 1,6-bisphosphate strongly prevented the decline of heart contractility due to the infusion of these oxidizing agents. On the other hand, fructose 1,6-bisphosphate had no effect on the release of total glutathione into the perfusate but prevented the loss of lactate dehydrogenase indicating a protective effect on cell membranes. Comparing the cytosolic and mitochondrial loss of glutathione, fructose 1,6-bisphosphate exerted a beneficial action only on the mitochondrial fraction. Several mechanisms of action have been considered to explain the protective action of fructose 1,6-bisphosphate. In our experimental conditions fructose 1,6-bisphosphate might stimulate its own production giving rise to dihydroxyacetone phosphate, that, after reduction to glycerol 3-phosphate, can permeate the mitochondrial membrane with the final production of energy.
Animals↗
Gluconeogenesis and its regulation.
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Amino Acids↗