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:4.1.2.13 (aldolase)
3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trivalent organic antimonials, such as stibophen, have been employed for the chemotherapy of schistosome and filariid infections. The effects of stibophen on adult Litomosoides carinii, Dipetalonema witei (= viteae), and Brugia pahangi were examined. In vitro, lactate accumulation was markedly inhibited by the antimonials as was phosphofructokinase activities in homogenates. Incubation of filariids with stibophen and determination of internal concentrations of hexose phosphate also indicated a decreased phosphofructokinase activity. In addition, a second inhibitory effect of stibophen on aldolase has been observed which appears to be specific for stibophen and is not displayed by potassium antimony tartrate. Both inhibitory activities may contribute to the chemotherapeutic effect of stibophen. In addition to the schistosomes and filariids, stibophen also inhibits Ascaris and Hymenolepis diminuta phosphofructokinases at low concentrations, where no inhibition of the corresponding mammalian liver enzyme was demonstrable.
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PMID:The effects of stibophen on phosphofructokinases and aldolases of adult filariids. 17 64

Optimal conditions necessary for the reversible inactivation of crystalline rabbit muscle phosphofructokinase by homogeneous rabbit liver fructose-1,6-bisphosphatase have been studied. At higher enzyme levels (to 530 mug/ml of phosphofructokinase) the two proteins were mixed and incubated in a pH 7.5 buffer composed of 50 mM Tris-HC1, 2 mM potassium phosphate, and 0.2 mM dithiothreitol. Aliquots were removed at various times and assayed for enzyme activity. A time dependent inactivation of phosphofructokinase caused by 1-2.3 times its weight of fructose-1,6-bisphosphatase was observed at 30, 23, and 0 degree C. This inactivation did not require the presence of adenosine 5'-triphosphate or Mg2+ in the incubation mixture, but an adenosine 5'-triphosphate concentration of 2.7 mM or greater was required in the assay to keep phosphofructokinase in an inactive form. A mixture of activators (inorganic phosphate, (NH4)2SO4, and adenosine 5'-monophosphate), when added to the assay cuvette, restored nearly all of the expected enzyme activity. Incubations with other proteins, including aldolase, at concentrations equal to or greater than the effective quantity of fructose-1,6-bisphosphatase had no inhibitory effect on phosphofructokinase activity. Removal of tightly bound fructose 1,6-bisphosphate from phosphofructokinase could not explain this inactivation, since several analyses of crystalline phosphofructokinase averaged less than 0.1 mol of fructose 1,6-bisphosphate/320 000 g of enzyme. Furthermore, the inactivation occurred in the absence of Mg2+ where the complete lack of fructose-1-6-bisphosphatase activity was confirmed directly. At lower phosphofructokinase concentrations (0.2-2 mug/ml) the inactivation was studied directly in the assay cuvette. Higher ratios of fructose-1,6-bisphosphatase to phosphofructokinase were necessary in these cases, but oleate and 3-phosphoglycerate acted synergistically with lower amounts of fructose-1,6-bisphosphatase to cause inactivation. The inactivation did not occur when high concentrations of fructose 6-phosphate were present in the assay, or when the level of adenosine 5'-triphosphate was decreased. However, the inactivation was found at pH 8, where the effects of allosteric regulators on phosphofructokinase are greatly reduced. Experiments with rat liver phosphofructokinase showed that this enzyme was also subject to inhibition by rabbit liver fructose 1,6-bisphosphatase under conditions similar to those used in the muscle enzyme studies. Attempts to demonstrate direct interaction between phosphofructokinase and fructose-1,6-bisphosphate by physical methods were unsuccessful. Nevertheless, our results suggest that, under conditions which approximate the physiological state, the presence of fructose-1,6bisphosphatase can cause phosphofructokinase to assume an inactive conformation. This interaction may have a significant role in vivo in controlling the interrelationship between glycolysis and gluconeogenesis.
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PMID:Specific, reversible inactivation of phosphofructokinase by fructose-1,6-bisphosphatase. Involvement of adenosine 5'-triphosphate, oleate, and 3-phosphoglycerate. 18 Oct 51

1. The regulation of glycolysis and pyruvate oxidation under varying conditions of ATP and oxygen consumption was studied in isolated perfused rat hearts. Potassium-induced arrest was employed to inhibit the ATP consumption of the heart. 2. Under the experimental conditions, the beating heart used solely glucose as the oxidisable substrate. The glycolytic flux through the aldolase step decreased in pace with the decreasing oxygen consumption during the potassium-induced arrest of the heart. The decrease in glucose oxidation was larger than the inhibition of the oxygen consumption, suggesting that the arrested heart switches to fatty acid oxidation. The time course and percentage changes of the inhibition of pyruvate oxidation and the decrease in the amount of the active form of pyruvate dehydrogenase suggest that the amount of active pyruvate dehydrogenase is the main regulator of pyruvate oxidation in the perfused heart. 3. To test the relative significance of the possible mechanisms regulating covalent interconversions of pyruvate dehydrogenase, the following parameters were measured in response to the potassium-induced cardiac arrest: concentrations of pyruvate, acetyl-CoA, CoA-SH, citrate, alpha-oxoglutarate, ATP, ADP, AMP, creatine, creatine phosphate and inorganic phosphate and the mitochondrial NADH/NAD+ ratio. In cardiac tissue the adenylate system is not a good indicator of the energy state of the mitochondrion, even when the concentrations of AMP and free cytosolic ADP are calculated from the adenylate kinase and creatine kinase equilibria. Only creatine phosphate and inorganic phosphate undergo significant changes, but evidence of the participation of the latter compounds in the regulation of the pyruvate dehydrogenase interconversions is lacking. The potassium-induced arrest of the heart resulted in a decrease in pyruvate, a slight increase in acetyl-CoA, a large increase in the concentration of citrate and an increase in the mitochondrial NADH/NAD+. The results can be interpreted as showing that in the heart, the pyruvate dehydrogenase interconversions are mainly regulated by the pyruvate concentration and the mitochondrial redox state. Concentrations of all the regulators tested shifted to directions which one would expect to result in a decrease in the amount of active pyruvate dehydrogenase, but the changes were quite small. Therefore, the energy-linked regulation of pyruvate dehydrogenase in intact tissue is possibly mediated by the equilibrium relations between the cellular redox state and the phosphorylation potential recently confirmed in cardiac tissue.
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PMID:Energy-linked regulation of glucose and pyruvate oxidation in isolated perfused rat heart. Role of pyruvate dehydrogenase. 18 44

4-Deoxy-4-fluoro-alpha-D-sorbose (6) was prepared in crystalline form by the action of potassium hydrogen fluoride on 3,4-anhydro-1,2-O-isopropylidene-beta-D-psicopyranose (3) followed by deacetonation. Under identical conditions, 3,4-anhydro-1,2-O-isopropylidene-beta-D-tagatopyranose (7) underwent epoxide migration to give 4,5-anhydro-1,2-O-isopropylidene-beta-D-fructopyranose (12), which after deacetonation yielded 4-deoxy-4-fluoro-D-tagatose (15) and 5-deoxy-5-fluoro-alpha-L-sorbopyranose (16), the latter as the crystalline, free sugar. The action of glycol-cleavage reagents on the isopropylidene acetals of the deoxyfluoro sugars was consistent with the assigned structures. The structures were established by 13-C n.m.r. studies of the free deoxyfluoro sugars 6 and 16 and of the isopropylidene acetal 13, and by 1-H n.m.r. studies on the acetylated isopropylidene acetals 5 diacetate, 13 diacetate, and 14 diacetate. 5-Deoxy-5-fluoro-L-sorbose (16) was biologically active, producing in mice effects characteristic of deoxyfluorotrioses and of fluoroacetate. 4-Deoxy-4-fluoro-D-tagatose (15) and 4-deoxy-4-fluoro-D-sorbose (6) produced no apparent effects in mice up to a dose of 500mg/kg. The implications of these findings with respect to transport, phosphorylation, and the action of aldolase on ketohexoses are discussed.
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PMID:Deoxyfluoroketohexoses: 4-deoxy-4-fluoro-D-sorbose and -tagatose and 5-deoxy-5-fluoro-L-sorbose. 114 54

In order to elucidate the effects of amphotericin B (AMB) on the glycolytic pathway, the metabolism of [1-13C]glucose in glucose-grown repressed Saccharomyces cerevisiae was studied. The cells were aerobically suspended in pyrophosphate solutions of high potassium concentration with or without 10(-6) M amphotericin B and measurements were made using 1H-, 13C-NMR spectroscopy and biochemical methods. The results were compared with those obtained under the same experimental conditions but in a medium rich in sodium salts containing the same antibiotic concentration. In general the presence of 10(-6) M AMB reduces the glucose consumption and the ethanol production while favouring the glycerol and trehalose formation. These effects are greatly reduced when a high K+ concentration was used. The AMB effects on the glucose consumption and the production of ethanol, glycerol and trehalose, observed in a suspension rich in Na+, can be fairly well explained by the leakage of K+ through AMB membrane channels. This outflux induces a substantial decrease in the activity of some K(+)-dependent enzymes, such as aldolase, phosphofructokinase and pyruvate kinase. The intensities of the glutamate C2 and C4 signals are higher with a suspension rich in Na+ than with a suspension rich in K+, suggesting that the Krebs cycle operates more effectively in a solution rich in Na+. In the absence of AMB, the passive diffusion of glycerol through the cell membrane is relatively slow and apparently depends on the ionic external medium: it is more efficient in solutions with a high K+ than with a high Na+ concentration. In the presence of 10(-6) M AMB, the glycerol C1,3 resonance drastically decreases at 20 min and then disappears in the noise. This rapid disappearance suggests that glycerol can easily pass through the pores arising from the interaction of AMB with the membrane sterols. However, the rate of pore formation is slow, independent of the external medium (Na+ or K+) and this process is not completed within 20 min.
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PMID:Comparative study of the effects of amphotericin B on the glucose metabolism in Saccharomyces cerevisiae in K(+)- and Na(+)-rich media. 132 8

The frequent association of myotonia with dystrophy and the knowledge that calcium is increased in injured skeletal muscle cells suggest a possible relationship between cell calcium and myotonic alterations. This investigation has been performed to study the role of calcium in experimental myotonia induced by anthracene-9-carboxylic acid (9-AC) in rats treated with several regimens of food and exercise. Thirty-two rats were divided into 4 groups of 8 rats each, one control and 3 experimental groups. The treatments included caffeine plus exercise (group 2), and a calcium-rich diet (group 3); these procedures were designed to increase intracellular calcium; another group was treated with 9-AC as a myotonia-inducer (group 4). The treatment for all groups lasted 60 days. No significant differences in plasma sodium, potassium, chloride and calcium between control and experimental groups were observed. Whole muscle calcium in wet tissue samples did no change with any treatment. On the contrary, mitochondrial calcium showed a significantly higher concentration in group 3 and 4. CPK and aldolase activities in groups 1, 2 and 3 were similar; but in group 4 these enzyme activities were significantly higher (p less than 0.05). The electrical and mechanical responses were not altered in any rat with any experimental treatment. Our data suggest that myotonia is a predisposing factor for an altered mitochondrial calcium homeostasis in this model; in addition, the enzyme activities of CPK and aldolase were increased in the rats of group 4 implicating that myotonia is a crucial factor in the development of enzymatic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of myotonia induced by anthracene-9-carboxylic acid on mitochondrial calcium, plasma creatinine-phosphokinase and aldolase activity in the rat. 139 15

Examinations of 176 children administered caries-preventing drugs for 2 years have shown that oral irrigation with 0.2% sodium fluoride solution, oral intake of fluorine in a dose of 1 mg, or of potassium orotate, or of calcium glucerophosphate improved the oral fluid resistance to carbohydrate action. Glycolytic enzyme activity of the oral fluid in these children was not augmenting during carbohydrate load, whereas in children not administered such preventive courses oral intake of 10% glucose solution resulted in essential elevation of salivary aldolase and lactate dehydrogenase activities, i.e. intensification of glycolytic processes, this leading to the development of acid potential in the oral cavity and, consequently, to a higher risk of caries development.
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PMID:[The carbohydrate-resistant mechanism of the action of caries-prophylactic agents on the oral fluid in children]. 179 7

We experienced 5 cases of acute renal failure due to rhabdomyolysis during the last two years and investigated those etiologies. Diagnosis of rhabdomyolysis was established by the detection of elevated serum creatine phosphokinase, myoglobin, aldolase, myoglobinuria as well as by the clinical course. The respective underlying illness of the 5 cases were grand mal seizures, infection (high fever), heat stroke, diabetes mellitus with hyperosmolar nonketotic coma and cerebral infarction treated by barbiturate. In this investigation, however, any single cause was not enough as the etiologies of rhabdomyolysis. There were multiple factors responsible to rhabdomyolysis in each case, such as hypokalemia, hypophosphatemia, shock, arteriosclerosis, etc. Some cases could not be classified as traumatic or non-traumatic rhabdomyolysis. Thus, in one case, acute renal failure due to rhabdomyolysis induced by the combination of grand mal seizures and serum potassium/phosphate depletion. 2 cases recovered without hemodialysis. 3 cases died in multiple organ failure, included a case treated by hemodialysis. We conclude that acute renal failure due to rhabdomyolysis induced easily by numerous diseases and early diagnosis is recommended.
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PMID:[Investigation of etiologies for acute renal failure due to rhabdomyolysis in 5 patients]. 212 50

Sialic acid has been assayed enzymatically by an immobilized two-enzyme system. The method includes cleavage of sialic acid to pyruvic acid by N-acetylneuraminic acid (NANA) aldolase and reduction of pyruvic acid by lactate dehydrogenase in the presence of NADH, which is followed photometrically at 349 nm. For the membrane preparation 5 units of lactate dehydrogenase and 1 unit of NANA-aldolase were used. The pH optimum of the reaction using potassium phosphate buffer was 7.0. This two-enzyme membrane remains 100% active for several weeks at 4 degrees C in the assay buffer and remains stable after performing experiments at 45 degrees C.
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PMID:An immobilized bienzyme system for assay of sialic acid. 287 18

In a randomised double-blind trial carried out on fit, unpremedicated patients undergoing standard minor operations with early postoperative mobility, using a standard form of anaesthesia, pretreatment with diazepam 0.15 mg/kg or midazolam 0.1 mg/kg failed to reduce significantly the incidence of postoperative muscle pains following suxamethonium 1 mg/kg. By contrast, tubocurarine 0.05 mg/kg proved to be effective as a pretreatment. Neither benzodiazepine influenced the incidence or severity of fasciculations seen with suxamethonium or the duration of neuromuscular block. Tubocurarine virtually abolished visible fasciculation and, in the dose used, reduced the intensity and duration of the neuromuscular block. There were no clinically significant changes in serum potassium, creatinine phosphokinase or aldolase after suxamethonium, although 5 out of 47 showed an atypical rise in creatinine phosphokinase.
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PMID:Failure of two benzodiazepines to prevent suxamethonium-induced muscle pain. 315 43


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