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)

The effect of mild doses of X-rays (three fractions, each of 100 R) on energy metabolism of the brain of starved rats has been investigated. It is inferred that X-radiation may cause serious detrimental changes of enzymes involved in glucose metabolism (glucose-6-phosphate dehydrogenase and fructose diphosphate aldolase) and in peroxidation (of catalase and lipid peroxidase), and of the acetylcholine activity which is determined by the cholinesterase level. Dynamics of changes in the protein and nucleic acid content of the brain has been studied. It has been shown that the level of 4-HIAA and 3M4HMA in the brain increases after irradiation of starved and normally fed rats.
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PMID:[The effect of low doses of x-rays on the biochemical processes in the brain and on urinary metabolites in fasted rats]. 188 96

Independently controlled, inducible, catabolic genes in Pseudomonas aeruginosa are subject to strong catabolite repression control by intermediates of the tricarboxylic acid cycle. Mutants which exhibited a pleiotropic loss of catabolite repression control of multiple pathways were isolated. The mutations mapped in the 11-min region of the P. aeruginosa chromosome near argB and pyrE and were designated crc. Crc- mutants no longer showed repression of mannitol and glucose transport, glucose-6-phosphate dehydrogenase, glucokinase, Entner-Doudoroff dehydratase and aldolase, and amidase when grown in the presence of succinate plus an inducer. These activities were not expressed constitutively in Crc- mutants but exhibited wild-type inducible expression.
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PMID:Isolation and characterization of catabolite repression control mutants of Pseudomonas aeruginosa PAO. 190 70

Effects of an 18 min exercise test, on three separate occasions during a one year jump-training programme, was studied in seven horses. Determinations were carried out on venous blood for packed cell volume, haemoglobin, total protein, lactate and pyruvate, glucose, free fatty acids, insulin, glucagon, blood gases, bicarbonate, pH, aldolase, aspartate aminotransferase and alanine amino-transferase. Exercise caused a slight increase in lactate and pyruvate, total protein, aldolase, alanine aminotransferase, pO2, bicarbonate and pH. Glucose, free fatty acids and pCO2 levels decreased. Training caused no significant difference in these changes. However, during the year, increases in lactate and decreases in pH (resting levels) were observed.
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PMID:Changes in some haematological and metabolic indices in young horses during the first year of jump-training. 191 34

The presence of glycolytic enzymes and a GLUT-1-type glucose transporter in rod and cone outer segments was determined by enzyme activity assays, glucose uptake measurements, Western blotting, and immunofluorescence microscopy. Enzyme activities of six glycolytic enzymes including hexokinase, phosphofructokinase, aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase, pyruvate kinase, and lactate dehydrogenase, were found to be present in purified rod outer segment (ROS) preparations. Immunofluorescence microscopy of bovine and chicken retina sections labeled with monoclonal antibodies against glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase, and lactate dehydrogenase have confirmed that these enzymes are present in rod and cone outer segments and not simply contaminants from the inner segments or other cells. Rod outer segments were also found to contain glucose transport activity as detected by 3-O-[14C]methylglucose uptake and exchange. The glucose transporter had a Km of 6.3 mM and a Vmax of 0.15 nmol of 3-O-methylglucose/s/mg of ROS membrane protein for net uptake and a Km of 29 mM and a Vmax of 1.06 nmol of 3-O-methylglucose/s/mg of ROS membrane protein for equilibrium exchange. These Km values for net uptake and equilibrium exchange are similar to values obtained for human red blood cells and are characteristic of GLUT-1-type glucose transporter. The transport was inhibited by both cytochalasin B and phloretin. Western blot analysis and immunofluorescence microscopy using type-specific glucose transporter antibodies indicated that both rod and cone outer segment plasma membranes have a GLUT-1 glucose transporter of Mr 45K as found in red blood cells and brain microsomal membranes. Solid-phase radioimmune competitive inhibition studies indicated that rod outer segment plasma membranes contained 15% the number of glucose transporters found in human red blood cell membranes and had an estimated density of 400 glucose transporter per micron2 of plasma membrane. These studies support the view that outer segments can generate energy in the form of ATP and GTP by anaerobic glycolysis to supply at least some of the energy requirements for phototransduction and other metabolic processes.
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PMID:Glycolytic enzymes and a GLUT-1 glucose transporter in the outer segments of rod and cone photoreceptor cells. 193 98

After her first grand mal seizure a 30-year-old woman was given a fructose infusion by an emergency doctor. On admission to hospital she complained of severe nausea. Ultrasonography revealed hepatosplenomegaly and the gamma-GT concentration was raised to 25 U/l. As hyperinsulinism was suspected an oral glucose tolerance test was suggested, but refused by the patient. She reported marked aversion to all sweet foods. Examination of an endoscopically obtained liver biopsy revealed clear reduction in fructoaldolase activity in liver tissue, i.e. the diagnosis of hereditary fructose intolerance. Three of the patient's siblings were also affected. The widespread use of infusion solutions containing sorbitol and fructose has twice proved acutely hazardous in this patient and is generally life-threatening for persons with an inborn error of metabolism whose pathologic status often remains undiagnosed to an adult age.
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PMID:[Adults with hereditary fructose intolerance: risks of fructose infusion]. 196 93

Glucose carbon recycling, glucose production and glucose turnover in glycogen storage disease type I and type II patients and control subjects were determined by a novel approach--mass isotopomer analysis of plasma 13C glucose. Changes in the isotopomer distribution of plasma 13C glucose were found only in glycogen storage disease type III patients and control subjects. Glucose carbon recycling parameters were also derived from 13C NMR spectra of plasma glucose C-1 splitting pattern. Our results eliminate a mechanism for glucose production in glycogen storage disease type I children involving gluconeogenesis. However, glucose release by amylo-1,6-glucosidase activity is in agreement with our results. A quantitative determination of the metabolic pathways of fructose conversion to glucose in normal children, and in children with disorders of fructose metabolism was derived from 13C NMR measurement of plasma 13C glucose isotopomer populations following [U-13C]fructose administration. A direct pathway from fructose, bypassing fructose-1-phosphate aldolase, to fructose-1,6-diphosphate in controls and hereditary fructose intolerant children (47% and 27%, respectively) was identified. In children with fructose-1,6-diphosphatase deficiency, only the gluconeogenic substrates were 13C labelled but no synthesis of glucose from [U-13C]fructose occurred. The significantly lower (by 68%) conversion of fructose to glucose in hereditary fructose intolerance, as compared to control subjects, and non-conversion in fructose-1,6-diphosphatase deficient subjects after [U-13C]fructose (approximately 20 mg/kg) administration can serve as the basis of a safe diagnostic test for patients suspected of inborn errors of fructose metabolism and other defects involving gluconeogenesis.
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PMID:Inherited disorders of carbohydrate metabolism in children studied by 13C-labelled precursors, NMR and GC-MS. 212 13

A single fructose-1,6-bisphosphate (FBP) aldolase has been detected in extracts from carrot storage roots (Daucus carota L.). The enzyme was purified 850-fold to electrophoretic homogeneity and a final specific activity of 26.3 mumols of FBP utilized/min per mg of protein. SDS/PAGE of the final preparation revealed a single protein-staining band of 40 kDa. The native molecular mass was determined by analytical gel filtration to be 159 kDa, indicating that the enzyme is a homotetramer. Denaturing isoelectric focusing revealed two predominant protein-staining bands, with pI values of 5.6 and 5.7. The enzyme is a class I aldolase, since EDTA or metal ions had no effect on its activity. The enzyme was relatively heat-stable, had an activation energy (Ea) of 68.3 kJ.mol-1, and had an absorption coefficient of 8.08 x 10(4) M-1.cm-1 at 280 nm. Km values for FBP and sedoheptulose 1,7-bisphosphate (SBP) were both determined to be 6 microM (pH optima 7.4). The specificity constant with FBP was 2.6 times that obtained with SBP. Ribose 5-phosphate, 6-phosphogluconate, MgAMP, glucose 1-phosphate and phosphoenolpyruvate (PEP) were inhibitors. PEP was a mixed-type inhibitor with respect to FBP (Ki = 3.2 mM, K'i = 5.1 mM). No activators were found. Rabbit anti-(carrot aldolase) polyclonal antibodies immunoprecipitated the activity of both carrot root aldolase and spinach leaf cytosolic aldolase, but not that of spinach leaf plastid aldolase. Western-blot analysis also revealed cross-reactivity with cytosolic, but not plastid, spinach leaf aldolase, indicating that the single carrot root aldolase is cytosolic.
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PMID:Purification and characterization of cytosolic aldolase from carrot storage root. 219 22

We have studied the effect of T3 administration (50 micrograms/Kg/day) on the phenotype expression of several glucose-metabolizing enzymes (hexokinase, HK, glucose-6-phosphate dehydrogenase, G6P-DH, aldolase, ALD, phosphofructokinase, PFK, lactate dehydrogenase, LDH) in the different myocardial layers of the left ventricle wall. In the control rats, most of these enzyme activities are uniformly distributed across the left ventricle wall, G6P-DH being the only exception. In the rats given T3 for 14 days, the mean levels of PFK, HK and ALD activities increased significantly. With regard to the transmural distribution patterns, that of PFK was unchanged, unlike those of HK and ALD which exhibited their maximum increase in activity in the midmyocardium or in the mid- and subepicardial myocardium. With LDH, a significant increase in activity was found in the subepicardial layers which escaped detection on the whole homogenate. It is concluded that the administration of thyroid hormone has different effects on enzyme phenotype expression of cardiomyocytes in different regions of the cardiac wall.
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PMID:Regional differences in the response of cardiac cells to triiodothyronine administration across the left ventricle free wall of rat heart. 231 6

Exposure of foundry workers to mixtures of different heavy metals is a very important toxicological problem. In this paper the estimation of the effects of lead, zinc, and copper on erythrocyte metabolism is presented. Concentrations of copper and zinc at work posts of the group examined did not exceed TLV, while lead concentration was 1.5 to 4 times higher than TLV. Erythrocyte metabolism was measured through activities of such glycolytic pathway enzymes as PFK, PGI, PK, aldolase and G6-PD from the hexose monophosphate pathway. Additionally the free erythrocyte protoporphyrin (FEP) level, D-ALA activity, serum GSH level, 2,3 DPG level in erythrocytes and lactic acid production during a 2-h incubation of red blood cells (RBC) was estimated. The blood-lead level, FEP level, copper concentration in erythrocytes in exposed group were significantly higher than in control group while the zinc level in erythrocytes was significantly lower. Measuring erythrocyte metabolism we showed that the activity of PGI, PFK, aldolase, lactic production and 2,3 DPG levels was significantly higher in the exposed group, probably as a result of anaerobic glycolysis activation.
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PMID:Influence of heavy metal mixtures on erythrocyte metabolism. 234 40

An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-[U-13C]fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of 13C NMR spectra of plasma glucose. The conversion parameters in the control and HFI children were estimated on the basis of doublet/singlet values of the plasma beta-glucose C-1 splitting pattern as a function of the rate of fructose infusion (0.26-0.5 mg/kg per min). Significantly lower values (approximately 3-fold) for fructose conversion to glucose were obtained for the HFI patients as compared to the controls. A quantitative determination of the metabolic pathways of fructose conversion to glucose was derived from 13C NMR measurement of plasma [13C]glucose isotopomer populations. The finding of isotopomer populations of three adjacent 13C atoms at glucose C-4 (13C3-13C4-13C5) suggests that there is a direct pathway from fructose, by-passing fructose-1-phosphate aldolase, to fructose 1,6-bisphosphate. The metabolism of fructose by fructose-1-phosphate aldolase activity accounts for only approximately 50% of the total amount of hepatic fructose conversion to glucose. It is suggested that phosphorylation of fructose 1-phosphate to fructose 1,6-bisphosphate by 1-phosphofructokinase occurs in human liver (and intestine) when fructose is administered nasogastrically; 47% and 27% of the total fructose conversion to glucose in controls and in HFI children, respectively, takes place by way of this pathway. In view of the marked decline by 67% in synthesis of glucose from fructose in HFI subjects found in this study, the extent of [13C]glucose formation from a "trace" amount (approximately 20 mg/kg) of [U-13C]fructose infused into the patient can be used as a safe and noninvasive diagnostic test for inherent faulty fructose metabolism.
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PMID:Determination of fructose metabolic pathways in normal and fructose-intolerant children: a 13C NMR study using [U-13C]fructose. 237 Dec 80


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