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 cellular distribution of free and bound glycolytic enzymes in vivo was estimated by means of a model based on previously determined association constants for individual binding interactions and in vivo protein concentrations. The calculations revealed that a significant proportion of the enzymes would be either associated with F-actin, or bound in binary enzyme-enzyme complexes in vivo. An analysis of the relative concentration, and relative activity, of F-actin-bound enzymes suggested that a complete glycolytic complex, composed of all enzymatic steps from phosphofructokinase (PFK) to lactate dehydrogenase (LDH) does not exist. This was indicated by a very low concentration of F-actin-associated phosphoglycerate kinase (PGK) and by a very low activity of F-actin bound aldolase and PGK; this model showed that aldolase and PGK would be absent from any F-actin bound complex. An analysis of soluble enzyme-enzyme associations indicated that formation of binary enzyme complexes may lead to an increased overall flux through glyceraldehyde 3-phosphate dehydrogenase and LDH, but would serve to decrease flux through PFK and aldolase. A 1.4-fold activation of PFK, which occurs when the soluble enzyme binds to F-actin, suggested that reversible binding of PFK to F-actin may represent a novel cellular mechanism for controlling glycolytic flux during periods of increased metabolic demand by controlling the key regulatory enzyme of glycolysis.
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PMID:A quantitative evaluation of the effect of enzyme complexes on the glycolytic rate in vivo: mathematical modeling of the glycolytic complex. 206 1

The purpose of the present study was to investigate the effects of 8 months of a specific and controlled sprint training programme on three groups of young athletes (two groups of males and one of females). Biopsies of vastus lateralis were taken before and after the period of training. The type percentage and diameter of the fibres, as well as the glycogen content and the activities of the enzymes of glycogen metabolism (glycogen synthase and glycogen phosphorylase), glycolysis (phosphofructokinase, pyruvate kinase, aldolase and lactate dehydrogenase), oxidative metabolism (succinate dehydrogenase) and creatine kinase and aminotransferases were studied. The results show an increase in the percentage of type I fibres and an increase in the diameter of both fibre types. A significant increase was also observed in glycogen content, and in the activities of glycogen synthase, glycogen phosphorylase, phosphofructokinase, pyruvate kinase, succinate dehydrogenase, aspartate aminotransferase and alanine aminotransferase. We conclude that a long period of sprint training induces a biochemical muscle adaptation to anaerobic exercise. This metabolic adaptation is followed by a morphological adaptation, although this is probably not as specific as the biochemical one.
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PMID:Biochemical and histochemical adaptation to sprint training in young athletes. 208 3

1. Turnover of the sarcoplasmic proteins aldolase, phosphoglycerate mutase, lactate dehydrogenase and creatine phosphokinase isolated from chicken breast muscle was investigated using a pulse labelling technique. 2. A single injection of [U-14C]leucine was given and the proteins were extracted and purified at 2, 6, 15, 30, 48 and 72 hr following administration. Specific radioactivity in all of these isolated enzymes showed unexpected multiple peak profiles which did not intersect with the specific radioactivity profile of the blood plasma. 3. These results were interpreted as showing that either a large proportion of these proteins was not turned over in rapidly growing muscle or that the plasma amino acid pool was not the precursor pool for muscle protein synthesis. 4. The results also suggested that at least two sub-populations of the proteins exist within the muscle tissue. 5. A further conclusion drawn from these data was that established techniques of pulse labelling may seriously overestimate the rate of protein synthesis in growing muscle.
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PMID:Turnover of sarcoplasmic proteins in the breast muscle of rapidly growing chicks. 213 16

Partition equilibrium experiments have been used to characterize the interactions of erythrocyte ghosts with four glycolytic enzymes, namely aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphofructokinase and lactate dehydrogenase, in 5 mM sodium phosphate buffer (pH 7.4). For each of these tetrameric enzymes a single intrinsic association constant sufficed to describe its interaction with erythrocyte matrix sites, the membrane capacity for the first three enzymes coinciding with the band 3 protein content. For lactate dehydrogenase the erythrocyte membrane capacity was twice as great. The membrane interactions of aldolase and glyceraldehyde-3-phosphate dehydrogenase were mutually inhibitory, as were those involving either of these enzymes and lactate dehydrogenase. Although the binding of phosphofructokinase to erythrocyte membranes was inhibited by aldolase, there was a transient concentration range of aldolase for which its interaction with matrix sites was enhanced by the presence of phosphofructokinase. In the presence of a moderate concentration of bovine serum albumin (15 mg/ml) the binding of aldolase to erythrocyte ghosts was enhanced in accordance with the prediction of thermodynamic nonideality based on excluded volume. At higher concentrations of albumin, however, the measured association constant decreased due to very weak binding of the space-filling protein to either the enzyme or the erythrocyte membrane. The implications of these findings are discussed in relation to the likely subcellular distribution of glycolytic enzymes in the red blood cell.
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PMID:Interactions of glycolytic enzymes with erythrocyte membranes. 214 Feb 76

A case of mitochondrial encephalomyopathy with a partial cytochrome c oxidase deficiency was reported with special reference to electrophysiological studies. A 56-year-old man was readmitted to Himeji Central Hospital due to mental deterioration and character change. At the age of 44 when he was attacked by his first epileptic seizure, he was admitted to Himeji Central Hospital, where EEG abnormalities and cerebral atrophy were found. Anticonvulsants helped to relieve his generalized convulsions but the EEG abnormalities persisted. At age 46, he had the second generalized seizure, so he quit his job as a crane operator. His family began to notice deterioration of his intellectual function and hyperaggressive behavior. His daily activities, intellectual performance and mental condition gradually deteriorated (WAIS FIQ less than 60). Other clinical and laboratory findings are as follows: bilateral impaired hearing, no optic nerve atrophy, no disturbance of extra ocular muscle movements, mild wasting and weakness of his extremities, normal coordination and sensation, no myoclonus or other involuntary movements, normal laboratory data of serum creatinine kinase, lactate dehydrogenase and aldolase, and increased amount of lactate and pyruvate in serum and cerebrospinal fluid (CSF), no abnormal amino acids in urine. A biopsy specimen of right biceps brachii muscle revealed numerous ragged-red fibers in frozen sections stained by the Gomori trichrome method. These fibers did not react to a cytochrome c oxidase staining. An ATPase staining demonstrated an atrophy of type-2 fibers. An electron micrograph showed many mitochondria in the sarcoplasm but few paracrystalline inclusions. A biochemical analysis of the muscle biopsy also revealed a significant decrease in the cytochrome c oxidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A mitochondrial encephalomyopathy due to partial cytochrome c oxidase deficiency with giant evoked potentials--a case report]. 217 89

Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
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PMID:Tryptophan-induced eosinophilia-myalgia syndrome. 221 1

The activity of lactate dehydrogenase (LDH), indophenol oxidase, aspartate aminotransferase (AsAT), alkaline phosphatase, acid phosphatase and aldolase at different stages of rat development was measured. We have also determined changes in the activity of these enzymes resulting from transplantation of embryonic nerve tissue (ENT) into the brain of adult animals. During development from the embryo to the adult animal, LDH and AsAT activities increased, while alkaline phosphatase activity diminished. After ENT transplantation, the most prominent changes were in the alkaline phosphatase activity whereas the activity of LDH, AsAT and acid phosphatase remained unchanged and similar to that in the brain cortex of intact adult animals. Changes in the enzyme activity resulting from ENT transplantation changed in a manner characteristic of the transplant. Local brain damage did not change the activity of the studied enzymes fifty days after surgery.
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PMID:[Changes in the activity of different classes of enzymes in the cerebral cortex of rats in ontogeny and after the transplantation of embryonic nerve tissue]. 223 89

Some biochemical parameters of liver and liver microsomes were studied in albino rats following administration of cobra and viper venoms at dose of 2 mg/kg body weight. The total protein content in cobra venom treated (CVT) animals and DNA and RNA contents of liver and liver microsomes were almost unaltered in both the venom treated animals while total protein content was significantly reduced in viper venom treated (VVT) animals. Alkaline and acid phosphatases activities of whole liver showed significant increase in both the venom treated animals whereas the rise in cholinesterase activity in CVT animals was not significant. Lactic acid content was significantly higher in CVT animals compared to either VVT animals or controls. The glycolytic enzymes viz., aldolase, phosphohexose isomerase and lactate dehydrogenase measured in hepatic microsomal fraction were significantly reduced while alanine and aspartate aminotransferases and gamma-glutamyl transpeptidase activities of liver microsomes were significantly elevated in both the venom treated animals compared to controls.
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PMID:Biochemical studies of liver & liver microsomes in envenomated rats. 227 76

Experimental alcoholic myopathy was induced in rats by a combination of prolonged alcohol intake (mean 15.3 g ethanol/kg/day for up to 10 weeks) and a short fast. In view of literature evidence for impairment of both glycolytic and oxidative metabolism in alcoholic myopathy, we combined histological and histochemical observations with biochemical studies comprising assay of all glycolytic enzymes and measurement of respiration rates and cytochrome content in isolated intact mitochondria. The predominant histological finding was Type IIb fibre atrophy, while levels of the glycolytic enzymes aldolase, pyruvate kinase and lactate dehydrogenase were significantly depressed. Evidence of rhabdomyolysis was seen in a minority of animals. Mean mitochondrial respiratory rates were significantly lower with the Site I substrate glutamate in alcohol-treated animals. It is postulated that chronic alcoholic myopathy is associated with glycolytic deficiency and that acute rhabdomyolysis may arise from a superimposed mitochondrial failure, resulting in a severe energy crisis in muscle.
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PMID:Biochemical and morphological studies of skeletal muscle in experimental chronic alcoholic myopathy. 229

Seven patients who developed a syndrome of eosinophilia, connective-tissue disease, and cutaneous abnormalities while ingesting tryptophan were examined. Other clinical manifestations commonly seen were pulmonary symptoms, fever, lymphadenopathy, and the development of myopathy. Laboratory features included mild elevations of aldolase and lactate dehydrogenase levels, with essentially normal creatine kinase levels, erythrocyte sedimentation rates, and C-reactive protein levels. Biopsy findings included features of scleroderma, small-vessel vasculitis, fasciitis, and myopathy. Discontinuation of tryptophan administration and implementation of corticosteroid therapy were of some benefit in relieving the intense myalgias and cutaneous findings that developed. Although temporally related to tryptophan ingestion, it is unclear whether this substance, a metabolite, or a contaminant were causal. We speculate that the pathogenesis of this syndrome may relate to abnormalities in tryptophan metabolism.
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PMID:Tryptophan-associated eosinophilic connective-tissue disease. A new clinical entity? 230 82


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