Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new, weakly hydrophobic, high-performance liquid chromatography column has been developed for the separation of native proteins based on their relative hydrophobicities. Starting with a covalently bound, hydrophilic polyamine matrix, packing materials were synthesized through acylation with anhydrides and acid chlorides of increasing chain length to obtain increasingly hydrophobic surfaces. Proteins in aqueous buffers were induced to bind hydrophobically to the columns by the use of high salt concentrations in the mobile phase. Elution was achieved by decreasing the ionic strength of the solvent in a linear gradient. A mixture of cytochrome c, conalbumin, and beta-glucosidase was used as a standard to test the resolving power of newly synthesized columns. On a 4-cm butyrate column, baseline resolution was achieved in 20 min with a gradient of 3.0 mu sodium sulfate in 0.1 M potassium phosphate buffer, pH 7.0, to water. The static loading capacity for each column was determined using a hemoglobin binding assay. Capacities normally ranged between 150 and 180 mg of hemoglobin per gram of support. Since proteins are not denatured in hydrophobic interaction chromatography, enzymes eluted from the column retained enzymatic activity. Samples of alpha-amylase and beta-glucosidase ranging in size from 10 to 200 micrograms were recovered from the butyrate column with greater than 92% enzymatic activity in all cases. In a single trial, the enzyme citrate synthase was recovered from the benzoate column with 92% retention of enzymatic activity.
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PMID:High-performance hydrophobic interaction chromatography of proteins. 642 67

Rats were given a daily injection of L-epinephrine, 100 micrograms/100 g body wt, for 6 wk. The hearts of the epinephrine-treated animals were heavier (11.5%), and blood glucose and plasma insulin concentrations were lower than those of control rats. Acute responses to epinephrine were compared in the two groups. An increase in blood glucose and decreases in plasma insulin, liver glycogen, and muscle glycogen occurred in both groups. The magnitude of these responses were similar in the two groups except for the decrease in muscle glycogen, which was smaller in the chronic epinephrine-treatment group. There were no changes in respiratory capacity, citrate synthase or succinate dehydrogenase activities, or in cytochrome c concentration in skeletal muscle in response to 6 wk of epinephrine treatment. These results are compatible with the suggestion that catecholamines may play a role in some of the metabolic and cardiac adaptations to exercise training. However, they argue strongly against the hypothesis that catecholamines are responsible for inducing the increase in muscle mitochondria that occurs in response to exercise training.
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PMID:Adaptive responses of rats to prolonged treatment with epinephrine. 645 52

Plasmid vectors for the acetic acid-producing strains of Acetobacter and Gluconobacter were constructed from their cryptic plasmids and the efficient transformation conditions were established. The systems allowed to reveal the genetic background of the strains used in the acetic acid fermentation. Genes encoding indispensable components in the acetic acid fermentation, such as alcohol dehydrogenase, aldehyde dehydrogenase and terminal oxidase, were cloned and characterized. Spontaneous mutations at high frequencies in the acetic acid bacteria to cause the deficiency in ethanol oxidation were analyzed. A new insertion sequence element, IS1380, was identified as a major factor of the genetic instability, which causes insertional inactivation of the gene encoding cytochrome c, an essential component of the functional alcohol dehydrogenase complex. Several genes including the citrate synthase gene of A. aceti were identified to confer acetic acid resistance, and the histidinolphosphate aminotransferase gene was cloned as a multicopy suppressor of an ethanol sensitive mutant. Improvement of the acetic acid productivity of an A. aceti strain was achieved through amplification of the aldehyde dehydrogenase gene with a multicopy vector. In addition, spheroplast fusion of the Acetobacter strains was developed and applied to improve their properties.
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PMID:Genetic organization of Acetobacter for acetic acid fermentation. 809 54

Mitochondrial enzyme activities (cytochrome c-oxidase = COX, carnitine acyl-transferase = CAT, citrate synthase = CS, lipoamide dehydrogenase = lipDH from the pyruvate-dehydrogenase complex, lactate dehydrogenase = LDH, and malate-dehydrogenase = MDH) were measured from progressive myopathy/encephalomyopathy. Cytochrome oxidase (COX) deficiency was detected from muscle or liver tissues, adult type of COX defectus had been diagnosed in 1 case and infantile type in further 6 cases. The 3 familial atactic children showed decreased activity of carnitine acetyl-transferase, too.
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PMID:[Specific enzyme diagnosis in mitochondrial myopathies and encephalomyopathies]. 817 Jun 74

We evaluated a simplified method for preparation and analysis of platelet cytochrome c oxidase activity in Alzheimer's disease (AD) and control patients. Mean cytochrome c oxidase activity in controls (n = 17) was 0.233 sec-1/mg whereas mean cytochrome c oxidase activity in Alzheimer patients (n = 19) was 0.193 sec-1/mg, p = 0.033. Complex III (ubiquinol:cytochrome c oxidoreductase), complex II (succinic dehydrogenase), and citrate synthase were all assayed as internal controls and were not significantly different in controls and Alzheimer patients. There is a relatively specific loss of platelet cytochrome c oxidase activity in Alzheimer disease patients.
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PMID:Reduced platelet cytochrome c oxidase activity in Alzheimer's disease. 761 12

Feeding rats beta-guanidinopropionic acid (beta-GPA), a creatine analogue, results in depletion of creatine and phosphocreatine and induces increases in mitochondrial oxidative enzymes and hexokinase in skeletal muscle. Comparisons of different muscle types and studies of the adaptation to exercise suggest that 1) the levels of the insulin-responsive glucose transporter (GLUT-4), mitochondrial oxidative enzymes, and hexokinase may be coregulated and 2) GLUT-4 content can determine maximal glucose transport activity in muscle. To further evaluate these possibilities, we examined the effects of feeding rats 1% beta-GPA in their diet for 6 wk on muscle GLUT-4 expression and glucose transport activity. beta-GPA feeding induced 40-50% increases in cytochrome c concentration, citrate synthase activity, and hexokinase activity in plantaris muscle. GLUT-4 protein concentration was increased approximately 50% in plantaris and epitrochlearis muscles, while GLUT-4 mRNA was increased approximately 40% in plantaris muscles of beta-GPA-fed rats. Glucose transport activity maximally stimulated by insulin was increased in parallel with GLUT-4 protein concentration in the epitrochlearis. These results provide evidence that chronic creatine depletion increases GLUT-4 expression by pretranslational mechanisms. They support the hypothesis that the levels of mitochondrial enzymes, hexokinase, and GLUT-4 protein are coregulated in striated muscles. They also support the concept that the GLUT-4 content of a muscle determines its maximal glucose transport activity when the signaling pathways for glucose transport activation are intact.
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PMID:Adaptation of muscle to creatine depletion: effect on GLUT-4 glucose transporter expression. 843 Jul 63

We studied two diagnostic aspects of fatal infantile defects of the mitochondrial respiratory chain: the age dependence of muscle mitochondrial enzyme activities and the reliability of diagnosis from autopsy samples. In morphologically normal quadriceps muscle samples of 46 children between the ages of 3 days and 15 years, activities of complex I plus III (NADH:cytochrome c oxidoreductase) and complex II plus III (succinate:cytochrome c oxidoreductase) increased 2-fold during the first three years of life, while that of complex II (succinate dehydrogenase), complex IV (cytochrome c oxidase), and citrate synthase did not show significant correlation with age. We suggest that these changes are related to age and stress the importance of strictly age-matched controls when diagnosing a mitochondrial disease of early childhood. The value of autopsy samples in diagnostic studies was evaluated by comparing mitochondrial enzyme activities in quadriceps muscle from autopsies and from surgical biopsies. In quadriceps muscle mitochondria, all the enzyme activities studied remained stable for at least 3 h after death. Using age-matched controls and autopsy samples, we diagnosed a respiratory chain enzyme deficiency in two infants, and the defects were confirmed in cultured skin fibroblasts.
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PMID:Diagnosis of fatal infantile defects of the mitochondrial respiratory chain: age dependence and postmortem analysis of enzyme activities. 874 50

Treatment with the combination of almitrine-raubasine increases both arterial oxygen partial pressure and haemoglobin oxygen saturation, reflecting an actual increase in the oxygen content of arterial blood. Furthermore, at the trans-cerebral carotid artery/internal jugular vein level, the treatment increases cerebral arterio-venous oxygen and glucose differences, suggesting an actual increase both in oxygen and glucose availability and uptake in cerebral tissues. The increased glucose transfer to the brain is supported also by enhancement of the 3H-deoxyglucose uptake induced by drug pre-treatment both in normoxia and hypoxia. Both almitrine and raubasine act at cerebral mitochondrial levels by decreasing the 'loss' of the 'biological' free energy for phosphorylation supported by the age-related drop in the cerebral enzyme activities, such as phosphofructokinase, pyruvate dehydrogenase and citrate synthase. Furthermore, the components interfere with the alterations induced by peroxidative stress acting at the level of cytochrome c, cytochrome c oxidase and succinate dehydrogenase. Treatment with the combination almitrine-raubasine increases the concentration of noradrenaline metabolites, while alteration of the dopaminergic system is less important. The interference with the noradrenergic system is possibly linked to the electroencephalographic changes induced by drug treatment: increasing alpha-rhythm distribution and reactivity, and increases in beta-rhythm amplitude. Pharmacological effects of almitrine-raubasine, obtained in experimental conditions, correlate with clinical therapeutic efficacy, e.g., in the treatment of cognitive disorders associated with ageing and other cerebral and neurosensory impairments. It is difficult to summarise, in a few pages, the large number of papers related to the cerebral pharmacometabolic and pharmacodynamic activities of the almitrine-raubasine combination. Thus, this review presents in sequential steps some of the interrelated research in humans and laboratory animals which describes in a critical way preclinical to clinical results.
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PMID:Pharmacological features of an almitrine-raubasine combination. Activity at cerebral levels. 951 73

We report automated methods for assaying the activities of the mitochondrial respiratory chain enzyme cytochrome c oxidase (COX), the matrix enzyme citrate synthase (CS), and the cytoplasmic enzyme lactate dehydrogenase (LDH) on a random access analyzer, the Roche Mira S. COX activity was assayed by measuring the initial rate of oxidation of reduced cytochrome c. The CS assay was based on the reaction of this enzyme with oxaloacetate and acetyl-CoA to produce CoASH, which further reacts with dithionitrobenzoic acid producing a free thionitrobenzoate ion. LDH activity was assayed by measuring the reduction of nicotinamide adenine dinucleotide during the oxidation of lactate to pyruvate. Precision of the COX assay was 2. 3%, CS assay 0.7%, and LDH 5.6%. These automated methods were faster by as much as 80%, cheaper by 50%, and used less than half the sample material needed for traditional manual methods. While these assays are often performed by specialized laboratories using dedicated staff, the automated methods presented here are easily performed by staff trained in the regular diagnostic laboratory.
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PMID:Automated analysis of mitochondrial enzymes in cultured skin fibroblasts. 961 94

Prolonged heart ischaemia causes an inhibition of oxidative phosphorylation and an increase of Ca2+ in mitochondria. We investigated whether elevated Ca2+ induces changes in the oxidative phosphorylation system relevant to ischaemic damage, and whether Ca2+ and other inducers of mitochondrial permeability transition cause the release of cytochrome c from isolated heart mitochondria. We found that 5 microM free Ca2+ induced changes in oxidative phosphorylation system similar to ischaemic damage: increase in the proton leak and inhibition of the substrate oxidation system related to the release of cytochrome c from mitochondria. The phosphorylating system was not directly affected by high Ca2+ and ischaemia. The release of cytochrome c from mitochondria was caused by Ca2+ and 0.175-0.9 mM peroxynitrite but not by NO, and was prevented by cyclosporin A. Adenylate kinase and creatine kinase were also released after incubation of mitochondria with Ca2+, however, the activity of citrate synthase in the incubation medium with high and low Ca2+ did not change. The data suggest that release of cytochrome c and other proteins of intermembrane space may be due to the opening of the mitochondrial permeability transition pore, and may be partially responsible for inhibition of mitochondrial respiration induced by ischaemia, high calcium, and oxidants.
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PMID:Release of cytochrome c from heart mitochondria is induced by high Ca2+ and peroxynitrite and is responsible for Ca(2+)-induced inhibition of substrate oxidation. 998 44


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