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:2.3.3.1 (citrate synthase)
4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic effects on rat cardiac and skeletal muscle of a strenous program of swimming, of cold acclimation and of isoprenaline treatment (0.3 mg/kg daily for 5 five-day weeks) were compared. Exercised and cold-exposed rats gained less body weight than did controls or isoprenaline-treated rats. In all treated groups the heart and the intercapular brown adipose tissue hypertrophied. The size of the adrenals increased only in isoprenaline-treated animals. Cold-acclimation and physical training increased and isoprenaline treatment reduced or did not affect the activities of succinate dehydrogenase, malate dehydrogenase and citrate synthase of cardiac muscle. In the skeletal muscle all treatments resulted in increased activities of these enzymes. Of the anaerobic enzymes analysed, only the activity of hexokinase increased in response to the treatements used. This increase was the same in cardiac as in skeletal muscle, but it was significantly greater with isoprenaline-treatment than with training or with cold-acclimation. The activities of lactate dehydrogenase and phosphofructokinase did not differ significantly. All treatments improved cold resistance, but only swimming exercise and cold acclimation significantly increased tolerance to exercise. It is concluded that prolonged stimulation of adrenergic beta-receptors by catecholamines is responsible for the metabolic changes observed.
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PMID:Comparison of the effects of physical exercise, cold acclimation and repeated injections of isoprenaline on rat muscle enzymes. 12 87

The effects of chronic "steady-state" and high-speed interval running were investigated on time-course changes in certain biochemical properties of cardiac and skeletal muscle fiber types of rats. Nine weeks of the interval program resulted in significant increased (15%) in both cardiac enlargement and ATPase activity of myofibrils; whereas increases in these parameters were only transient and not significant at the termination of the program involving steady-state running. Neither program induced appreciable alterations in citrate synthase and phosphofructokinase activity in cardiac muscle. In fast-twitch white fibers, "steady-state" training induced only a transient 45% increase in citrate synthase activity in contrast to a progressive twofold change with interval training. Both programs resulted in similar increases (45-50%) in citrate synthase activity in fast-twitch and slow-twitch red fibers. However, the patterns of increase for both fiber types differed between the two programs. These findings suggest that training programs incorporating elements of both "steady-state" incline and high-speed interval running can potentially induce respiratory enzyme adaptations in the greatest spectrum of rodent skeletal muscle fibers in addition to inducing adaptations to enhance contractile potential in cardiac muscle.
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PMID:Time course adaptations in cardiac and skeletal muscle to different running programs. 13 67

Fifty-seven isolated, blood perfused, continuously weighed canine hearts have been utilized to study the development of abnormal myocardial fluid retention during early myocardial ischemic injury. Inflatable balloon catheters were positioned around the left anterior descending coronary arteries (LAD) of 54 hearts or the proximal left circumflex coronary arteries of three hearts for study of the following intervals of coronary occlusion: a) 10 minutes followed by 20 minutes of reflow, b) 40 minutes followed by either no reflow or by 20 minutes of reflow, and c) 60 minutes without reflow. After 60 minutes of fixed coronary occlusion, histologic and ultrastructural examination revealed mild swelling of many ischemic cardiac muscle cells in the absence of interstitial edema, cardiac weight gain, and obvious structural defects in cell membrane integrity. After 40 minutes of coronary occlusion and 20 minutes of reflow, significant cardiac weight gain occurred in association with characteristic alterations in the ischemic region, including widespread interstitial edema and focal vascular congestion and hemorrhage and swelling of cardiac muscle cells. Focal structural defects in cell membrane integrity were also noted. The development of abnormal myocardial fluid retention after 40 minutes of LAD occlusion occurred in association with a significant reduction in sodium-potassium-ATPase activity in the ischemic area, but with no significant alteration in either creatine phosphokinase or citrate synthase activity in the same region. Despite the abnormal myocardial fluid retention in these hearts, it was possible pharmacologically to vasodilate coronary vessels with adenosine and nitroglycerin infusion to maintain a consistently high coronary flow following release of the coronary occlusion after 40 minutes and to even exceed initial hyperemic flow values following release of the occlusion when adenosine and nitroglycerin infusion was delayed until 15 minutes after reflow. Thus, the data indicate that impaired cell volume regulation and interstitial fluid accumulation and focal structural defects in cell membrane integrity are early manifestations of ischemic injury followed by reflow, but fail to establish a major role for the abnormal fluid retention in altering coronary blood flow prior to the development of extensive myocardial necrosis. In contrast, fixed coronary occlusion for 60 minutes results in mild intracellular swelling but no significant interstitial edema and no obvious structural defects in cell membrane integrity.
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PMID:Abnormal myocardial fluid retention as an early manifestation of ischemic injury. 13 29

The effects of thyroid deficiency (Td) and of chemical sympathectomy (Sx) were studied on marker enzymes of energy metabolism in cardiac muscle of neonatal and of adult rats. Td prevented the normal development of neonatal body weight, relative heart mass, and cardiac levels of cytochrome c (-22%), citrate synthase (-27%), phosphofructokinase (-20%) and Mg2+- and Ca2+-ATPase activity of purified myofibrils (-33%, -44%). Exogenous thyroxin replacement restored those parameters studied to normal with the exception that it persistently elevated citrate synthase activity significantly above normal control levels. Responses similar to those of Td neonates occurred when adult rats were similarly treated. Sx produced no consistent effects on respiratory and glycogenolytic marker enzymes, but caused a 20% reduction in Ca2+-ATPase activity of both neonatal and adult cardiac myofibrils. These findings suggest that cardiac muscle cells require thyroxin for normal growth and enzyme development. Also, Sx may impair cardiac functional capacity by altering Ca2+ activity of actomyosin ATPase.
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PMID:Effects of thyroid deficiency and sympathectomy on cardiac enzymes. 21 2

Rats were treated by daily alprenolol (10, 20 and 50 mg/kg) injections for 5 days a week for 4 weeks. At 20--21 degrees C alprenolol treatment retarded the weight gain of the animals and increased the weight of the adrenals. These changes were not seen at 29 degrees C. The reduction in size and fat content of the interscapular brovin adipose tissue in drug-treated rats was independent of experimental temperature. At 20--21 degrees C prolonged beta-blockade did not cause any changes in the enzymes of the energy metabolism. At 29 degrees C, however, alprenolol treatment antagonized the decrease in activity of oxidative enzymes (succinate dehydrogenase, malate dehydrogenase, citrate synthase) and the decrease in protein concentration of the cardiac muscle. In skeletal muscle alprenolol treatment significantly decreased the activities of oxidative enzymes and antagonized the rise in the activity of lactate dehydrogenase resulting from warm acclimation. The increased activities of oxidative enzymes in interscapular brown adipose tissue of aprenolol treated rats were coupled with an increase in protein concentration of the tissue. Although these changes were more marked at 29 degree C they were observable at 20--21 degree C, too. The difference in the drug effects at 20--21 degrees C and 29 degrees C can be accounted for by the compensatory catecholamine release at the lower temperature, due to impaired thermoregulatory capacity after alprenolol. Prolonged beta blockade decreased the exercise tolerance and cold tolerance of the rats. An increased response of the diastolic blood pressure to an alpha-adrenergic drug, noradrenaline, and a decreased response to a beta-adrenergic drug, isoprenaline, in alprenolol-treated rats indicates a shift from beta- to alpha-receptors.
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PMID:Effect of prolonged beta-blockade on energy metabolism and adrenergic responses in the rat. 59 3

Two populations of mitochondria were observed upon ultrastructural examination of cardiac muscle tissue, one located directly beneath the sarcolemma (subsarcolemmal mitochondria) and another between the myofibrils (interfibrillar mitochondria). Subsarcolemmal mitochondria were released by treatment of heart muscle with a Polytron tissue processor, while interfibrillar mitochondria were released by nagarse digestion of the remaining tissue. These results were supported by electron microscopy of Polytron-treated heart tissue showing rupture and loss of sarcolemma with release of the underlying mitochondria but with retention of intact mitochondria between the myofibrils. Electron microscopy of the isolated mitochondria indicated that both mitochondrial types maintained their structural integrity throughout the isolation procedure. Specific activities of succinate dehydrogenase and citrate synthase were higher in the interfibrillar mitochondria as compared to the subsarcolemmal mitochondria, while those of carnitine palmitoyltransferase and alpha-glycerophosphate dehydrogenase were nearly the same in both. Interfibrillar mitochondria oxidized all substrates tested approximately 1.5 times faster than did the subsarcolemmal mitochondria. Thus the two mitochondrial types differed not only in their respective locations in the cell, but also in certain biochemical properties.
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PMID:Biochemical properties of subsarcolemmal and interfibrillar mitochondria isolated from rat cardiac muscle. 92 18

The purpose of this study was to determine whether cardiac biochemical adaptations are induced by chronic exercise training (ET) of miniature swine. Female Yucatan miniature swine were trained on a treadmill or were cage confined (C) for 16-22 wk. After training, the ET pigs had increased exercise tolerance, lower heart rates during exercise at submaximal intensities, moderate cardiac hypertrophy, increased coronary blood flow capacity, and increased oxidative capacity of skeletal muscle. Myosin from both the C and ET hearts was 100% of the V3 isozyme, and there were no differences between the myosin adenosine triphosphatase (ATPase) or myofibrillar ATPase activities of C and ET hearts. Also, the sarcoplasmic reticulum Ca(2+)-ATPase activity and Na(+)-Ca2+ exchange activity of sarcolemmal vesicles were the same in cardiac muscle of C and ET hearts. Finally, the glycolytic and oxidative capacity of ET cardiac muscle was not different from control, since phosphofructokinase, citrate synthase, and 3-hydroxyacyl-CoA dehydrogenase activities were the same in cardiac tissue from ET and C pigs. We conclude that endurance exercise training does not provide sufficient stress on the heart of a large mammal to induce changes in any of the three major cardiac biochemical systems of the porcine myocardium: the contractile system, the Ca2+ regulatory systems, or the metabolic system.
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PMID:Biochemical characterization of exercise-trained porcine myocardium. 183 67

Disuse (inactivity, bed rest, and spaceflight) may lead to a loss of muscle mass and a decrease in oxidative capacity in skeletal muscle. If such changes were to occur in hibernating animals, both locomotor and thermogenic function would be compromised. Muscle masses and oxidative capacities (as assessed by citrate synthase activity) were measured in the gastrocnemius and semitendinosus muscles, cardiac muscle (ventricle), and brown fat (axillary pad) in a group (n = 7) of prehibernating ground squirrels (Spermophilus lateralis) and after 6 mo of hibernation (n = 8). Hibernation produced significant atrophy in the gastrocnemius (14%) and semitendinosus (42%) muscles. Cardiac tissue increased (21%) in mass, as did brown adipose tissue (150%). That such changes were not due simply to fluid shifts was evidenced by similar protein concentrations between groups. In contrast to many other disuse studies, oxidative capacity was increased significantly in the gastrocnemius (65%) and semitendinosus (37%). Citrate synthase was also higher in cardiac tissue of hibernators (20%) but was not significantly different in brown fat.
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PMID:Disuse atrophy in the hibernating golden-mantled ground squirrel, Spermophilus lateralis. 195 70

This study investigates the effects of physiological increments in plasma thyroxine (T4) at three levels of biological organization in thyroid-intact and thyroidectomized captive western fence lizards, Sceloporus occidentalis. Two doses of T4-loaded pellets elevated plasma T4 in thyroid-intact lizards from 4.8 +/- 0.47 to 10.7 +/- 2.25 and 20.4 +/- 5.77 ng/ml (mean +/- SE). Surgical thyroidectomy reduced T4 to 1.8 +/- 0.23 ng/ml, and subsequent T4 pellet implantation raised T4 to 14.8 +/- 4.30 ng/ml. Minimal resting metabolic rate (= standard metabolic rate; SMR), a common organismal metric of thyroid perturbation, was reduced 31% (P less than 0.0001) by thyroidectomy and was restored by T4 replacement but was not stimulated by T4 supplementation in thyroid-intact lizards. In T4-replaced, thyroidectomized lizards, SMR was significantly correlated with plasma T4 (r2 = 0.626, P = 0.003, n = 11). At the organ level, liver mass was not changed by any treatment; heart mass was decreased by thyroid deficiency and restored by T4 replacement. At the molecular level, citrate synthase activity was significantly reduced by thyroidectomy and was returned to control levels by T4 replacement in liver and skeletal muscle (gastrocnemius) but was not changed in cardiac muscle. Citrate synthase was not affected in any tissue by T4 supplementation in thyroid-intact lizards. Pyruvate kinase activity was not affected by any of the treatments in any of the tissues. Cytosolic alpha-glycerophosphate dehydrogenase was significantly reduced in liver by all treatments and in skeletal muscle by T4 replacement after thyroidectomy. These results indicate that SMR and cardiac muscle mass in lizards are dependent on normal thyroid function and are expressed maximally in euthyroid animals. The stimulatory effect of T4 on SMR in thyroid-intact lizards, which has been reported previously by several investigators, is a nonphysiological response to pharmacological T4 levels, at least in these captive lizards. Molecular responses are tissue and enzyme dependent and cannot be generalized. Pellet implantation is an effective means of inducing physiological increments in plasma T4 and should replace previously used injection protocols. This new method can be used in capture-recapture experiments involving field-active lizards.
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PMID:Thyroid regulation of resting metabolic rate and intermediary metabolic enzymes in a lizard (Sceloporus occidentalis). 229 23

Metabolic differences of the cardiac muscle in children with normoxaemic and hypoxaemic congenital heart disease were analyzed by means of representative enzymes of the energy metabolism in 95 specimens in 80 children with congenital heart disease. Tissue specimens from the right atria and ventricles were obtained during surgical operations. It was revealed that the myocardial metabolism of patients with congenital heart disease was markedly influenced by hypoxaemia: the aerobic capacity was significantly reduced in the atria as well as in the ventricles. Changes in the atrial musculature were, however, more marked: in addition to citrate synthase - similarly as in the ventricles - in the atria also activities of enzymes associated with lactate metabolism (LDH) and with glycolysis (TPDH, GPDH) were reduced. Patients with an atrial septal defect had a significantly lower activity of the enzyme involved in the fatty acid breakdown (HOADH) than patients with a ventricular septal defect. The described new adaptive mechanism is of practical importance for the treatment of congenital heart disease and other conditions associated with prolonged hypoxaemia.
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PMID:[Adaptation of cardiac energy metabolism in children with congenital heart defects]. 280 25


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