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 postnatal development of mitochondrial ATP-producing pathways and Na-K-adenosinetriphosphatase (ATPase) in the rat medullary thick ascending limb of Henle (MTAL) was studied by measuring the activities of 3-ketoacid-CoA transferase, fumarase, citrate synthase, and Na-K-ATPase in microdissected MTAL of 16, 21, and 30-day-old pups and in adults. The role of adrenal steroids in the development of these four markers was also investigated by studying 21-day-old rats adrenalectomized on day 16 and given dexamethasone or aldosterone or NaCl injections from day 16 to day 21. There were large and correlated increases in the activities of the oxidative enzymes in the MTAL of control rat kidneys between 16 and 30 days after birth; Na-K-ATPase activity in the MTAL also greatly increased during the same period. Adrenalectomy completely prevented the developmental increases in MTAL oxidative enzymes and Na-K-ATPase; dexamethasone restored the development of all four enzymes, whereas aldosterone had no effect. We conclude that the postnatal maturation of Na+ reabsorption functions in MTAL cells involves coordinated increases in the capacity to produce ATP by oxidative metabolism and in Na-K-ATPase activity. This maturation process is probably triggered by the rise in circulating glucocorticoids that occurs during the weaning period.
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PMID:Coordinate development of oxidative enzymes and Na-K-ATPase in thick ascending limb: role of corticosteroids. 132 5

The mechanical and energetic consequences of long-term volume-overload (VOL) hypertrophy have been investigated in rabbits and compared with the consequence in sham-operated controls (SOC). Hypertrophy was induced by creating an aortocaval shunt, and the mechanical, biochemical, and energetic properties of the compensated heart were examined approximately 12 wk later. At 27 degrees C and a stimulus frequency of 1 Hz there were no significant changes in peak stress development, 10-90% rise times, shortening velocity, work, and mechanical power output. There was, however, a prolongation of contractile duration. The inverse relationship between peak stress and cross-sectional area was unchanged in the VOL and SOC groups. Polarographic and myothermic experiments were made on papillary muscles. Hypertrophy produced a small increment in basal metabolism. In isometric studies there were no significant changes in either the activation heat magnitude or the slope of the heat-stress relationship. In isotonic contractions there was no change in work output or total enthalpy (heat + work), and as a result mechanical efficiency was unchanged. A force-length-area (FLA) analysis of the isotonic data showed no significant change in intercept or FLA contractile efficiency. Biochemical studies showed no significant difference in the myosin isoenzyme profile at the time of death. The Ca(2+)-stimulated adenosinetriphosphatase activity of the sarcoplasmic reticulum was unchanged as were the enzymatic activities of mitochondrial citrate synthase and alpha-ketoglutarate dehydrogenase. Interestingly essentially the same data were obtained from the hearts of four animals in failure and from the hearts of seven compensated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanical, energetic, and biochemical changes in long-term volume overload of rabbit heart. 153 94

Skeletal muscle grafts performed with neurovascular repair are used extensively in clinical situations. However, most controlled experimental studies on the efficacy of such grafts have been conducted on muscles with a relatively small mass and over a limited recovery period. Therefore, selected cellular and matrix component properties of the comparatively large dog gracilis muscle (75 g) were studied 9-12 mo after orthotopic neurovascular grafting. The grafted muscle wet weights were 71% of the contralateral control (sham-operated) muscles. In addition, the concentrations of noncollagenous protein (13%), DNA (28%), and RNA (34%) were significantly reduced in the grafts. However, the concentration of collagen was significantly higher (41%) in the grafts. In this regard, the type III collagen phenotype showed the greatest relative increase. There was no difference between the grafted and control proteoglycan concentration. The metabolic profiles of the grafted muscles were significantly different from control. The activities of myofibrillar adenosinetriphosphatase (34%) and alpha-glycerophosphate dehydrogenase (25%) were reduced, whereas citrate synthase remained unchanged. These data suggest that recovery of up to 1 yr was insufficient for the normalization of several connective tissue matrix components and biochemical properties of the grafts.
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PMID:Incomplete normalization of dog gracilis muscle grafts with neurovascular repair despite long-term recovery. 169 Jun 97

The purpose was to determine the biochemical and hemodynamic adaptations of the myocardium to chronic tachycardia. Cardiac pacemakers were implanted in Yorkshire pigs and set at a rate of 180 beats/min for a period of 35-42 days. Animals were then anesthetized with pentobarbital sodium. Myocardial blood flow and hemodynamics were determined at three different heart rates (i.e., 120, 180, and 220 beats/min). Tissue samples were then taken for microsphere and biochemical analyses. Chronically paced hearts maintained better cardiac function and had consistently higher left ventricular blood flow with a higher endocardial-to-epicardial ratio. The activities of citrate synthase and 3-hydroxyacyl-CoA dehydrogenase were 23 and 45% greater in the paced hearts, respectively. The sarcoplasmic reticulum adenosinetriphosphatase activity was 55% greater in the paced hearts, whereas the myosin adenosinetriphosphatase was the same as in the control hearts. Polyacrylamide gels of the ventricular myosin isoforms showed only the V3 type to be present in both the control and paced hearts. These findings show that the heart of a large mammal adapts to chronic tachycardia (i.e., 180 beats/min) by elevating the aerobic and calcium-sequestering capacities without altering its myosin type.
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PMID:Myocardial biochemical and hemodynamic adaptations to chronic tachycardia. 182 10

The purpose of this study was to determine the extent to which functional demand regulates the biochemical character and enzyme capacities of the rat myocardium. Hearts from donor rats were heterotopically transplanted onto the abdominal aorta and inferior vena cava of isogenic recipients. The procedure results in a perfused but nonpumping heart that has a reduced heart rate (HR) and performs essentially no stroke work (SW). After 30 days, metabolic enzyme activities (phosphorylase, 6-phosphofructokinase, citrate synthase, and 3-hydroxyacyl-CoA dehydrogenase) were significantly lower (40-60%) in the nonworking heart. Specific sarcoplasmic reticulum Ca2(+)-adenosinetriphosphatase (ATPase) activity was unchanged, but activity per gram of heart was 41% lower. Myosin isozymes were 58% V1, 21% V2, and 21% V3 in the nonworking heart compared with 100% V1 in the working heart. Myosin and myofibrillar ATPase activities each decreased by 28%. These findings suggest that both HR and SW play major and specific roles in regulating myocardial biochemical capacities and determining the myosin phenotype.
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PMID:Role of cardiac work in regulating myocardial biochemical characteristics. 214 21

Skeletal muscle has an inherent biochemical phenotypic plasticity that provides the possibility for it to be remodeled into a "heart-like" muscle for use in cardiac-assist devices. The purpose of this study was to chronically stimulate skeletal muscle electrically to transform the biochemical capacities of the three major subcellular systems (i.e., metabolic, calcium regulating, and contractile) to resemble those of heart muscle. The latissimus dorsi muscle (LDM) of mongrel dogs weighing 22-27 kg was stimulated via the thoracodorsal nerve at 2 Hz for 6-8 wk. This stimulation protocol reduced the phosphorylase (glycogenolytic) and phosphofructokinase (glycolytic) activities by 70%. The aerobic (citrate synthase activity) and fatty acid oxidative (3-hydroxyacyl-CoA dehydrogenase activity) capacities were not significantly increased by chronic stimulation and remained at about one-fourth those in the canine heart. The calcium-dependent sarcoplasmic reticulum adenosinetriphosphatase (ATPase) activity in the microsomal fraction, which was sixfold greater in the nonstimulated LDM than in the heart, was reduced by electrical stimulation to a level similar to that of the dog heart. The contractile capacity was evaluated by determining the percentage of types I and II fibers, the myofibrillar ATPase activity, and the proportion of myosin isoforms. The transformed muscle was comprised of 93 +/- 2% type I fibers, a myofibrillar ATPase activity similar to that in heart with primarily a slow-twitch muscle myosin isoform. In conclusion, electrical stimulation of canine LDM at 2 Hz for 6-8 wk resulted in two of the three biochemical systems, which confer physiological expression and fatigue resistance to muscle being transformed to resemble those of the myocardium.
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PMID:Biochemical transformation of canine skeletal muscle for use in cardiac-assist devices. 214 Aug 28

The purpose of this study was to investigate metabolic changes in equine muscle from birth to 1 yr of age. Duplicate biopsies from the middle portion of the gluteus medius were obtained from a depth of 2 cm beneath the superficial fascia at 1 day, 7 days, 1 mo, 3 mo, 6 mo, and 1 yr of age in 11 quarter horses and at 1 day, 3 mo, 6 mo, and 1 yr of age in 5 Standardbreds. Muscle enzyme activities determined were citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, phosphorylase, and lactate dehydrogenase. Percent fast-twitch, fast-twitch high oxidative, and slow-twitch oxidative fiber types were determined using succinate dehydrogenase and myosin adenosinetriphosphatase (pH 9.4) histochemical stains. Histochemically determined muscle fiber-type percents did not change dramatically with increasing age. However, lactate dehydrogenase activity increased threefold in quarter horses and twofold in Standardbreds, and phosphorylase activity increased sixfold in quarter horses and sevenfold in Standardbreds from 1 day to 6 mo of age. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities decreased during the first 3 mo of age in quarter horses.
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PMID:Changes in the metabolic profile of equine muscle from birth through 1 yr of age. 234 82

This study was undertaken to examine the influence of guanethidine monosulfate-induced sympathectomy on exercise-induced adaptations of cardiac contractile protein and on acute hemodynamic responses to exercise involving female neonatal rats. Four groups of rats were studied: 1) normal sedentary (NS), 2) normal trained (NT), 3) sympathectomized sedentary (SS), and 4) sympathectomized trained (ST). The 9-wk running program, which began at 20 days of age, induced increases in whole-body maximal O2 consumption and skeletal-muscle citrate synthase activity in both NT and ST groups compared with NS (P less than 0.05). Submaximal exercise tests demonstrated circulatory adaptations for NT, SS, and ST groups compared with NC; however, the ST group demonstrated the greatest degree of altered cardiac function (decreased heart rate, left ventricular pressure, and contractility index) during exercise. Also, significant reductions in both myosin- and Ca2+-regulated myofibril adenosinetriphosphatase (ATPase) activity and increases in the relative content of the low ATPase myosin isozyme, V3, occurred in the hearts of the two trained groups (P less than 0.05). These findings suggest that chronic exercise involving normal and sympathectomized neonatal rats improves cardiac function without compromising maximal exercise capacity. Also, the exercise-related adaptation involving myosin isozyme shifts are exaggerated when involvement of the sympathetic nervous system is reduced during training.
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PMID:Cardiac biochemical and functional adaptations to exercise in sympathectomized neonatal rats. 293 64

Biopsy samples were obtained from the middle gluteal muscle of 10 Thoroughbred horses undergoing a commercial race-training program. Samples were obtained before the program began and again after 6 and 12 weeks of training. All horses had raced at least once by the 12th week of training. Serial sections of muscle were examined histochemically for myosin adenosinetriphosphatase after either acid (pH 4.3 and 4.6) or alkaline (pH 10.3) preincubation, and then muscle fibers were identified as types I, IIA, IIB, or IIC. The oxidative capacity of individual fibers was assessed, using the reduced nicotinamide dinucleotide tetrazolium-reductase stain, and the number of intermyofibrillar capillaries adjacent to each fiber were counted after staining, using the alpha-amylase-periodic acid-Schiff technique. Biochemical analyses involved the fluorometric measurement of 3 enzymes--citrate synthase, 3-hydroxy-acyl coenzyme A dehydrogenase, and lactate dehydrogenase--as markers of end terminal oxidative, beta-oxidative, and glycolytic potentials, respectively. Changes in fiber-type percentages did not occur in response to training. There was a significant (P less than 0.01) increase in the percentage of type IIB fibers, having high nicotinamide dinucleotide-tetrazolium reductase staining after 12 weeks of training. Alterations in the number of capillaries adjacent to each fiber type did not occur during the training period. There were increases in the activities of both citrate synthase and 3-hydroxy-acyl coenzyme A dehydrogenase after 6 weeks (P less than 0.05) and 12 weeks (P less than 0.001) of training. Alterations in the activity of lactate dehydrogenase did not occur in response to training.
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PMID:Effects of training on muscle composition in horses. 394 89

This study was designed to test the hypothesis that rats trained with marked reductions in exercise heart rate respond with adaptations indicative of increased intrinsic myocardial performance. Therefore, we measured changes in maximum work capacity (VO2max), biochemical-functional indexes of cardiac contractile capacity, and skeletal muscle oxidative capacity in normal-trained (NT) rats and in rats trained while receiving the selective cardiac beta 1-blocking drug atenolol (AT). Training consisted of treadmill running at approximately 80% VO2max (untrained) for 1-h duration, 6 days/wk, for a total of 8 wk. Exercise heart rate of the AT group was markedly reduced and averaged 140 beats/min below the NT group for any given session. Compared with sedentary controls, VO2max was increased by 11%, and red vastus lateralis muscle citrate synthase activity was increased by 28% in both AT and NT groups (P less than 0.05). There were no differences between trained and nontrained groups with regard to Ca2+-regulated myofibril adenosinetriphosphatase. In situ derived left ventricular pressure and the maximum rate of left ventricular pressure development were not augmented relative to sedentary control values when the trained hearts were either stimulated inotropically or maximally afterloaded . These findings suggest that maximum exercise capacity can be enhanced in rodents conditioned with and without limited elevation in exercise heart rate; however, this reduction of exercise heart rate acceleration does not provide a stimulus to enhance the intrinsic functional capacity of the rodent heart.
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PMID:Adaptive responses of rats trained with reductions in exercise heart rate. 623 46


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