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)

Fast-twitch plantaris muscles of female rats were subjected to unilateral compensatory overload, induced by partial excision of synergistic muscles. One group of rats remained sedentary whereas another was subjected to a supplemental program of treadmill exercise consisting of walking 3 m/min, 65% grade, 2 h/day, 5 days/week. Groups of rats were sacrificed after 1, 2, 4, and 8 weeks and their muscles were weighed and analyzed for protein, citrate synthase, phosphofructokinase (PFK) and myofibril ATPase. Absolute and relative (muscle weight/body weight) muscle weights were much greater in both overloaded groups as compared to contralateral controls. However, treadmill exercise also increased the absolute and relative muscle mass of control plantaris muscles in the exercising group as compared tonormal sedentary contralateral controls. Citrate synthase activity was decreased in overloaded, sedentary muscles as compared to contralateral controls, but after 8 weeks of exercise, it returned to normal levels. PFK was decreased in both sedentary and exercised overloaded muscles throughout the 8 week period. Myofibril ATPase showed a tendency to be reduced in sedentary, overloaded muscles, and was significantly reduced in overloaded, exercising muscles. These results collectively suggest that certain fibers of overloaded fast-patterns take on similar in certain aspects to that normally seen in differentiated slow-twitch muscle fibers.
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PMID:Enzymatic changes in hypertrophied fast-twitch skeletal muscle. 13 54

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

The effects of bilateral functional overload on enzyme changes in fast-twitch plantaris muscles were studied on different groups of rats: 1) normal-control; 2) normal-exercise; 3) overload-control; and 4) overload-exercise. Overload was accomplished by surgical elimination of synergists. Exercising groups walked up a 65% grade, 3 m/min, 2 h/day. Peak muscle enlargement of the overload groups was reached after 5 wk. Citrate synthase, phosphofructokinase, and myofibril ATPase activities were consistantly depressed by approximately 30%, 40%, and 18%, respectively, in overload as compared to normal groups. Daily exercise prevented the decrease in only citrate synthase activity. Unilateral overload of medial gastrocnemius muscle indicated that both fast-twitch oxidative-glycogenolytic and fast-twitch glycogenolytic fiber types undergo enzyme changes in response to the functional stress. However, changes in the former were in closer agreement with the net changes seen in the plantaris than the latter. Soleus muscle responded to overload primarily with marked reductions in respiratory capacity. These findings suggest that certain enzyme systems are altered with functional overload in different fiber types. However, the alterations in certain enzyme systems may, in part, be independent of the process of hypertrophy.
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PMID:Effect of functional overload on enzyme levels in different types of skeletal muscle. 13 68

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

The mitochondrial matrix subfractions from rat liver, kidney cortex, brain, heart, and skeletal muscle were isolated and their protein components were resolved by two-dimensional polyacrylamide gel electrophoresis, revealing between 120 and 150 components for each matrix subfraction. Excellent resolution was obtained utilizing a pH 5 to 8 gradient in the first dimension and in 8 to 13% exponential acrylamide gradient in the second dimension, increasing the number of mitochondrial matrix proteins observed 3-fold over one-dimensional systems. Protein components tentatively identified by co-migration with pure enzymes and by known tissue distributions are carbamoyl-phosphate synthetase (EC 2.7.2.5), ornithine transcarbamylase (EC 2.1.3.3), glutamate dehydrogenase (EC 1.4.1.3), pyruvate carboxylase (EC 6.4.1.1), citrate synthase (EC 4.1.3.7), fumarase (EC 4.2.1.2), aconitase (EC 4.2.1.3), alpha-ketoglutarate dehydrogenase (EC 1.2.4.2), dihydrolipoyl transsuccinylase (EC 2.3.1.12), lipoamide dehydrogenase (EC 1.6.4.3), glutamate-aspartate aminotransferase (EC 2.6.1.1), and the two subunits of pyruvate dehydrogenase (EC 1.2.4.1). Protein components unambiguously identified by peptide mapping are citrate synthase, aconitase, and pyruvate carboxylase. The inner membrane subfraction from rat liver mitochondria was also resolved two dimensionally; the alpha and beta subunits of ATPase (F1) (EC 3.6.1.3) were identified by peptide mapping.
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PMID:Resolution of rat mitochondrial matrix proteins by two-dimensional polyacrylamide gel electrophoresis. 44 63

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

Chronic low-frequency stimulation of rabbit fast-twitch muscle induced time-dependent increases in the concentration of the sarcolemmal Na+,K(+)-ATPase and in mitochondrial citrate synthase activity. The almost twofold increase in Na+,K(+)-ATPase preceded the rise in citrate synthase and was complete after 10 days of stimulation. We suggest that the increase in Na+,K(+)-ATPase enhances resistance to fatigue of low-frequency-stimulated muscle prior to elevations in aerobic-oxidative capacity.
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PMID:Time-dependent increases in Na+,K(+)-ATPase content of low-frequency-stimulated rabbit muscle. 132 68

It has recently been discovered that both mineralocorticoid (MC) and glucocorticoid (GC) hormones can stimulate electrogenic Na+ absorption by mammalian collecting duct cells in culture. In primary cultures of rat inner medullary collecting duct (IMCD) cells, 24-h incubation with either MC or GC agonist stimulates Na+ transport approximately threefold. We have now determined that the effects were not additive, but the time courses were different. As aldosterone is known to stimulate citrate synthase, Na+/K+ ATPase activity, and ouabain binding in cortical collecting duct principal cells, we determined the effects of steroids on these parameters in IMCD cells. MC and GC agonists both produced a small increase in citrate synthase activity. There was no increase in Na+/K+ ATPase activity but specific ouabain binding was increased more than two-fold by either agonist. To determine the role of apical Na+ entry in the steroid-induced effects, the Na+ channel inhibitor, benzamil, was used. Benzamil did not alter the stimulation of citrate synthase activity by either steroid. In contrast, GC stimulation of ouabain binding was prevented by benzamil, whereas MC stimulation was not. We conclude that there are differences in the way that MC and GC hormones produce an increased Na+ transport. Both appear to produce translocation (or activation) of pumps into the basolateral membrane. GC stimulation of pump translocation requires increased Na+ entry whereas MC stimulation does not.
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PMID:Cellular responses to steroids in the enhancement of Na+ transport by rat collecting duct cells in culture. Differences between glucocorticoid and mineralocorticoid hormones. 132 98

Although the soleus muscle comprises only 6% of the ankle plantar flexor mass in the rat, a major role in stance and walking has been ascribed to it. The purpose of this study was to determine if removal of the soleus muscle would result in adaptations in the remaining gastrocnemius and plantaris muscles due to the new demands for force production imposed on them during stance or walking. A second purpose was to determine whether the mass or the fiber type of the muscle(s) removed was a more important determinant of compensatory adaptations. Male Sprague-Dawley rats underwent bilateral removal of soleus muscle, plantaris muscle, or both muscles. For comparison, compensatory hypertrophy was induced in soleus and plantaris muscles by gastrocnemius muscle ablation. After forty days, synergist muscles remaining intact were removed. Mass, and oxidative, glycolytic, and contractile enzyme activities were determined. Despite its role in stance and slow walking, removal of the soleus muscle did not elicit a measurable alteration in muscle mass, or in citrate synthase, lactate dehydrogenase, or myofibrillar ATPase activity in gastrocnemius or plantaris muscles. Similarly, removal of the plantaris muscle, or soleus and plantaris muscles, had no effect on the gastrocnemius muscle, suggesting that this muscle was able to easily meet the new demands placed on it. These results suggest that amount of muscle mass removed, rather than fiber type, is the most important stimulus for compensatory hypertrophy. They also suggest that slow-twitch motor units in the gastrocnemius muscle play an important role during stance and locomotion in the intact animal.
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PMID:Adaptation in synergistic muscles to soleus and plantaris muscle removal in the rat hindlimb. 143 77


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