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 structural changes accompanying digitonin-induced release of enzymes and metabolites from isolated hepatocytes have been studied by scanning and transmission electron microscopy. In the initial phase, characterized by total release of the cytosolic marker enzyme, lactate dehydrogenase, the plasma membrane was immediately damaged, rapidly followed by extensive damage to the endoplasmic reticulum. The shape of the cell, however, was maintained, and the mitochondria and nucleus remained tightly held together by the cytoskeleton. Mitochondria remained intact initially, whereas the cytosol became less electron dense and the nuclear chromatin was more dispersed. An intermediate phase was characterized by total release of adenylate kinase and most of the glucose-6-phosphatase, marker enzymes for the mitochondrial intermembrane space and the endoplasmic reticulum, respectively. The outer mitochondrial membrane was ruptured, but mitochondria maintained their normal matrix electron density. In the final phase, characterized by the beginning of citrate synthase release from the mitochondrial matrix space, the mitochondria became swollen, and only the nucleus, inner and outer mitochondrial membranes, and the cytoskeleton could be clearly distinguished. Although the plasma membrane could not be readily discerned in electron micrographs after the initial phase, the plasma membrane marker enzyme 5'-nucleotidase remained associated with digitonin-treated hepatocytes. Acetyl-CoA carboxylase was released much more slowly than lactate dehydrogenase, indicating some severe restriction on its release. The release of acetyl-CoA carboxylase closely paralleled the release of glucose-6-phosphatase. The controlled exposure of hepatocytes to digitonin, therefore, leads to the sequential release of soluble, compartmentalized cellular components and some membrane-bound components, but the mitochondrial membrane, cytoskeleton and the nucleoskeleton survive even long-term digitonin treatment.
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PMID:Structural changes of isolated hepatocytes during treatment with digitonin. 614 31

The purpose of this investigation was to examine the effects of chronic and acute exercise on the main components involved in excitation-contraction coupling and relaxation in rat heart. Sixty male Wistar rats were divided into a sedentary (S) and three 12-wk treadmill-trained groups (T-1, moderate intensity; T-2, high intensity; T-3, interval running). After 12-wk, 15 rats from the S group and 15 rats from the T-2 group were subjected to a single treadmill-exercise session until exhaustion before being killed at 0, 24, or 48 h (acute exercise). The remaining animals were killed 48 h after the last standard exercise session (chronic exercise). The efficacy of the training programs was confirmed by an increase in treadmill endurance time and in skeletal muscle citrate synthase activity. None of the exercise programs modified heart weight or cardiac oxidative capacity. [(3)H]PN200-110 and [(3)H]ryanodine binding to cardiac homogenates indicated that the density of L-type and sarcoplasmic reticulum (SR) Ca(2+) channels was the same in S and trained rats. The SR Ca(2+)-ATPase activity was also unmodified. Finally, the activities of the ectoenzymes Mg(2+)-ATPase and 5'-nucleotidase, which are involved in degradation of extracellular nucleotides, were not affected by either of the running programs. After the acute exercise session, no changes were detected in either of the tested parameters in heart homogenates of S and T-2 animals. We conclude that neither treadmill-exercise training for 12 wk nor exhaustive exercise alters the density of Ca(2+) channels involved in excitation-contraction coupling or the SR Ca(2+)-ATPase and the ectonucleotidase activities in rat heart.
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PMID:Chronic and acute exercise do not alter Ca2+ regulatory systems and ectonucleotidase activities in rat heart. 1040 69

The present study was conducted to investigate the effects of long-term exercise training on the main components involved in excitation-contraction coupling and relaxation in rat myocardium. Twenty male Wistar rats were divided into sedentary (S) and treadmill-trained (T) groups. Group T was trained for 24 weeks, 5 days/week (25 m/min, 45-60 min, 0% slope). 48 h after the last exercise session, animals were killed and ventricular and soleus muscle homogenates were obtained. The citrate synthase activity in soleus muscle was significantly increased (163%) in T compared with S rats ( P<0.01), confirming the exercise training efficacy. Although heart weight and cardiac oxidative capacity were not modified by exercise training, the binding of [(3)H] ryanodine and the dihydropyridine [(3)H]PN200-110 to cardiac homogenates, and sarcoplasmic reticulum Ca(2+)-ATPase activity were increased significantly in the ventricular homogenates from T compared with S animals ( P<0.01). Western blot analysis of ventricular homogenates failed to show significant alterations in dihydropyridine receptor and Ca(2+)-ATPase levels in T animals, but revealed an increase of ryanodine receptor density in this group ( P<0.01). The activity of the ectoenzymes 5'-nucleotidase and Mg(2+)-ATPase was not affected by training ( P>0.05). In conclusion, long-term treadmill training induces adaptive changes in some of the components of myocardial rat excitation-contraction coupling and relaxation systems that could contribute to the improvement of cardiac function.
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PMID:Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training. 1273 53