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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several of the adenosinetriphosphatase enzymes that are responsible for cardiac muscle contraction rely on high-energy phosphates supplied by the creatine kinase (CK) system. Experimental diabetes mellitus has been shown to cause a decrease in the maximal contractile performance of the heart. We postulated that the decrease in contractile performance may be explained in part by a decrease in CK enzyme activity. To evaluate this possibility, we determined the level of CK activity and isoenzyme distribution in ventricular homogenates from normal, diabetic, and insulin-treated diabetic rats. We found that total CK activity was decreased by 35% in diabetic hearts and that a 66% reduction in the cardiac-specific MB isoenzyme occurs. Using a cDNA probe for CK-muscle (M) RNA in Northern blot analysis, we determined that a 61.1% decrease in CK-M mRNA occurs in diabetes. Chronic insulin therapy for 1 mo restores CK-M mRNA levels and enzyme activity. In conclusion, diabetes-induced CK enzyme decreases are mediated in part by a lower level of CK-M mRNA that codes for the major CK-M subunit protein. Decreased performance of the CK system may contribute to diabetic cardiomyopathy.
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PMID:Diabetes decreases creatine kinase enzyme activity and mRNA level in the rat heart. 267 31

N-methyl-D-aspartate (NMDA) is an agonist used to identify neuronal receptive sites for dicarboxylic amino acid neurotransmitters; NMDA receptors are implicated in neuronal damage of ischemic or hypoglycemic origin in newborns although involved mechanisms remain to be identified. In the present study, 31P magnetic resonance spectroscopy with fast (6/min) data acquisition was used in newborn rat brain slices to measure changes of intracellular phosphocreatine and nucleotide triphosphate levels following extracellular NMDA applications. The rapid exhaustion of phosphocreatine stores in 50% of the total population of brain cells was induced in all cases by application of NMDA (30-45 s, 25-100 mM). It was not reproduced by other excitatory agents: potassium ions (24.6 mM, 4 min), isobutylxanthine (1mM), muscarine (10 mM), serotonin (0.1 mM) or substance P (10 microM). Such an effect of NMDA was not modified after tetrodotoxin (1 microM) and was reduced by extracellular 2-amino-5-phosphonovalerate (50 microM) or magnesium ions (2.2 mM). However it did develop during NMDA-induce neuronal excitations and was reversible within 10-30 min. This action of NMDA was followed by an irreversible decrease of phosphorus metabolites if mitochondrial creatine kinase and adenosine triphosphatase were decoupled by atractyloside (50 microM). Experiments revealed a link between selective NMDA action at neuronal plasma membranes, neurotoxicity and energy production by mitochondria.
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PMID:Metabolic action of N-methyl-D-aspartate in newborn rat brain ex vivo: 31p magnetic resonance spectroscopy. 268 43

The present investigation was undertaken to compare the effects of cold crystalloid and blood cardioplegia on the functional recovery of the heart; on Ca++ binding and uptake, Ca++-ATPase of the sarcoplasmic reticulum (SR), and sarcolemmal (SL) ATPase; and on serum MB fraction of creatine kinase (MBCK) after one and half hours of reperfusion following one hour of ischemic cardiac arrest in dog. This study was made also to determine if the functional changes are related to the changes in biochemistry at the molecular level. The dogs were divided into three groups: sham bypass (SB), cold crystalloid cardioplegia (CC), and pump blood cardioplegia (PB). There was a decrease in the cardiac index (CI), left ventricular work index (LVWI), and mean aortic pressure (MAP) in all three groups. The index of myocardial contractility [dp/dt)/IIP) and CI were lower in the CC group as compared with the SB and PB groups. All the hemodynamic values for the PB group were similar to those of the SB group except total systemic vascular resistance (TSVR) and left ventricular end-diastolic pressure (LVEDP) which were lower in the PB group. The index of myocardial contractility and cardiac index appeared to be greater in the PB group than in the CC group. There was a decrease in the Ca++ uptake by SR from both the CC and PB groups. Ca++ binding and Ca++,-ATPase of SR from the PB group were depressed. The sarcolemmal ATPase was unaffected in both groups. The serum MBCK increased in both PB and CC groups, though the increase was smaller in the PB group. These results indicate that the functional recovery of the heart was slightly better with pump blood cardioplegia than with cold crystalloid cardioplegia. The depressed myocardial contractility and cardiac function in the CC group were associated with a decrease in the Ca++ uptake by SR. However, the decreases in the Ca++ binding, Ca++ uptake, and Ca++ ATPase by SR from the pump blood cardioplegic group were not accompanied by decreases in the cardiac contractility and cardiac function. Myocardial damage as assessed by serum MBCK was smaller in the PB group than in the CC group.
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PMID:Effects of blood and crystalloid cardioplegia on cardiac function at organ and cellular levels during hypothermic cardiac arrest. 282 61

The cardiac myofibrillar component of the phosphorylcreatine shuttle mechanism enzymatically couples the functionally significant processes of energy utilization (ATPase) with substrate regeneration by creatine kinase (CK). Both components have isoenzyme forms that are transcriptionally regulated. Propylthiouracil-induced (PTU) hypothyroidism reduced rat cardiac contractile protein ATPase activity by shifting isomyosin predominance from the V1 to the V3 form. However, neither CK specific activity or CK isoenzyme composition was altered by PTU treatment. Thus, myofibrillar components of the phosphorylcreatine shuttle, ATPase and CK, are not coordinately regulated under hypothyroid conditions.
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PMID:Cardiac myofibrillar creatine kinase is not influenced by hypothyroidism. 293 Nov 68

The precipitation patterns of the following ultracytochemical methods in rat muscle cells were compared and examined critically: the potassium pyroantimonate method for calcium demonstration; the calcium phosphate technique for the Ca2+--ATPase reaction; the formazan reaction for the demonstration of creatine kinase activity (all performed on heart muscle); and the lead phosphate technique for the Mg2+--ATPase reaction in skeletal muscle. Using X-ray microanalysis, it was found that the antimonate precipitate contains only calcium as the precipitated ion in the vast majority of cases. Most probably it consists of pure calcium pyroantimonate. However, in myocytes showing the well-established precipitation pattern, the concentration of calcium was estimated to be about two orders of magnitude higher than the native concentration of total intracellular calcium. It is concluded that calcium ions diffuse freely from the extracellular space and from adjacent cells into cells containing antimonate and are precipitated mostly at sites where heterogeneous nucleation is facilitated by intracellular catalysts (biopolymers). As shown by the similar precipitation patterns for the four reactions compared, these catalysts are not specific to any of these reactions and are most probably neither calcium-binding sites nor sites of any one of the enzymes examined in the native cell.
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PMID:Localization artefacts in ultracytochemical ion precipitation reactions. 294 Feb 4

Thirteen horses with histories of exertional rhabdomyolysis were exercised for 20 minutes to induce clinical signs of lameness, elevated serum creatine kinase (CK), and aspartate aminotransferase (AST) activities and skeletal muscle morphologic lesions. The clinical signs exhibited by affected horses included trembling, sweating, increased rate of respiration, and restricted limb movement. Serum CK reached maximal activity between 4 and 8 hours after the exercise period and serum AST activity peaked between 24 and 48 hours. Histologically, the skeletal muscle lesions in muscle biopsies 24 hours after the exercise period consisted of segmental muscle fiber degeneration. Damaged muscle fibers were repaired by myoblastic regeneration. Horses with moderate (greater than 1,500 U/liter) to severe (greater than 5,000 U/liter) elevations of serum CK activity accompanied by clinical signs of muscle soreness induced by exercise, had visible muscle fiber degeneration microscopically. Frozen sections of biopsies of the gluteus medius muscle from affected (n = 13) and control (n = 11) groups of horses were processed to demonstrate myofibrillar ATPase activity. These sections were then used to determine fiber types, area percentages, and mean cross sectional fiber sizes. The mean type I, type II, and intermediate fiber sizes were significantly larger in the affected group than in the control group. In the gluteus medius muscles of the affected group, there was a significantly greater percentage of intermediate fibers and a significantly greater percentage of area occupied by intermediate fibers than in the control group. In the muscle samples with acute lesions of exertional rhabdomyolysis, type II fibers were selectively but not exclusively affected. In one horse which was subsequently necropsied 24 hours after the exercise period, lesions were present in several postural muscles, the masseter muscle and the heart. We conclude that the gluteus medius muscle fibers of affected horses are larger in cross sectional area than those of control horses and that there is preferential degeneration of type II fibers in acute lesions of exertional rhabdomyolysis.
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PMID:Histochemical and morphometric evaluation of skeletal muscle from horses with exertional rhabdomyolysis (tying-up). 294 76

The muscle enzymatic changes subsequent to 6 months of strength training followed by 3 months of detraining were examined in 21 physically active men. They were assigned either to a heavy-resistance (HR) or an explosive strength (EX) training program. Muscle biopsies were obtained from m. vastus lateralis for the assessment of activities of the enzymes hexokinase (HK), myofibrillar ATPase (ATPase), citrate synthase (CS), phosphofructokinase (PFK), lactate dehydrogenase (LDH), myokinase (MK) and creatine kinase (CK). The activities were measured on freeze-dried tissue samples using fluorometrical assays. Both groups displayed increased (P less than 0.01-0.001) fast-twitch (FT) fiber area consequent to training with no concomitant hypertrophy of slow-twitch (ST) fiber area. Mean fiber area increased by 16% (P less than 0.001) in HR and 9% (NS) in EX. Following detraining, mean fiber area returned to pretraining value only in EX. HK decreased in both groups (P less than 0.01-0.001) and CK decreased in HR (P less than 0.05). When the two groups were treated together, all enzymes, except for LDH, decreased their activity (P less than 0.05-0.001). It is concluded that 6 months of strength training performed either as heavy-resistance or explosive training is not associated with any increased activities of enzymes reflecting phosphagen, glycolytic, or oxidative metabolism. Instead, the present results suggest that exercise-induced hypertrophy is accompanied by attenuation of certain enzyme activities of importance for ATP regeneration.
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PMID:Enzymatic adaptations consequent to long-term strength training. 295 91

Rat heart myofibrils were isolated and purified in three different media: sucrose medium; EGTA medium; EGTA+ATP medium. All preparations were characterized by similar Ca2+-sensitive ATPase activities and were practically free of mitochondrial and sarcolemmal contaminations. However, they contained different amounts of creatine kinase. In preparations which showed the most intact ultrastructure, the activity of creatine kinase was 0.99 +/- 0.12 IU/mg. It was found that creatine kinase can be bound to myofibrils in a reversible manner with Kd = 0.16 mg/ml = 1.8 X 10(-6) M; the creatine kinase/myosin ratio was estimated to be approximately 1:10. The localization of creatine kinase was found to be a basis for the high turnover rate of ATP in the coupled creatine kinase and ATPase reactions occurring in cardiac myofibrils.
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PMID:[Myofibrillar creatine kinase: reversible binding to contractile proteins, stoichiometric ratio to myosin and its functional role]. 295 89

Mammalian heart development, from the time of weaning until adulthood, is characterized by progressive and significant enhancement in functional performance. Aerobic metabolism and contractile protein ATPase activity increase in parallel with augmented cardiac function. The present studies examined the potential contribution of phosphorylcreatine shuttle enzymes to the developmentally linked alterations in heart performance. Mitochondrial ATPase specific activity was not altered between weanling and adult heart; however, creatine kinase activity was enhanced approximately threefold. Myofibrillar ATPase activity doubled over the developmental time course, while creatine kinase activity increased to an even greater extent. Enhanced myofibrillar ATPase activity was not due to alterations in either calcium sensitivity or ATPase activity measured in purified myosin. Both the mitochondrial and myofibrillar creatine kinase enzyme activities are enhanced during normal heart growth; however, relatively greater enhancement of the myofibrillar component occurs. Thus, enzymatic reactions comprising the phosphorylcreatine shuttle system are dramatically increased during normal heart development. This mechanism deserves consideration as a potentially powerful contributor to enhanced cardiac function during the perinatal period.
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PMID:Phosphorylcreatine shuttle enzymes during perinatal heart development. 295 1

A study was undertaken to assess the effectiveness of cold crystalloid cardioplegia with or without verapamil on the functional recovery of the heart, Ca++ binding and uptake, Ca++ ATPase of sarcoplasmic reticulum, sarcolemmal ATPase and the MB fraction of creatine kinase (MBCK) after 1.5 h of reperfusion following 1 h of ischemic cardiac arrest. The dogs were divided into three groups: group I, sham bypass; group II, cold crystalloid cardioplegia; group III, cold crystalloid cardioplegia with verapamil. There was a decrease in the cardiac index (CI), left ventricular work index (LVWI) and mean aortic pressure (MAP) in the sham bypass group at the end of the protocol (time period corresponding to 60 mins off bypass). There was a decrease in the Cl and index of myocardial contractility in the cold crystalloid cardioplegic group compared to sham bypass group. The decrease in the cardiac function in cold crystalloid group was associated with a decrease in Ca++ uptake by sarcoplasmic reticulum and a tendency for an increase in the sarcolemmal Na+-K+ ATPase. The Ca++ binding and the Ca++ ATPase of sarcoplasmic reticulum were not affected. The index of myocardial contractility and cardiac function were better with cold crystalloid containing verapamil than with cold crystalloid alone. This improvement, although partial, in cardiac contractility and function with cold crystalloid cardioplegia containing verapamil was associated with an improvement in the Ca++ uptake by the sarcoplasmic reticulum. The Ca++ ATPase and Ca++ binding were depressed in group III. The MBCK in systemic and coronary sinus blood increased progressively in groups II and III. Although there was an increase in MBCK in group I the increase was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of crystalloid cardioplegia and verapamil on cardiac function and cellular biochemistry during hypothermic cardiac arrest. 296 3


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