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)

In vivo administration of L-thyroxine (L-T4) in Anabas testudineus, while significantly stimulated the activities of cytochrome c oxidase and alpha-glycerophosphate dehydrogenase (alpha-GPDH), inhibited glucose-6-phosphate dehydrogenase (G-6-PDH), cytosolic and mitochondrial malate dehydrogenase (cyt. MDH; mit. MDH), and Mg2+ DNP-dependent adenosine triphosphatase (Mg2+ ATPase) activities. The activities of lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), and catalase remained unaltered after L-T4 treatment. Administration of protein synthesis inhibitors such as actinomycin D, while significantly inhibited cytochrome oxidase, alpha-GPDH, catalase, SDH, and Mg2+ ATPase activities, did not change LDH, cyt. MDH, and mit. MDH activities. Chloramphenicol injection significantly stimulated cytochrome oxidase, alpha-GPDH, and G-6-PDH activities. Simultaneous injections of actinomycin D or chloramphenicol with 3,5,3'-triiodo-L-thyronine (L-T3) or L-T4 prevented the effects of thyroid hormones on enzyme activities, when compared to the respective controls.
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PMID:Oxidative metabolism in a teleost, Anabas testudineus Bloch: effect of thyroid hormones on hepatic enzyme activities. 292 Sep 3

The effects of heating blood to 57 degrees C on intraerythrocytic calcium, membrane ATPase activity and cell shape have been studied in canine blood. Intraerythrocytic calcium was determined by use of arsenazo III, membrane ATPase activity was determined by inorganic phosphorous formation and erythrocyte shape was determined by scanning electron microscopy. The results of this study showed that this degree of thermal trauma would cause a 27% increase in intraerythrocytic calcium and a 38% decrease in ATPase activity. During these changes in calcium and ATPase activity the erythrocyte changed form from biconcave to spherical. Addition of catalase (3,200 U/ml) to the blood prior to heating prevented the changes observed in intraerythrocytic calcium, membrane ATPase activity and shape. The addition of the free-radical generating combination of hypoxanthine-xanthine oxidase to blood produced a 20% decrease in membrane ATPase activity and a change in erythrocyte shape, but did not alter intraerythrocytic calcium. These results suggest that free-radicals are responsible for the changes in membrane ATPase activity. The observation that shape change occurs when ATPase activity has been decreased, but calcium has not been increased, suggests that membrane ATPase activity levels are more important in producing changes in erythrocyte shape than are intraerythrocytic calcium levels.
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PMID:Relationship between membrane ATPase and shape changes in the dog erythrocyte. 294 79

The superoxide radicals generated by the xanthine oxidase reaction reduced the myofibrillar Ca2+-ATPase activity. This negative effect was prevented by superoxide dismutase or by dithiothreitol, a protective thiol compound. Partial protection was achieved by catalase, while mannitol was ineffective. The myofibrillar Ca2+-ATPase exposed to O2-. radicals did not modify the affinity for Ca2+ while it showed a remarkable reduction of Vmax measured at the saturating level of Ca2+. The O2-. inhibited myofibrillar ATPase showed a higher value of Km for the cofactor associated to a reduced value of Vmax when studied in the presence of increasing concentration of ATP. Thus, circumstances that enhance the production of cardiac O2- radicals can be considered a negative metabolic event capable of depressing the myofibrillar Ca2+-ATPase activity.
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PMID:Inhibitory effect of superoxide radicals on cardiac myofibrillar ATPase activity. 299 80

The present study has examined early cellular effects of chronic adriamycin administration to dogs using a protocol (1 mg/kg/week to a total cumulative dose of 240 mg/m2) producing significant but small reductions in ejection fraction and stroke volume as determined echocardiographically prior to the development of clinical or radiological manifestations of heart failure. At this early phase of cardiomyopathy, significant reduction (P less than 0.05) in sarcoplasmic reticulum Ca2+, K+-ATPase was observed without any change in mitochondrial, lysosomal or sarcolemmal marker enzymes. Myocardial calcium (P less than 0.01) and glutathione (P less than 0.001) levels were increased significantly. Detailed analysis of myocardial phospholipid profiles failed to show any significant differences between control and treated dogs. In contrast, red cell membranes showed increased phosphatidylcholine (PC) and decreased phosphatidylserine (PS) contents, resulting in a significant increase in PC/PS ratio (P less than 0.05). No significant changes were detected in activities of catalase, superoxide dismutase or glutathione peroxidase in erythrocytes or myocardial tissue from control and adriamycin-treated animals. A significant (P less than 0.05) elevation in plasma sialic acid was observed following adriamycin treatment. Our results suggest that early adriamycin-induced damage is unlikely to result from alterations in cellular processes protecting tissues against oxidant injury. Regression analysis indicated that, of the various abnormalities observed, only the elevated myocardial calcium levels and the increases in plasma sialic acid correlated with the degree of myocardial functional impairment. Our findings suggest the presence of sarcolemmal alterations in Ca2+ handling in early adriamycin-induced myocardial injury and indicate that measurement of plasma sialic acid should be further investigated as a possible noninvasive indicator of impending adriamycin cardiotoxicity.
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PMID:Adriamycin cardiomyopathy: implications of cellular changes in a canine model with mild impairment of left ventricular function. 299 97

Studies have been carried out on dog erythrocytes to determine the effects of heating to 57 degrees C on membrane ATPase and erythrocyte shape. The results of these studies showed that after heating the blood there was approximately a 30 per cent decrease in membrane ATPase and an alteration of erythrocyte shape from biconcave to spherical. Additional studies of the effects of addition of arachidonic acid to erythrocyte-membrane homogenates demonstrated that this substance produced a dose-related inhibition of ATPase. If the additions were made to membranes from blood which had previously been heated, the effects of arachidonic acid and heat were additive. Addition of the hydroxyl-radical scavenger catalase to the blood before heating prevented the observed decrease in ATPase and prevented the change in shape to spherical. These results confirm the previous findings of Bessis that heat will cause a change in the erythrocyte shape from biconcave to spherical and suggest that the mechanism responsible for this change is an alteration in membrane ATPase. The observation that a similar response can be produced by arachidonic acid suggests that metabolism of this substance may generate agents which are capable of inhibiting erythrocyte membrane ATPase. The observation that catalase will prevent the ATPase inhibition and the change in erythrocyte shape suggests that hydroxyl-free radicals play an important part in this thermal trauma-induced response.
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PMID:Effects of thermal trauma on dog erythrocyte ATPase and shape. 300 74

Incubation of Trypanosoma cruzi mitochondrial ATPase (Fo-F1) with the xanthine oxidase system (XO), Fenton's reagent (Fe2+ + H2O2) and the ascorbate-Cu system, caused gradual loss of enzyme activity, which increased as a function of incubation time and rate of oxygen radical generation. The essential role of OH. radicals for ATPase inactivation was supported by a) the enzyme protection afforded by superoxide dismutase, catalase and mannitol, when using the XO system; b) the similar effect of mannitol and benzoate with Fenton's reagent; c) the similar effect of catalase, EDTA and histidine with the ascorbate-Cu system; d) the increased rate of ATPase inactivation by 1) the XO system supplemented with chelated iron, and 2) the ascorbate-Cu system supplemented with H2O2. Comparison of oxygen radical generators for their action on membrane-bound (Fo-F1) and soluble F1 revealed that ascorbate-Cu was the most effective one, possibly because of its capability of producing OH. radicals that react preferentially with the enzyme at their formation site.
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PMID:Inactivation of mitochondrial adenosine triphosphatase from Trypanosoma cruzi by oxygen radicals. 301 49

The role of O2 free radicals in the reduction of sarcolemmal Na+-K+-ATPase, which occurs during reperfusion of ischemic heart, was examined in isolated guinea pig heart using exogenous scavengers of O2 radicals and an inhibitor of xanthine oxidase. Ischemia and reperfusion reduced Na+-K+-ATPase activity and specific [3H]ouabain binding to the enzyme in ventricular muscle homogenates and also markedly lowered sodium pump activity estimated from ouabain-sensitive 86Rb+ uptake by ventricular muscle slices. These effects of ischemia and reperfusion were prevented to various degrees by O2-radical scavengers, such as superoxide dismutase, catalase, dimethyl-sulfoxide, histidine, or vitamin E or by the xanthine oxidase inhibitor, allopurinol. The degree of protection afforded by these agents paralleled that of reduction in enhanced lipid peroxidation of myocardial tissue as estimated from malondialdehyde production. These results strongly suggest that O2 radicals play a crucial role in the injury to sarcolemmal Na+-K+-ATPase during reperfusion of ischemic heart.
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PMID:O2 free radicals: cause of ischemia-reperfusion injury to cardiac Na+-K+-ATPase. 302 76

Experiments were conducted to determine whether ultraviolet (UV) radiation exerts its effect through the generation of oxygen intermediates on Langerhans cells (LC). Guinea pigs were exposed to one single dose of UVB (0.9-2.7J/cm2), and biopsy specimens were taken 5 days after the irradiation. The population of LC was evaluated using ATPase-stained epidermal sheets. These exposures reduced the number of LC to 20-25% of the original density. On the other hand, superoxide dismutase (SOD) (0.02-0.2 mg), a scavenger of superoxide anion, which had been injected intradermally just before UV radiation, significantly prevented the depletion of LC, although not completely (37-40% of the original density). The injection immediately after the exposure was still significantly effective, but less so. Other scavengers of oxygen intermediates including catalase, D-mannitol, and L-histidine revealed no detectable effect. A single exposure of UVB at doses of 0.3-0.6 J/cm2 did not deplete the ATPase-positive LC. However, the same dose of UVB reduced the number of LC to 70%, when exposed after the injection of an SOD inactivator, diethyldithiocarbamate, possibly due to inactivation of physiologically existing SOD. These observations indicate that oxygen intermediates such as superoxide anion or its subsequent species are generated by UV radiation exposure and damage the epidermal LC.
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PMID:Oxygen intermediates are involved in ultraviolet radiation-induced damage of Langerhans cells. 303 31

The effects of sublethal heat pulses on cell division have provided insights into possible molecular mechanisms. Thus Zeuthen's findings of 'set-backs' up to a transition point provides the basis for the idea that the continuous accumulation of a compound needed for cell division spans a major portion of the cell cycle. The accumulating substance is a 'division protein' which forms part of a structure which is unstable until completely assembled at the transition point. Experiments showing phase resetting of mammalian cells by temperature perturbation indicate limit-cycle oscillator control of the cell cycle with a phase-response curve with a repeat interval equal to the period of the clock. As well as providing a method for establishing synchronized cultures these observations have found application in the selective effects of hyperthermia as an antitumour agent. Circadian rhythms display several unique features distinguishing them from other periodic processes. Only recently has it been recognized that some of these characteristics may be properties of ultradian rhythms as well. The probably most striking feature of circadian timekeeping, i.e. independence of ambient temperature, was found for ultradian rhythmicity even at the level of the unicellular organization. Synchronous cultures of some lower eukaryotes were prepared by centrifugal size selection methods. Experiments with asynchronous control cultures substantiated the view that the conditions employed were such as to minimize any perturbative effects: most importantly the organisms were never removed from their culture medium. Whereas the control cultures showed smoothly increasing respiration rates, total RNA, total protein, enzyme activities and enzyme protein (e.g. for cytochrome aa3, ATPase, catalase), in synchronous cultures all these parameters showed oscillatory behaviour. Different periods were observed in different organisms: thus in Acanthamoeba castellanii the period was about 70 min, in Tetrahymena pyriformis strain ST it was about 50 min, in T. pyriformis AII it was 30 min, and in Candida utilis it was about 30 min (all measurements at 30 degrees C). In A. castellanii the periods of both the oscillations in rate of respiration and the total cell protein were hardly affected by the temperature of growth over the range 20 to 30 degrees C. The oscillations show no damping during experiments lasting 12 h: these properties suggest that we are observing temperature-compensated endogenous rhythms which presumably serve a timekeeping function in cells undergoing growth and division.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A temperature-compensated ultradian clock explains temperature-dependent quantal cell cycle times. 333 82

Erythrocyte membrane (EM) abnormalities in a 16-yr-old boy with hypoalphalipoproteinemia resembling fish eye disease (FED-LS) were investigated. The proband's erythrocytes had markedly decreased osmotic fragility with target cells observed in the peripheral film. Analysis of his EM lipids revealed normal cholesterol and phospholipid content but a marked increase in phosphatidylcholine with concomitant decreases in phosphatidylethanolamine and sphingomyelin. Of the EM enzymes examined, acetylcholinesterase and superoxide dismutase activities were decreased while those of Na+-K+ ATPase, catalase and glutathione reductase were normal. 51Cr erythrocyte survival in the patient was slightly decreased. The observed changes in a number of structural and functional properties of erythrocytes in this disorder are indistinguishable from those previously described in homozygotes for familial lecithin:cholesterol acyltransferase (LCAT) deficiency. Thus, it is possible that in both of these disorders an abnormality of plasma LCAT activity causes, either directly or indirectly, functional and structural changes in the erythrocyte membrane.
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PMID:Erythrocyte abnormalities in a hypoalphalipoproteinemia syndrome resembling fish eye disease. 341 11


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