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

---

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

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.
...
PMID:[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels]. 300 17

Microtubules have been isolated from immature (3-4 weeks' old) and old (11-13 years' old) bovine brains. Quantitative studies revealed that the concentration of extractable microtubule protein per gram of wet brain decreased from 0.47 mg (immature animals) to 0.34 mg (old animals). The major components of microtubule protein (tubulin and high-molecular-weight microtubule-associated proteins) do not undergo an age-correlated change. Determination of the endogenous protein kinase activity revealed that the activity associated with "immature" calf brain microtubules was six times higher than the activity present in "old" preparations. In contrast, the stimulatory effect of cyclic AMP on protein phosphorylation in microtubules from old bovine brains exceeds nine-fold the value obtained from immature animals. After addition of casein (exogenous acceptor), the basal activities increased in both preparations without altering the age-correlated difference in the specific activity. By comparing the radioactivity pattern of sodium dodecyl sulfate polyacrylamide gels after autophosphorylation of microtubule protein with [gamma-32P]ATP, 1.5 moles of phosphate per mole of high-molecular-weight microtubule-associated protein were estimated to be incorporated in preparations from immature animals and 0.9 mole of phosphate per mole of associated protein in the experiments with "old" microtubule protein. Adenosine triphosphatase activity, associated with the high-molecular-weight microtubule-associated protein 1, was determined to be 15% reduced in preparations from old animals, compared to the activity in "young" preparations. In contrast, the guanosine triphosphatase activity increased five-fold during ageing; the higher activity of this enzyme was observed both during the initial and the steady-state phases of microtubule formation.
...
PMID:Age-dependent alterations of microtubule-associated enzyme activities from bovine brain (protein kinase, adenosine triphosphatase, guanosine triphosphatase). 613 97

Development of brain edema following various pathological insults occurs after some delay. The mechanism of the delay is poorly understood. Using an in vivo model of cold-injury to study the time course of edema development, the present study indicates that the initiation of phospholipid degradation and rapid release of endogenous polyunsaturated fatty acids occurs within 1 min. Evans blue staining was slightly increased in the lesioned area at 1 min and was more profound at 30 min and at 24 h. The cerebral water content was unchanged at 1 min but was significantly increased at later times. The content of thiobarbituric acid-reactive malondialdehyde (MDA) was normal at 1 min but decreased at 30 min and at 24 h. The lipid-soluble fluorescence of MDA conjugates was also decreased concomitant with the degradation of membrane phospholipids at 24 h. Furthermore, Na+, K+-ATPase activities were consistently decreased in traumatized cortex from 24 h to 48 h after the cold-injury. These data indicate that the degradation of membrane phospholipids, the rapid release of polyunsaturated fatty acids and increased blood-brain barrier permeability are very early events underlying the subsequent development of vasogenic edema induced by cold-injury.
...
PMID:Phospholipid degradation and edema development in cold-injured rat brain. 613 47

Alkaline phosphatase (AP) is one of the enzymes which is highly active in the plasmalemma of endothelial cells (ECs) of BBB-type microvessels. In the ECs of non-BBB type vessels, the reaction for AP (and other phosphatases) is negative (e.g. choroid plexus, area postrema, hypophysis). After BBB damage, the leakage of the vessels can be demonstrated by the use of horseradish peroxidase (HRP). Concomitantly, changes in polar distribution of AP in the ECs occur, paralleled by the appearance of numerous pinocytic vesicles, deep invaginations of the plasmalemma and channel-like structures. The delimiting membranes of these structures possess AP, 5'-nucleotidase, nucleoside diphosphatase and Na+, K+-ATPase activities. These observations suggest that the redistribution of plasmalemma bound enzymes from luminal to abluminal surface results from membrane flow associated with formation of pinocytic vesicles and channel-like structures in affected ECs. In the area of brain where the process of resolution of brain edema occurs, the shift of the enzymatic activity from luminal to abluminal plasmalemma of the ECs is observed probably because of the need to remove various solutes present in the edematous fluid. The appearance of positive reaction for AP in the abluminal side of the EC can be a reflection of the changed functional polarity of these cells associated with reverse transport of solutes from brain, back into the blood stream.
...
PMID:Enzyme cytochemistry of blood-brain barrier (BBB) disturbances. 630 82

The effects of polyunsaturated fatty acids on brain edema formation have been studied in rats. Intracerebral injection of polyunsaturated fatty acids (PUFAs), including linolenic acid (18:3) and arachidonic acid (20:4), caused significant increases in cerebral water and sodium content concomitant with decreases in potassium content and Na+- and K+- dependent adenosine triphosphatase activity. There was gross and microscopic evidence of edema. Saturated fatty acids and monounsaturated fatty acid were not effective in inducing brain edema. The [125I]-bovine serum albumin spaces increased twofold and threefold at 24 hours with 18:3 and 20:4, respectively, indicating vasogenic edema with increased permeability of brain endothelial cells. Staining of the brain was observed five minutes after injection of Evans blue dye followed by arachidonic acid perfusion. A major decrease in brain potassium content was evidence of concurrent cellular (cytotoxic) edema as well. The induction of brain edema by arachidonic acid was dose dependent and maximal between 24 and 48 hours after perfusion. Dexamethasone (10 mg/kg) was effective in ameliorating the brain edema, whereas a cyclooxygenase inhibitor, indomethacin (10 mg/kg), was not. These data indicate that arachidonic acid and other PUFAs have the ability to induce vasogenic and cellular brain edema and further support the hypothesis that the degradation of phospholipids and accumulation of PUFAs, particularly arachidonic acid, initiate the development of brain edema in various disease states.
...
PMID:Induction of brain edema following intracerebral injection of arachidonic acid. 630 72

This study investigates the functioning of synaptosomal ouabain-sensitive Na+ -K+ -ATPase in cold-induced edema. During vasogenic brain edema development, the enzyme affinities for Na+ and K+ are progressively decreased paralleling the increase in the tissue water content, whereas maximal velocity of the reaction is not changed. On the basis of these data, it is likely that Na+ -K+ -ATPase impairment accounts for the intracellular uptake of water in this model of edema.
...
PMID:Modifications of synaptosomal Na+ -K+ -ATPase activity during vasogenic brain edema in the rabbit. 631 90

Arachidonic acid is released rapidly from cellular membrane phospholipids after pathological insults associated with the delayed development of brain edema. Intracerebral injection of arachidonic acid caused significant increases in brain water and sodium content with decreases in potassium content and Na+,K+-ATPase activity. The 125I-labeled bovine serum albumin spaces in brain (a measure of blood-brain barrier permeability) rose threefold 24 h after arachidonic acid injection. There was gross and microscopic evidence of edema. Saturated fatty acids and monounsaturated fatty acids were not effective. These data indicate that the endothelial cells of the blood-brain barrier are target sites for the action of arachidonic acid. It is hypothesized that the increased permeability of endothelial cells to macromolecules and water results from alterations of membrane phospholipids and increased vesicular transport, changes that are responsible for the delayed development of vasogenic edema.
...
PMID:The role of arachidonic acid in vasogenic brain edema. 642 Jan 96

The in vitro model presented provides an approach to study the nature of cell volume control as well as of swelling mechanisms under pathophysiological conditions. Pertinent parameters of cell volume control can be analyzed in isolation due to a virtually infinite extracellular environment precluding secondary effects of the suspended cells. Exposure of C6 glial cells to hypotonic medium was investigated as a model to study fundamental aspects of cell volume control. In confirmation of studies on other cell types glial cells suspended in hypotonic medium recover cell volume after transient swelling. Normalization of cell volume is associated with stimulation of respiration. Moreover, normalization of cell volume in hypotonic medium can be pharmacologically influenced. Addition of naftidrofuryl which enhances cellular O2-consumption led to acceleration of cell volume recovery. On the other hand, inhibition of Na+-K+-ATPase by ouabain did not prevent regulatory volume decrease ruling out a major role of the Na+-transport enzyme in this process. Contrary to hypotonic suspension, hypertonic exposure did not result in volume regulation during an observation period of 3 h. However, this may not necessarily exclude a capability of cell volume to normalize in hypertonic conditions as observed in vivo. Volume control of glial cells in abnormal osmotic medium may--on a cellular basis--reflect fundamental adaptive processes of central nervous tissue. Knowledge of the physiological and biochemical basis of cell volume control is not only of scientific interest but also of therapeutical significance in patients suffering from cytotoxic brain edema.
...
PMID:Volume regulation and metabolism of suspended C6 glioma cells: an in vitro model to study cytotoxic brain edema. 664 Mar 40

The adhesion molecule on glia (AMOG) has been reported to function as cell adhesion molecule and also to constitute the beta 2-subunit of the murine Na,K-ATPase. In order to elucidate these functions in vivo, Magyar et al. have generated mice carrying a targeted deletion of the AMOG gene. These mice exhibit behaviourally normal development till postnatal day P16. At this time, they develop muscular weakness, incoordination, and tremor. Death invariably occurs 24-36 hours after onset of the symptoms. Histological and ultrastructural examination of brain sections show enlarged ventricles, brain edema, and swelling of astrocyte end feet. However, no disturbances of the architecture or cell migration in the brain can be detected. In order to identify long-term consequences of AMOG deficiency which might not yet be detectable at the time of death, we have established a CNS grafting model. The embryonal brain anlage (E10.5-E13.5) was grafted into the caudoputamen of wild type mice. The graft recipients are sacrificed up to 7 months after the procedure. Both wild type and AMOG deficient grafts develop and form solid neural tissue with neurons, myelinated axons, glial cells, and ventricular structures, as shown by histological and immunocytochemical analysis. However, no differences in grafts derived from wild type, heterozygous, and AMOG-deficient donors can be detected. Proliferation has been examined by BrdU immunocytochemistry. The blood-brain barrier as examined by repeated magnetic resonance imaging after injection of Gadolinium-DTPA has been shown to be largely reconstituted five weeks after grafting.
...
PMID:[Morphology and development of neural transplants of AMOG-deficient mice]. 753 17

Na(+)K(+)-ATPase activity, water content, and Na+/K+ concentrations in the parietal cortex were measured in untreated and phenytoin-treated rats following global cerebral ischemia. Inhibitory effects of phenytoin treatment on brain edema and changes in Na(+)-K+ concentration with ischemia or ischemia followed by recirculation of varying intervals were assessed. The cortical Na(+)-K(+)-ATPase activity increased in the phenytoin-treated group during and after ischemia. Based on these results, we conclude that phenytoin provides ischemic brain protection by activating cortical Na(+)-K(+)-ATPase activity and by reducing intracellular Na+ and water content.
...
PMID:Effect of phenytoin on cortical Na(+)-K(+)-ATPase activity in global ischemic rat brain. 762 69


<< Previous 1 2 3 4 5 Next >>

---