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)

The calcium theory of neuronal damage has been recently adapted to subarachnoid haemorrhage (SAH). It is proposed that haemorrhagic insult to the brain causes free radical-mediated destructive reactions of membrane phospholipids, and the consequent decrease of phospholipid-dependent enzymatic activities, such as Na(+)-K+ ATPase. In the present study we have studied the effects of Nicardipine treatment on lipid peroxidation and Na(+)-K+ ATPase activity after experimental induction of SAH. SAH was induced in anaesthesized rats by slow injection of 0.3 ml of autologous arterial blood into the cisterna magna. We assessed the extent of lipid peroxidation by measuring the level of thiobarbituric acid reactive substances (TBARS) and Na(+)-K+ ATPase activity in 3 different rat brain areas (cerebral cortex, hippocampus and brain stem) of sham-operated (0.3 ml of mock CSF into cisterna magna) and at 1 hour, 6 hours and 48 hours after SAH induction; simultaneously, we investigated the capacity of cerebral lipid peroxidation by measuring the accumulation of TBRAS in homogenates of brain areas incubated under aerobic conditions. Na(+)-K+ ATPase activity decreased in the cerebral cortex at 1 hour and 6 hours and in brain stem at 1 hour after SAH, while the same enzymatic activity did not change in the hippocampus. There was no significant difference in lipid peroxide content between sham-operated and haemorrhagic animals; Nicardipine treatment reduced the TBRAS content and induced the recovery of Na(+)-K+ ATPase activity, exerting a brain protective role against the detrimental effects of the haemorrhage.
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PMID:Effects of nicardipine treatment on Na(+)-K+ ATPase and lipid peroxidation after experimental subarachnoid haemorrhage. 185 1

The production of oxygen-free radicals and their subsequent peroxidative action on membrane unsaturated fatty acids could be enhanced after subarachnoid hemorrhage. High-dose methylprednisolone (30 mg/Kg i.v.) treatment can antagonize acute SAH-induced brain hypoperfusion and protect the ultrastructural integrity of endothelial cell membranes. Experimental subarachnoid hemorrhage (SAH) was induced in anesthesized rats by slow injection of 0.3 ml of autologous arterial blood into cisterna magna. Tissue lipid peroxidation, quantified as thiobarbituric acid reactive material (TBAR) and Na(+)-K+ ATPase activity were assayed in three different rat brain areas (cerebral cortex, hippocampus and brain stem) of controls (without any surgical manipulation), sham-operated (0.3 ml. of mock CSF into cisterna magna) and after SAH induction, at 1 h, 6 h and 48 h. Na(+)-K+ ATPase activity decreased in the cerebral cortex at 1 h and 6 h and in brain stem at 1 h after SAH, while the same enzymatic activity was unchanged in the hippocampus. High-dose methyl-prednisolone treatment (started immediately after SAH induction) enhanced the Na(+)-K+ ATPase activity until control levels. There was no significant difference in lipid peroxide content between sham-operated and hemorrhagic animals; however, the injection itself induces a transient increase of TBAR (1 h after injection) and methylprednisolone treatment decreases the products of lipid peroxidation in all brain areas.
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PMID:Effects of high-dose methylprednisolone on Na(+)-K+ ATPase and lipid peroxidation after experimental subarachnoid hemorrhage. 217 70

Subarachnoid hemorrhage was produced experimentally in cats by intracisternal injection of non-heparinized autologous arterial blood obtained by cardiac puncture under ketamine and xylazine anesthesia. Cats were sacrificed at varying time intervals between 30 min and 7 days post ictus. Measurements of resting membrane potential were recorded from smooth muscle cells of the basilar artery. These measurements were obtained by impalement from the adventitial surface of isolated but otherwise intact segments of the artery using glass microelectrodes with tip sizes less than 0.1 micron. The resting membrane potential recorded in vitro from animals previously subjected to subarachnoid hemorrhage in vivo was consistently and significantly depolarized when compared to normal controls. This depolarization was present as early as 30 min post ictus. Addition of the cardiac glycoside, ouabain, in a concentration of 10(-5)M depolarized cells from both control and experimental animals. There is a significant electrogenic pump potential contribution to the resting membrane potential of vascular smooth muscle cells. Ouabain is a potent blocker of Na+, K+-ATPase, the enzyme responsible for maintaining the cation electrochemical gradients. The depolarization recorded in these cells following subarachnoid hemorrhage is not, therefore, due to impairment of the electrogenic pump. The significance and implications of these findings are discussed.
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PMID:Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em. 241 49

Subarachnoid hemorrhage (SAH) was produced in Sprague Dawley rats by injection of 0.30 mL of autologous arterial blood into the cisterna magna. Tissue lipid peroxide, quantified as thiobarbituric acid reactive material (TBAR), and Na+,K(+)-ATPase activity were assayed in three different rat brain areas (cerebral cortex, hippocampus, and brain stem) of sham-operated rats and in four hemorrhagic rat groups at 30 min, 1 h, 6 h, and 2 d after SAH. Na+,K(+)-ATPase activity decreased in the cerebral cortex at 30 min, 1 h, and 6 h and in the brain stem at 1 h after SAH induction, whereas enzymatic activity was unchanged in the hippocampus. There was no evident difference in lipid peroxide content between sham-operated animals and hemorrhagic animals. These results indicate that little modifications in lipid peroxidative process (as expressed in TBAR) are not responsible for changes in the ATPase activity.
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PMID:Experimental subarachnoid hemorrhage. Lipid peroxidation and Na+,K(+)-ATPase in different rat brain areas. 256 16

The phosphorylation of an M(r) 20,000 myosin light chain (MLC20) promotes the generation of contractile force through actin-myosin adenosine triphosphatase in most agonist-mediated vascular smooth muscle cell contraction. However, the role of calcium-mediated contractile processes in sustained arterial narrowing after subarachnoid hemorrhage remains unknown. In a femoral artery model of vasospasm, whole blood was applied to arteries in 54 rats for periods of 2 to 10 days; the contralateral artery treated with platelet-rich plasma served as matched control. During the early stage of vasospasm (Days 2-5), in the media of arteries exposed to blood, MLC20 phosphorylation (including diphosphorylated forms) increased significantly (30-38%; P < 0.05); total medial MLC20 during this interval was comparable to that in controls. After 5 days, however, total MLC20 decreased markedly (> 90%; P < 0.01) compared with controls; phosphorylated MLC20 was undetectable during this interval. MLC20-mediated contractile processes may be prominent in the early stages of arterial narrowing after subarachnoid hemorrhage; later stages are associated with the loss of MLC20 and the possible persistence of arterial narrowing by other mechanisms.
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PMID:The time course of myosin light-chain phosphorylation in blood-induced vasospasm. 764

1. In the present study we have studied the effects of deferoxamine treatment on lipid peroxidation and Na-K ATPase activity after experimental induction of subarachnoid haemorrhage (SAH) in guinea pigs. 2. We assessed the extent of lipid peroxidation by measuring the level of malondialdehyde and Na-K ATPase activity in 3 different groups (sham-operated, SAH, SAH + deferoxamine). 3. There was no significant difference in lipid peroxide content between sham-operated and haemorrhagic animals, but Na-K ATPase activity decreased after SAH. 4. Deferoxamine treatment reduced the malondialdehyde content and induced the recovery of Na-K ATPase activity, exerting a brain protective role against the detrimental effects of the haemorrhage.
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PMID:The effect of deferoxamine on brain lipid peroxide levels and Na-K ATPase activity following experimental subarachnoid hemorrhage. 792 96

It is reported that CNS hemorrhage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K(+)-ATPase activity measurement and spin-label studies were performed on crude synaptosomal membranes. Subarachnoid hemorrhage decreased Na+, K(+)-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.
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PMID:Effect of hyperbaric oxygenation on the Na+, K(+)-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage. 823 20

Changes in Ca(++)-adenosine triphosphatase (ATPase) activity in the plasma membrane of smooth-muscle cells in the basilar arteries of dogs with experimental subarachnoid hemorrhage (SAH) were examined. The study methods included electron microscopic histochemistry and bioassay of the enzyme that exports cytoplasmic Ca++ to extracellular spaces. The Ca(++)-ATPase activity in the basilar artery increased significantly in response to the application of vasoconstrictive agents (prostaglandin F2 alpha and a phorbol ester), but decreased significantly 24 hours after experimental SAH, inversely with basilar artery contraction. Dogs that had undergone two arterial blood injections (double SAH) exhibited a further decrease in Ca(++)-ATPase activity as well as persistent contraction of the basilar artery for a longer period (at least 7 days) than was seen in animals with a single arterial blood injection. Bioassay of the enzyme also demonstrated a decrease in vascular Ca(++)-ATPase activity in dogs subjected to double SAH. These findings suggest that the early occurrence of and long-lasting decrease in Ca(++)-ATPase activity in dogs with experimental SAH induces a persistent disturbance of Ca++ homeostasis and indicates that damage to the plasma membrane in the cerebral arterial smooth-muscle cells proceeds to myonecrosis after SAH.
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PMID:Changes in Ca(++)-ATPase activity in smooth-muscle cell membranes of the canine basilar artery with experimental subarachnoid hemorrhage. 828 66

Recent evidence indicates the presence of naturally occurring digitalis-like compounds in mammals, collectively known as either digitalis-like (DLF) or ouabain-like (OLF) factors, presumed to be endogenous hormones regulating the biological activity of the NA+/ K(+)-ATPase and its isoforms. This substance has been postulated to enhance renal tubular sodium excretion and to increase peripheral vascular resistance. Digoxin-like immunoreactive substance (DLIS) was observed in plasma of some patients with spontaneous subarachnoid haemorrhage (SSAH). Accumulating evidence suggests the central nervous system as a site of synthesis, but also as a site of hypertensinogenic action of endogenous cardioglycosides. The present study intends to establish the ratio of the DLIS in plasma to that in cerebrospinal fluid (CSF) in patients with SSAH and to investigate possible connection of this substance with development of arterial vasospasm. A prospective analysis of DLIS levels was performed on plasma and CSF samples obtained in 40 patients who had suffered a recent SSAH. DLIS levels were determined by the fluorescence polarisation immuno-assay method immediately after the admission to the Ward, and again seven days later. The comparison of CSF and plasma DLIS levels did not show statistically significant differences between the results--neither for the first (Z = 0.530; P = 0.591) nor for the seventh day after the disease onset (Z = 0.448; P = 0.654). Three possible hypothetical explanations of these results are offered: a) substance determined by digoxin immuno-assay has no essential likeness to digoxin; b) loss of the haemato-encephalic barrier integrity enabling free substance exchange between plasma and central nervous system; c) digoxin-like substance production within the central nervous system. Further, comparison of DLIS plasma levels (7th day from onset of SSAH) with angiography results showed that patients with multiple vasospasm had essentially higher plasma DLIS levels compared to patients with no vasospasms (Z = 2.59; P = 0.0097). The amount of extravasated blood, assessed on the basis of cranial CT scanning, was also connected with higher plasma DLIS levels (X2 = 3.29; P = 0.0305). The enhanced arterial narrowing which occurs in SSAH may be in part mediated by increased digitalis-like factor activity.
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PMID:Plasma and cerebrospinal fluid endogenous digoxin-like immunoreactivity in patients with aneurysmal subarachnoid haemorrhage. 1048 79

Oxidative stress plays an important role in the pathogenesis of amyotrophic lateral sclerosis (ALS). In the present study, we investigated the expression of two major human enzymes that prevent errors caused by 8-oxoguanine (8-oxoG), a mitochondrial form of 8-oxoG DNA glycosylase (hOGG1) and oxidized purine nucleoside triphosphatase (hMTH1). We also investigated the relationship between their expression and the 8-oxoG accumulation observed in the large motor neurons of the lumbar spinal cord in seven cases of adult onset sporadic ALS, four cases of subarachnoid hemorrhage (SAH) and four control cases. 8-oxoG immunoreactivity increased in most large motor neurons in both the ALS and SAH cases. However, the large motor neurons in the control cases often lacked hOGG1 immunoreactivity, although some neurons expressed hOGG1 in either homogeneous or fine granular patterns. In SAH cases, most large motor neurons showed a fine granular pattern proportional to the increased 8-oxoG immunoreactivity. However, only half of the remaining motor neurons in ALS expressed hOGG1 in the fine granular pattern, and the rest did not show any immunoreactivity. In addition, small aggregates of hMTH1 in the nuclei of the anterior horn cells were present in several ALS cases. Our results indicate that the oxidative damage accumulates in the mitochondria of motor neurons in ALS, and that hOGG1 does not repair the damage efficiently, which may lead to a loss of motor neurons in ALS.
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PMID:Impairment of mitochondrial DNA repair enzymes against accumulation of 8-oxo-guanine in the spinal motor neurons of amyotrophic lateral sclerosis. 1190 61


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