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)

Using the fluorescent probe technique, it was shown that activation of lipid peroxidation decreases the value of transmembrane potential of rat brain synaptosomes. Depolarization of synaptosomes may be due to the impairment of the "barrier" properties of synaptosomal membranes and the decrease in Na,K-ATPase activity. alpha-Tocopherol and its model derivative devoid of the phytol chain--2,2,5,7,8-pentamethyl-6-oxychromanol--stabilize the transmembrane potential value during inhibition of lipid peroxidation. alpha-Tocopherol acetate causes no stabilizing or inhibiting effects. Unlike 2,2,5,7,8-pentamethyl-6-oxychromanol, alpha-tocopherol exerts a structuralizing action which manifests itself in the stabilization of the synaptosomal membrane potential during incomplete inhibition of lipid peroxidation. The previously established ability of alpha-tocopherol to protect synaptosomes from the damaging action of phospholipases and the experimental results of this work permit to regard vitamin E as a universal stabilizer of brain synaptosomal membranes.
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PMID:[Mechanism of the stabilization of synaptosomes with alpha-tocopherol during activation of lipid peroxidation]. 369 20

We studied the effect of arachidonic acid on function and CPK release of normal, ischemic and reperfused isolated rat hearts. Under control conditions arachidonate (10 micrograms/ml) produced a transient inotropic effect which gradually reversed during a 90 minute perfusion. Creatinephosphokinase (CPK) release was augmented by arachidonic acid, particularly under high flow (pre-ischemia and reperfusion) conditions. Recovery of contractility following reperfusion of ischemic myocardium was significantly depressed by arachidonic acid. Vitamin E (100 ng/ml) an antioxidant and free radical scavenger, reduced the enzyme leakage and enhanced recovery of contractility of reperfused myocardium. It also prevented the depression in contractility during control perfusion. Similar protective effects were observed by perfusing the heart with reduced calcium but not by nifedipine; a calcium channel blocker, indomethacin; a prostaglandin synthesis inhibitor or nordihydroguarietic acid; a lipoxygenase inhibitor. Arachidonic acid also inhibited membrane Na+/K+-ATPase although it is unlikely that this property mediated its cardiotoxic influence since it was not prevented by vitamin E. In addition, we observed that arachidonic acid increased the coronary resistance of isolated hearts, probably through enhanced calcium influx as this constriction was reduced by low calcium as well as by nifedipine. Thus, arachidonic acid possesses distinct properties. Its cardiotoxic influence is likely mediated by free radical generation.
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PMID:Toxic properties of arachidonic acid on normal, ischemic and reperfused hearts. Indirect evidence for free radical involvement. 392 Jun 82

Vitamin E is known to have an interaction with pyridoxine. To understand the functional significance of this interaction a study was carried out on the effect of simultaneous administration of vitamin E and pyridoxine on erythrocyte membrane Na+K+ ATPase activity. Adult male volunteers belonging to low socio-economic class with prior consent were used as subjects for the study. The results of the study have shown that administration of vitamin E alone brings about a transient increase in the total and ouabain insensitive Na+K+ ATPase. Administration of B6 along with vitamin E brought about an increase in the total and true Na+K+ ATPase activity. B6 administration alone showed a statistically insignificant increase in true ATPase activity. The results of the study are interpreted to show that administration of vitamin E along with B6 is beneficial to membrane function.
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PMID:Effect of simultaneous administration of vitamin E and pyridoxine on erythrocyte membrane Na+K+ ATPase activity. 609 64

Feeding rats the diet enriched with vitamin E or addition of alpha-tocopherol to the suspension of sarcoplasmic reticular membranes of rat and rabbit skeletal muscles protects Ca2+-dependent ATPase against thermal inactivation aggravated by the action of free fatty acids.
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PMID:[Vitamin E protection of membranes of the sarcoplasmic reticulum against the damaging effect of free fatty acids]. 622 47

The effects of temperature on reconstituted sarcoplasmic Ca-ATPase preparations from vitamin E-deficient dystrophic and control rabbits were studied. Delipidated Ca-ATPase from vitamin E-deficient sarcoplasmic reticulum (SR) reconstituted with lipid of control SR exhibited properties similar to preparations reconstituted with lipid of vitamin E-deficient SR, namely low Ca-ATPase activity and a linear Arrhenius plot of enzyme activity. On the other hand, delipidated control SR Ca-ATPase reconstituted with lipid of vitamin E-deficient SR showed a reduction in activity but retained the discontinuity in the Arrhenius plot. These results indicated that the altered property of sarcoplasmic Ca-ATPase from vitamin E-deficient dystrophic rabbit was associated with the protein and not the lipid component.
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PMID:Altered property of sarcoplasmic Ca-ATPase from vitamin E-deficient dystrophic rabbit is associated with the protein and not the lipid component. 623 17

The mechanism of light-induced changes in the activity of Na,K-ATPase from plasma membranes (PM) of photoreceptor cells was studied in vitro. Illumination resulted in inhibition of the ATPase activity and an increase of 18O exchange between water and Pi. The maximum light effect was revealed when the PM contained both the inner segments of the rods (RIS) and rod outer segments (ROS) of the photoreceptor cells. Lipid peroxidation stimulated by the FeSO4+ascorbate system induced a decrease of the ATPase activity. Antioxidants (ionol, Na2SeO3, vitamin E) prevented the effect of the lipid peroxidation products on NA,K-ATPase and the photoinduced changes of the enzyme activity. It is supposed that the photoinduced changes of the Na,K-ATPase activity in vitro are due to lipid peroxidation of photoreceptor PM.
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PMID:[Light-induced changes in activity of Na, K-ATPase from the retinal photoreceptors of vertebrates: possible mechanism]. 624 78

Several membrane properties of vitamin E-deficient and normal erythrocytes were studied after incubation of these cells with hydrogen peroxide. Measurements of mean corpuscular volume, cation permeability, membrane Na+, K+ ATPase activity, red cell filterability through 5 mu millipore filters, and membrane protein pattern on sodium dodecyle sulfate-gel electrophoresis revealed marked alterations before lysis. Vitamin E sufficient cells were unaffected by a similar incubation with hydrogen peroxide. We speculate that the changes in membrane function, which follow peroxidant injury, contribute to the shortened red cell survival in the vitamin E deficient state.
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PMID:Properties of vitamin E-deficient erythrocytes following peroxidant injury. 629 51

This work reports a study about the influence of some lipophilic substances like cholesterol, calciferol and tocopherol on the ATP-hydrolase activity in mitochondria. It is found that the steroids cholesterol and calciferol inhibit ATPase activity and behave like uncompetitive factors towards the enzymatic kinetics. Tocopherol, instead, affects significantly only the DCCD sensitivity of ATPase. Such effects are very probably due to the action of the physico-chemical state of th mitochondrial membrane produced by these lipophilic compounds.
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PMID:Effect of some lipophilic substances on mitochondrial ATPase. 644 55

Male rats fed on pellet diet to an average weight of 105 g were placed on a vitamin E deficient diet containing 20% coconut oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Rats on 20% casein diet showed a definite weight loss but not so at the 10% casein level. A marked increase in the liver in vitro lipid peroxidation was observed at both protein levels. Feeding of retinyl palmitate at 100,000 IU/100 g body weight for 4 consecutive days inhibited the liver, brain and kidney in vitro peroxidation; megadoses of ascorbic acid produced less inhibition of the liver peroxidation, but the same degree of inhibition for brain and kidney peroxidation as in vitamin A loaded rats. Both dietary palmitate or ascorbic acid. Acetylcholine esterase and ATPase, two of the membrane enzymes of erythrocytes, were depressed in all the groups. The glutathione content of erythrocytes was increased in rats given ascorbic acid. In all the groups the higher dietary protein levels produced greater loss of body and tissue weights. It is concluded vitamin E deficient diet supplemented with dietary coconut oil (saturated fat) induces increased in vitro lipid peroxidation and oxidative lysis of erythrocytes and that megadoses of vitamin A or C suppress the in vitro lipid peroxidation but enhance the lysis.
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PMID:Effect of dietary coconut oil and casein and megadoses of vitamin A or C on tissue lipid peroxidation and hemolysis in vitamin E deficiency. 665 Mar 2

Rats were maintained on a vitamin E free diet containing 20% safflower oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Enhanced in vitro tissue lipid peroxidation and lysis of erythrocytes were noticed at both the protein levels. A reduction in body mass and tissue weights were observed in both the protein groups but more so at 20% protein level. Feeding of retinyl palmitate (100 000 IU/100 g body weight) for 4 consecutive days to -E rats inhibited liver and kidney in vitro lipid peroxidation. Ascorbic acid (150 mg/100 g body weight) given orally for 5 days to -E rats inhibited liver brain and kidney in vitro peroxidation. Lysis of erythrocytes from -E rats was further increased by dosing with both the vitamins "A" and "C", the latter being more effective. The stromal enzymes acetyl choline esterase and ATPase were lowered, following the hemolysis profile of the erythrocytes from the different groups. Glutathione content of erythrocytes were unaffected except in -E +C group. In all groups the higher protein level (20%) produced greater lysis as compared to 10% level. It is concluded that 20% protein is more injurious in vitamin E deficiency simultaneously made hypervitaminosis A or C.
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PMID:Effect of dietary protein and hypervitaminosis A or C on tissue peroxidation and erythrocyte lysis of vitamin E deficiency. 716 Sep 64


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