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)

We evaluated whether fish oil or vitamin E administration affected ethanol-induced changes in membrane ATPases. Male Wistar rats (225-250 g) were fed, through a gastric tube a liquid diet containing fish oil (25% of calories) and ethanol for one month. Another group of animals was given supplemental vitamin E (300 u/kg). In the pair-fed control animals, ethanol-derived calories were replaced with dextrose. The blood ethanol levels were maintained between 150 and 350 mg/dL. At sacrifice, the red cells were immediately washed with ice-cold saline, membranes were prepared and ATPases measured. These was no difference in the Na+K+ ATPase, Ca2+ ATPase and Mg2+ ATPase activities between the fish oil-dextrose and corn oil-dextrose groups. A decrease in Ca2+ ATPase and an increase in Na+K+ ATPase was seen with ethanol feeding; these change are similar to those seen in corn oil-ethanol fed rats. In contrast, Vitamin E administration prevented the ethanol-induced changes in ATPase. This observation provides support for the role of lipid peroxidation in alcohol-induced changes in cell membrane ATPase activities.
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PMID:Effect of fish oil and vitamin E on ethanol-induced changes in membrane ATPases. 805 50

At concentrations of 0.5 microM and upward, cyclosporin A (CsA) caused dose-related inhibition of the growth of a hamster renal tubular cell line (HAK ATCC; CCL15) in vitro. Inhibition of cell growth was due to the cytotoxic properties of CsA which were associated with enhancement of activity of phospholipase A2 (PLA2) according to the increased generation of arachidonic acid and lysophosphatidylcholine (LPC). Arachidonate per se, at concentrations of up to 20 microM, did not affect the growth of HAK cells, while cyclooxygenase and 5-lipoxygenase inhibitors failed to protect the cells against the antiproliferative effects of CsA. However, LPC caused dose-related inhibition of the growth of HAK cells. Moreover, coincubation with lysophospholipase or alpha-tocopherol (AT, vitamin E), a PLA2 inhibitory and lysophospholipid-complexing agent, protected the HAK cells against both CsA and LPC. The Na+, K(+)-ATPase activity of HAK cells was also inhibited by CsA, with the enzyme being protected by inclusion of AT or lysophospholipase. Increased activity of PLA2 and inhibition of Na+, K(+)-ATPase preceded cytotoxicity and cytolysis. Excessive production of lysophospholipids and consequent inhibition of Na+, K(+)-ATPase in renal tubular cells is a possible mechanism of CsA-induced nephrotoxicity. The protective effects of AT suggest that this agent may be clinically useful in preventing the renal side effects of CsA.
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PMID:Alpha-tocopherol prevents cyclosporin A-mediated activation of phospholipase A2 and inhibition of Na+, K(+)-adenosine triphosphatase activity in cultured hamster renal tubular cells. 817 26

The calcium uptake and ATPase activity were studied using fragmented sarcoplasmic reticulum (FSR) vesicles from normal and selenium (vitamin E)--deficient lambs. The latter group was suffering from white muscle disease (WMD). The calcium uptake of FSR vesicles from muscle of WMD lambs was reduced 10-fold as compared to those from normal lambs. An inverse relationship was found with the calcium uptake ability of the FSR vesicles and the severity of WMD. ATPase activity was nonsignificantly lower in vesicles from WMD lambs. The most active FSR vesicles from both normal and WMD lambs banded at 27% when purified on linear sucrose density gradients. The number of protein bands appearing in acrylamide gels of the purified vesicles appeared to be directly proportional to the severity of WMD. The 75Se cosedimented with the calcium uptake and ATPase activity when FSR vesicles from a lamb injected with 75Se-selenite were subjected to linear sucrose density gradient centrifugation, suggesting that selenium is incorporated into these vesicles. Injection of selenium into WMD lambs resulted in significantly greater calcium uptake activity in vesicles 18 and 38 days later as compared with untreated WMD lambs. Injection of selenium in WMD lambs resulted in a marked decrease in plasma CPK activity and a significant increase of glutathione peroxidase activity in the blood.
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PMID:Calcium uptake and ATPase activity of sarcoplasmic reticulum vesicles isolated from control and selenium deficient lambs. 821 48

The relationship between the phospholipase-stimulating and immunosuppressive properties of the riminophenazine anti-mycobacterial agent clofazimine and its experimental analogue, B669, has been investigated in vitro. At concentrations of 0.6 microM and upwards, both riminophenazines, particularly B669, caused dose-related inhibition of mitogen- and alloantigen-stimulated uptake of tritiated thymidine by human mononuclear leucocytes (MNL), while in short-term assays both agents increased the release of lysophosphatidylcholine (LPC) and arachidonic acid from these cells. Arachidonate per se at a concentration of 20 microM did not affect mitogen-activated lymphocyte proliferation, while cyclooxygenase and 5'-lipoxygenase inhibitors, as well as water- and lipid-soluble oxidant-scavengers and anti-oxidant enzymes, failed to protect the cells against the anti-proliferative effects of clofazimine and B669. However, LPC caused dose-related inhibition of lymphocyte proliferation. Moreover, co-incubation of NML with alpha-tocopherol (vitamin E), a lysophospholipid complex-forming agent, or with lysophospholipase, protected the cells against clofazimine and B669, as well as against LPC. Na+, K(+)-adenosine triphosphatase was identified as the primary target of riminophenazine/LPC-mediated inhibition of lymphocyte proliferation. Excessive release of anti-proliferative lysophospholipids during clofazimine or B669 treatment of mitogen- or antigen-activated lymphocytes is the probable biochemical mechanism of the immunosuppressive activity of these agents.
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PMID:Clofazimine and B669 inhibit the proliferative responses and Na+, K(+)-adenosine triphosphatase activity of human lymphocytes by a lysophospholipid-dependent mechanism. 826 51

The effect of vitamin E (VE) or diazepam (DZ) pretreatment on some carbohydrate metabolic aspects in the brains of stressed rats was studied. DZ and VE were given i.p. at doses of 5 mg/kg body wt for 6 days prior to subjecting the animals to single swimming stress (SSS). Pretreatment of the rats with DZ or VE diminished the stress-induced increases in plasma corticosterone and glucose levels and reversed the decrease due to stress on brain ATP, glucose, glycogen and pyruvate contents. The increase in brain ADP and lactate was brought back to levels which approached the pre-stressed values. Moreover, DZ and VE pretreatments helped in attenuating the stress-induced alteration in brain mitochondrial and cytosolic hexokinase as well as sodium, potassium adenosine triphosphatase (Na+,K(+)-ATPase) activities. The change in these metabolic parameters produced by VE pre-treatment was less than that exhibited by DZ. The effects of VE were explained in light of its antioxidant property in preventing the free radical production and lipid peroxide formation which are important factors in the pathogenesis of stress.
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PMID:Effect of pretreatment with vitamin E or diazepam on brain metabolism of stressed rats. 839 75

To clarify the pathogenesis of the vascular injury caused by the administration of anti-neoplastic drugs, cisplatin with lipiodol was infused into the superior mesenteric artery of rats. Morphological and biochemical changes in the vascular wall and the prophylactic effects of vitamin E were examined 4 days after administration. In the cisplatin-treated group, but not in the other groups, severe endothelial injury, such as vacuolation, subendothelial edema, and destruction of the internal elastic membrane, was observed. Superoxide dismutase, a potent scavenger of the superoxide anion, was markedly lower in the cisplatin group, and Na/K-ATPase, a marker of the plasma membrane, was also low in this group. These morphological changes were minimal, and enzyme activity was higher in the vitamin E-treated group than in the cisplatin-treated group. These findings indicate that endothelial injury after cisplatin administration could be caused by free radical-induced lipid peroxidation of the membrane system, and that such injury may be prevented by the co-administration of vitamin E.
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PMID:Vitamin E prevents endothelial injury associated with cisplatin injection into the superior mesenteric artery of rats. 853 Mar 21

The calmodulin-stimulated (Ca2+, Mg2+)-ATPase (calmodulin-ATPase) of the erythrocyte membrane is susceptible to oxidative stress induced by heme and non-heme iron. There is a time-and concentration-dependent inhibition of the calmodulin-ATPase activity when the erythrocyte membranes are treated with either iron or hemin. In the present study, the calmodulin-ATPase has been used as a model system to evaluate the protective effects of a vitamin E analog (U83836E) and two 21-aminosteroids (U74500A and U74389G) against calmodulin-ATPase inhibition induced by iron and hemin. The drugs, lazaroids from Upjohn, can significantly protect the enzyme against iron-induced inhibition and also causes a decrease in the formation of thiobarbituric acid reactive species, with an IC50 of 0.4 microM for the drug U83836E and 4 microM for the drug U74500A. The 21-aminosteroid U74389G does not restore iron-inhibited calmodulin-ATPase activity under similar conditions. At higher concentrations (> 100 microM) all three drugs inhibit the calmodulin-ATPase activity. None of the drugs tested can restore hemin-inhibited calmodulin-ATPase activity.
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PMID:Protection by lazaroids of the erythrocyte (Ca2+, Mg2+)-ATPase against iron-induced inhibition. 857 27

Treatment of bovine pulmonary artery smooth muscle tissue microsomes with H2O2 (1 mM) markedly stimulated protease activity tested with a synthetic substrate N-benzoyl-DL-arginine p-nitroanilide (BAPNA), and also enhanced Ca(2+)-ATPase activity. ATP-dependent Ca(2+) uptake was found to be stimulated upon treatment of the microsomes with H2O2. Pretreatment of the microsomes with vitamin E and aprotinin prevented the H2O2-induced stimulation of Ca(2+)-ATPase activity and also ATP-dependent Ca(2+) uptake. In contrast, H2O2-induced inhibition of Na(+)-dependent Ca(2+) uptake was reversed by vitamin E and aprotinin.
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PMID:Oxidant-mediated proteolytic activation of Ca(+)-ATPase in microsomes of pulmonary smooth muscle. 867 43

The oxidising actions of tert-butyl hydroperoxide (tBH) (0-3 mmol/l) on human erythrocyte membrane ion transport have been studied using measurements of 86Rb+ influx. Ouabain and bumetanide were used to distinguish Rb+ flux via the sodium pump (Na,K-ATPase), Na,K,2Cl cotransporter and through residual membrane permeability. The protective actions of antioxidants and related molecules (vitamin E, vitamin E acetate, Trolox, butylated hydroxytoluene (BHT) and dithioerythritol (DTE) were studied. The effects of tBH were concentration dependent and the mean residual (ouabain and bumetanide insensitive) Rb+ permeability was increased by a factor of 8.5 (S.E.M. 2.2, n = 15) by a 5-min exposure to 2 mmol/l tBH. This action was almost completely prevented by co-incubation with Trolox or BHT, and partially prevented by the presence of vitamin E or DTE. Incubation with 2 mmol/l tBH for 5 min increased intracellular Na+ by a factor of 1.8 (S.E.M. 0.1, n = 8) and reduced intracellular K+ by a factor of 0.93 (S.E.M. 0.03, n = 8). These effects were prevented by Trolox and partially prevented by vitamin E, whereas DTE and vitamin E acetate were ineffective. Incubation with 2 mmol/l tBH for 5 min reduced the mean apparent sodium pump Vmax by 43% (S.E.M. 4, n = 8). This effect was completely prevented by Trolox and partially prevented by vitamin E. Vitamin E acetate had no effect. The mean bumetanide-sensitive Rb+ influx via the Na,K,2Cl cotransporter was reduced by 30% (S.E.M. 8.7, n = 25) by a 5-min exposure to 2 mmol/l tBH. This action was variable and no significant actions of the antioxidants studied could be demonstrated. This study suggests that tBH-mediated oxidative damage occurs from a hydrophilic site and involves increased non-selective membrane cation permeability and inhibition of specific transport systems.
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PMID:The effects of tert-butyl hydroperoxide on human erythrocyte membrane ion transport and the protective actions of antioxidants. 873

We have investigated the effects of cyclosporin A (CsA, 3-50 ng/ml) in combination with the riminophenazine agents clofazimine and B669 (60-500 ng/ml) on the mitogen- and alloantigen-activated proliferative responses of human mononuclear leukocytes (MNL), as well as on the phospholipase A2 and Na+, K+- adenosine triphosphatase activities of these cells. When used in combination these agents caused inhibition of the proliferative responses of both mitogen- and alloantigen-activated MNL which was at least additive. Combinations of CsA with the riminophenazines also caused augmentative activation of PLA2 and inhibition of Na+, K+-ATPase. The inhibitory effects of these agents, both individually and in combination, on the Na+, K+-ATPase and proliferative responses of MNL were neutralized by the membrane-stabilizing, lysophospholipid complex-forming agent alpha-tocopherol (vitamin E, 20 microgram/ml). These observations suggest that combinations of CsA with riminophenazines cause interactive enhancement of the activity of PLA2 in MNL leading to lysophospholipid-mediated inactivation of Na+, K+-ATPase and consequent inhibition of the proliferative responses of these cells. In the therapeutic setting combinations of these agents may enable reduction in the dose of CsA required to achieve meaningful immunosuppression with a consequent decrease in the risk of chemotherapy-related organ toxicity.
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PMID:Augmentative inhibition of lymphocyte proliferation by cyclosporin A combined with the riminophenazine compounds clofazimine and B669. 884 96


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