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)

The activity of Na+,K+ATPase, gamma-glutamyltranspeptidase, ceruloplasmin, total antioxidative activity of water-soluble antioxidants, the contents of vitamins C and E, free amino-nitrogen and peroxide resistance of erythrocytes were determined at the blood's plasma of healthy persons (120 persons) and suffered from aged cataract (437 persons) of three aged groups (up to 40 years, 40-60 years and elder then 60 years). We have shown, that changes, which has been connected with cataractogenesis and age dependent changes are not equal. The lowering of activity of Na+,K(+)-ATPase, gamma-glutamyltranspeptidase and level of vitamin E was expressed less during the ageing, then during the development of lenses opacification. The increase of activity of oxidase during the cataractogenesis is less significant, then age depended inhibition of this enzyme. The opposite tendency (the lowering of activity at the patients with cataract is more expressed, then compensatory activations of these parameters at the persons of the corresponding age with transparent lenses) was revealed for total antioxidative activity of water-soluble antioxidants.
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PMID:[Biochemical blood parameters in people with a normal crystalline lens and in cataracts]. 1044 69

It has been shown that the lipid composition of plasma membrane can be modified in vivo by dietary fat. It has also been observed that an increase in the cholesterol content of plasma membranes results in decreased activities of ATPases. In the present study, we evaluated the changes in the activities of ATPases from erythrocytes, hepatocytes, and kidney cortex caused by cholesterol-rich diet in rats and subsequently examined the role of vitamin E administration on the cholesterol-induced effects in these tissues. Administration of hypercholesterolemic diet to the rats for 4.5 months, significantly decreased membrane Na(+)-K(+)-ATPase and Ca+2-ATPase activities in comparison to the controls in all tissues studied. Vitamin E supplementation to the hypercholesterolemic rats led to a recovery in membrane ATPase activities. In conclusion, vitamin E supplementation to the rats provided protection against hypercholesterolemic diet-induced impairment of membrane-bound ATPases.
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PMID:Vitamin E and ATPases: protection of ATPase activities by vitamin E supplementation in various tissues of hypercholesterolemic rats. 1068 54

Vascular complications in diabetes mellitus are known to be associated with the activation of the protein kinase C (PKC) pathway through the de novo synthesis of diacylglycerol (DAG) from glycolytic intermediates. Specific PKC isoforms, mainly the beta- and delta-isoforms, have been shown to be persistently activated in diabetic mellitus. Multiple studies have reported that the activation of PKC leads to increased production of extracellular matrix and cytokines, enhances contractility, permeability and vascular cell proliferation, induces the activation of cytosolic phospholipase A2 and inhibits the activity of Na+-K+-ATPase. These events are not only frequently observed in diabetes mellitus but are also involved in the actions of vasoactive agents or oxidative stress. Inhibition of PKC by two different kinds of PKC inhibitors - LY333531, a selective PKC-beta-isoform inhibitor, and vitamin E, d-alpha-tocopheron - were able to prevent or reverse the various vascular dysfunctions in vitro and in vivo. Clinical studies using these compounds are now ongoing to evaluate the significance of DAG-PKC pathway activation in the development of vascular complications in diabetic patients.
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PMID:Protein kinase C activation and its pharmacological inhibition in vascular disease. 1110

We examined whether opacification of rat lenses treated with diethylmaleate (DEM), a depletor of reduced glutathione (GSH), is associated with membrane dysfunction. When isolated rat lenses were incubated with 2 mM DEM for 1, 6, and 24 h, a cortical opacity appeared at 6 h and was more pronounced at 24 h. This opacification was accompanied by decreases in GSH and vitamin E (Vit. E) content and Na+,K+-ATPase activity, and an increase in water content, but not by a change in the content of thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation. Vit. E co-treatment caused a partial prevention of opacification, a complete recovery of decreased Vit. E content, attenuation of decreased Na+,K+-ATPase activity, and a decrease in TBARS content in rat lenses treated with 2 mM DEM for 24 h. Neither opacity formation nor changes in Vit. E, TBARS, and water content and Na+,K+-ATPase activity occurred in rat lenses treated for 48 h with 2 mM l-buthionine-(S,R)-sulfoximine, an inhibitor of glutathione synthesis, although a marked GSH depletion was observed. These results suggest that opacification of isolated rat lenses treated with DEM could be associated with impairment of Na+,K+-ATPase rather than GSH depletion.
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PMID:Opacification of isolated rat lenses intoxicated with diethylmaleate: relation to lens membrane dysfunction. 1131 74

The major goal of this study was to examine the ability of several antioxidants namely, vitamin E, beta-carotene and N-acetylcysteine, to protect the brain from oxidative stress induced by lipopolysaccharide (LPS, endotoxin). LPS, a component of the bacterial wall of gram-negative bacteria, has been recognized as one of the most potent bacterial products in the induction of host inflammatory responses and tissue injury and was used in this study to mimic infections. LPS injection resulted in a significant increase in the stress indices, plasma corticosterone and glucose concentration, a significant alteration of the brain oxidative status observed as elevation of the level of malondialdehyde (MDA, index of lipid peroxidation) and reduction of reduced glutathione (GSH), and a disturbance in the brain energy metabolism presented as a reduction in the ATP/ADP ratio and an increase in the mitochondrial/cytosolic hexokinase ratio. However, the activities of brain superoxide dismutase and Na+, K+-ATPase and contents of cholesterol and phospholipids were not altered. Administration of the aforementioned antioxidants prior to LPS injection ameliorated the oxidative stress by reducing levels of MDA, restoring GSH content and normalizing the mitochondrial/cytosolic hexokinase ratio in the brain in addition to lowering levels of plasma corticosterone and glucose. In conclusion, this study showed the increased free radical generation during infections and LPS-induced stress. It also suggests that brain oxidative status and energy is disturbed.
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PMID:Protective effect of vitamin E, beta-carotene and N-acetylcysteine from the brain oxidative stress induced in rats by lipopolysaccharide. 1133 Dec 2

Although an excessive amount of circulating catecholamines is known to induce cardiomyopathy, the mechanisms are poorly understood. This study was undertaken to investigate the role of oxidative stress in catecholamine-induced heart dysfunction. Treatment of rats for 24 h with a high dose (40 mg/kg) of a synthetic catecholamine, isoproterenol, resulted in increased left ventricular end diastolic pressure, depressed rates of pressure development, and pressure decay as well as increased myocardial Ca2+ content. The increased malondialdehyde content, as well as increased formation of conjugated dienes and low glutathione redox ratio were also observed in hearts from animals injected with isoproterenol. Furthermore, depressed cardiac sarcolemmal (SL) ATP-dependent Ca2+ uptake, Ca2+-stimulated ATPase activity, and Na+-dependent Ca2+ accumulation were detected in experimental hearts. All these catecholamine-induced changes in the heart were attenuated by pretreatment of animals with vitamin E, a well-known antioxidant (25 mg/kg/day for 2 days). Depressed cardiac performance, increased myocardial Ca2+ content, and decreased SL ATP-dependent, and Na+-dependent Ca2+ uptake activities were also seen in the isolated rat hearts perfused with adrenochrome, a catecholamine oxidation product (10 to 25 microg/ml). Incubation of SL membrane with different concentrations of adrenochrome also decreased the ATP-dependent and Na+-dependent Ca2+ uptake activities. These findings suggest the occurrence of oxidative stress, which may depress the SL Ca2+ transport and result in the development intracellular Ca2+ overload and heart dysfunction in catecholamine-induced cardiomyopathy.
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PMID:Role of oxidative stress in catecholamine-induced changes in cardiac sarcolemmal Ca2+ transport. 1136 87

To elucidate the significance of oxidative stress in the modulation of endothelial functions, we examined the effects of H(2)O(2) on the expression of two endothelium-derived vasoactive peptides, endothelin (ET) and adrenomedullin (Am), and their interaction. H(2)O(2) dose dependently suppressed ET secretion and ET-1 mRNA expression in bovine carotid endothelial cells (ECs). Menadion sodium bisulfate, a redox cycling drug, also decreased ET secretion in a dose-dependent manner. Catalase, a H(2)O(2) reductase, and dl-alpha-tocopherol (vitamin E) significantly inhibited H(2)O(2)-induced suppression of ET secretion. Downregulation of ET-1 mRNA under oxidative stress was regulated at the transcriptional level. In contrast, H(2)O(2) increased Am secretion (and its mRNA expression) accompanied by the augmentation of cAMP production. Am, as well as 8-bromo-cAMP and forskolin decreased ET secretion in a dose-dependent fashion. Furthermore, an anti-Am monoclonal antibody that we developed abolished H(2)O(2)-induced suppression of ET secretion at 6-24 h after the addition of H(2)O(2). H(2)O(2) increased the intracellular Ca(2+) concentration ([Ca(2+)](i)). Moreover, treatment with ionomycin, a Ca(2+) ionophore, and thapsigargin, an inhibitor of endoplasmic reticulum ATPase, decreased ET secretion dose dependently for 3 h. These results suggest that the production of ET was decreased via activation of the Am-cAMP pathway and by the elevation of [Ca(2+)](i) under oxidative stress. These findings elucidate the coordinate expression of two local vascular hormones, ET and Am, under oxidative stress, which may protect against vascular diseases.
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PMID:Coordinate regulation of endothelin and adrenomedullin secretion by oxidative stress in endothelial cells. 1151 8

The effects of the environmental contaminants methylmercury (MeHg) and inorganic mercury (HgCl(2)) on cell viability, intracellular calcium concentration ([Ca(2+)](i)), and reactive oxygen species (ROS) generation were studied in rat cerebellar granule neuron cultures using fluorescent methods. MeHg exhibited an LC(50) (2.47 microM) tenfold lower than that of HgCl(2) (26.40 microM). To study the involvement of oxidative stress and Ca(2+) homeostasis disruption in mercury-induced cytotoxicity, we tested the neuroprotective effects of several agents that selectively interfere with these mechanisms. After a 24 hr exposure, the cytotoxic effect of both mercury compounds was reduced by thapsigargin, an inhibitor of endoplasmic reticulum Ca(2+)-ATPase; the Ca(2+) channel blocker flunarizine; and the Na(+)/Ca(2+) exchanger blocker benzamil. All these compounds decreased the mercury-mediated [Ca(2+)](i) rise. These results indicate that Ca(2+) influx through Ca(2+) channels and the Na(+)/Ca(2+) exchanger and Ca(2+) mobilization from the endoplasmic reticulum are involved in mercury-mediated cytotoxicity. The antioxidants probucol and propyl gallate reduced the HgCl(2) toxicity. Probucol and vitamin E partially inhibited the MeHg toxicity after a 24 hr period, whereas propyl gallate completely prevented this effect. Probucol slightly reduced ROS generation in methylmercury-exposed cultures and decreased mercury-mediated rise of [Ca(2+)](i). Propyl gallate abolished ROS generation and partially inhibited the increase of [Ca(2+)](i) induced by both mercury compounds. Propyl gallate also protected human cerebral cortical neuron cultures from the MeHg effect even after 72 hr of MeHg exposure, thus showing a long-lasting effect. Our data suggest that disruption of redox equilibrium and Ca(2+) homeostasis contribute equally to HgCl(2)-mediated toxicity, whereas oxidative stress is the main cause of MeHg neurotoxicity.
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PMID:Antioxidant compounds and Ca(2+) pathway blockers differentially protect against methylmercury and mercuric chloride neurotoxicity. 1159 10

Perchloroethylene (PER) administered by oral gavage for 15 consecutive days, at a dose of 3000 mg/kg body wt. decreased the activities of Na+, K(+)-ATPase and Mg(2+)-ATPase with an increase in the activity of Ca(2+)-ATPase. It also decreased RBC and platelet counts but the WBC count was found to be increased. An investigation of the relative importance of the modulators, vitamin E, 2-deoxy-D-glucose (2DG) and taurine in rendering protection to tissues against PER induced membrane damage was performed. PER administered mice were subjected to vitamin E (400 mg/kg body wt/day), 2DG (500 mg/kg body wt/day by i.p.) and taurine (100 mg/kg body wt/day) administration for 15 days to study their individual effect on ATPase and on certain hematological parameters. Vitamin E, 2DG and taurine treated mice showed a marked reversal of these metabolic changes related to membrane damage caused by PER. These results suggest that PER induced membrane damage may be associated with energy metabolism and hemolysis, which can be effectively prevented by these modulators.
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PMID:Protective role of vitamin E, 2-deoxy-D-glucose, and taurine on perchloroethylene induced alterations in ATPases. 1166 51

Diabetes-prone BHE/Cdb and Sprague-Dawley (SD) rats were studied with respect to mitochondrial (mt) function and mt gene expression. The BHE/Cdb rats carry mutations in the mt ATPase 6 gene that phenotype as decreased OXPHOS efficiency with subsequent development of impaired glucose tolerance. The base substitutions result in amino acid substitutions in the proton channel and this, in turn, affects the efficiency of energy capture in the ATP molecule. Feeding studies showed that BHE/Cdb rats required 10 times more vitamin E and three times more vitamin A in their diets than do normal SD rats. Vitamin A supplementation 'normalized' mt OXPHOS as well as increased the amount of ATPase subunit a protein in the mt compartment. Western blot analysis of retinoic acid receptors in the mitochondrial and nuclear compartments showed that these proteins were present in the mt compartment. The effect of the vitamin A supplementation plus the observation of retinoic acid receptors suggest that vitamin A functions to enhance the transcription of the ATPase 6 gene. Work with primary cultures of hepatocytes showed that not only does retinoic acid increase mitochondrial ATPase 6 gene expression but so too does the steroid hormone intermediate, dehydroepiandrosterone (DHEA). Triiodothyronine also plays a role in this process but not as an independent factor. Rather, this hormone potentiates the effects of retinoic acid and DHEA on ATPase gene expression. These results suggest that mt gene expression requires more than just the mt transcription factor A. More than likely the process requires a number of factors in much the same way as does nuclear gene expression.
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PMID:Role of vitamin A in mitochondrial gene expression. 1173 5


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