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 aim of this study was to estimate the anticataract action of vitamin E using an in vitro methylprednisolone (MP)-induced cataract model. The same severity of early cortical cataract was induced in lenses isolated from male Wistar rats aged 6 weeks by incubation with MP (1.5 mg/ml) in TC-199 medium. The cataractous lenses showed slight increases in lipid peroxide (LPO) content and Na+/K+ ratio and slight decreases in reduced glutathione (GSH) content and glyceraldehyde-3-phosphate dehydrogenase (GAP-DH), a sensitive index of oxidative stress, and Na+,K(+)-ATPase activities. When the cataractous lenses were further incubated in TC-199 medium with and without vitamin E (250 micrograms/ml) for 48 h, the progression of cataract was prevented in the vitamin E-treated lenses, but not in the vitamin E-untreated lenses. The vitamin E-untreated lenses showed a decrease in vitamin E content and an increase in water content in addition to further increases in LPO content and Na+/K+ ratio and further decreases in GSH content and GAP-DH and Na+,K(+)-ATPase activities. In contrast, the changes of these components and enzymes except for GSH were attenuated in the vitamin E-treated lenses. From these results, it can be estimated that vitamin E prevents in vitro cataractogenesis in rat lenses treated with MP by protecting the lenses against oxidative damage and loss of membrane function.
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PMID:Anticataract action of vitamin E: its estimation using an in vitro steroid cataract model. 888 85

Lipid peroxidation is considered as one of the manifestations of cellular damage in the toxicity of ochratoxin A (OA). OA; its three natural analogs, OB, OC, and Oalpha; and four synthetic analogs, d-OA, the ethylamide of OA (OE-OA), O-methylated OA (OM-OA), and the lactone-opened OA (OP-OA) were used to study free radical generation in bacteria with Bacillus brevis as a model system. The uptake of the different ochratoxins by B. brevis varied substantially depending on the molecular structures. Electron paramagnetic resonance spectroscopy using alpha-(4-pyridyl-1-oxide)-N-tert-butyl nitrone as a spin trapping agent showed an enhanced free radical generation due to the addition of OA and most of the analogs. The EPR signals could be further enhanced by the addition of Ca2+, a calcium ionophore and an ATPase uncoupler, whereas they were eliminated by incubating the growing cells with vitamin E. The spin adduct hyperfine splitting constants indicate the presence of alpha-hydroxyethyl radicals resulting from generated hydroxyl radicals, which are trapped by alpha-(4-pyridyl-1-oxide)-N-tert-butyl nitrone. The results further suggest that OA induces free radical production in this model system by enhancing the permeability of the cellular membrane to Ca2+.
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PMID:Free radical generation as induced by ochratoxin A and its analogs in bacteria (Bacillus brevis). 891 Mar 17

Microsomes isolated from bovine pulmonary artery smooth muscle tissue treated with the oxidant t-buOOH stimulated Ca2+ ATPase activity dose-dependently as also protease activity when tested with a synthetic substrate N-benzoyl-DL-arginine p-nitroanilide. At 300 microM, t-buOOH optimally stimulated these activities. Treatment of the microsomes with t-buOOH stimulated ATP dependent Ca2+ uptake while Na+ dependent Ca2+ uptake was inhibited by t-buOOH. Pretreatment of the microsomes with vitamin E (1 mM) and aprotinin (1 mg/ml) prevented t-buOOH caused stimulation of protease activity and Ca2+ ATPase activity, and also stimulation of ATP dependent Ca2+ uptake while t-buOOH caused inhibition of Na+ dependent Ca2+ uptake was reversed by vitamin E and aprotinin. Treatment of the microsomes with trypsin (1 microgram/ml) stimulated Ca2+ ATPase and ATP dependent Ca2+ uptake while Na+ dependent Ca2+ uptake was inhibited. Pretreatment of the microsomes with aprotinin prevented trypsin caused stimulation of Ca2+ ATPase and ATP dependent Ca2+ uptake, while trypsin caused inhibition of Na+ dependent Ca2+ uptake was reversed by aprotinin.
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PMID:Involvement of a protease in tert-butylhydroperoxide-mediated activation of Ca2+ ATPase in microsomes of pulmonary smooth muscle. 902 24

The in vitro effects of membrane lipid peroxidation on ATPase-ADPase activities in synaptic plasma membranes from rat forebrain were investigated. Treatment of synaptic plasma membranes with an oxidant generating system (H(2)0(2)/Fe(2+)/ascorbate) resulted in lipid peroxidation and inhibition of the enzyme activity. Besides, trolox as a water soluble vitamin E analogue totally prevented lipid peroxidation and the inhibition of enzyme activity. These results demonstrate the susceptibility of ATPase-ADPase activities of synaptic plasma membranes to free radicals and suggest that the protective effect against lipid peroxidation by trolox prevents the inhibition of enzyme activity. Thus, inhibition of ATPase-ADPase activities of synaptic plasma membranes in cerebral oxidative stress probably is related to lipid peroxidation in the brain.
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PMID:Sensitivity of ATPase-ADPase activities from synaptic plasma membranes of rat forebrain to lipid peroxidation in vitro and the protective effect of vitamin E. 913 34

Anti-cataract activity of vitamin E analog with shortened side chain--2'-4'-methyl-pentenyl-acetoxy-2,5,7-tetramethylchroman has been studied. It is shown on the model system that the analog of vitamin E inhibits the increase of the lens agent fluorescence under irradiation of its homogenates by polychrome light. Taking no negative effect on the lens capsule epithelium, the drug normalizes the content of vitamin E in the blood and increases activity of Na+, K+, ATPase in the cortex and capsule of rabbits lenses in dynamics under simulation of light cataract in vivo.
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PMID:[Anti-cataract activity of a vitamin E analog]. 922 55

The structural elucidation and mechanism of action of a potential component, LLU-alpha, of what is possibly a multifactorial complex known as "natriuretic hormone" was recently reported [Wechter, W.J. et al. (1996a) Proc. Natl. Acad. Sci. U.S.A. 93: 6002-6007]. "Natriuretic hormone," a long-sought factor, is believed to regulate extracellular fluid volume and consequently be pathomimetic for hypertension, cirrhosis, congestive heart failure and other volume expanded states. The studies reported herein further characterize LLU-alpha. The precursor of the endogenous LLU-alpha was demonstrated to be gamma-tocopherol by radiolabeling studies. The pharmacokinetics of infused rac-LLU-alpha proved to be biphasic (half-lives: 12 min and 6 h). Specificity of the inhibition of the 70 pS potassium channel of the thick ascending limb of the loop of Henle was examined with the natural S-enantiomer being the most potent known inhibitor whereas the analogous alpha-tocopherol metabolite, rac-5-Me-LLU-alpha, showed no inhibition. Rac-LLU-alpha does not inhibit two isozymes of the Na+/K+-ATPase. LLU-alpha is natriuretic acting via inhibition of the 70 pS potassium channel and not Na+/K+-ATPase, the assumed mechanism of action of the "natriuretic hormone." LLU-alpha, a metabolite of a vitamin, if it were found to play a role in the regulation of extracellular fluid volume, would be the second example of a vitamin acting as a precursor for a hormone. Of considerable interest is the fact that this manuscript reports the first biological activity of gamma-tocopherol, a member of the vitamin E complex.
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PMID:Endogenous natriuretic factors 7: biospecificity of a natriuretic gamma-tocopherol metabolite LLU-alpha. 926 27

The effect of cyclosporin A, a highly effective immunosuppressant, was investigated on hyperoxaluric rats with and without vitamin E pretreatment. Hyperoxaluria was induced by oral feeding of 3% ammonium oxalate in water for 3 days. Cyclosporin A (50 mg/kg body wt.) was administered for 3 days. Pretreatment with vitamin E (50 mg/100 g body wt., once a week for 3 weeks) was carried out before the administration of cyclosporin A and ammonium oxalate. Nonenzymatic ascorbate-induced lipid peroxidation was increased to 1.55-fold in either cyclosporin A-administered or hyperoxaluric rat kidney and liver when compared to control. The lipid peroxidation was further elevated to 1.9-fold when both cyclosporin A and ammonium oxalate were coadministered. The activities of renal and hepatic ATPase, glucose-6-phosphatase as well as the concentrations of thiols were decreased significantly (p < 0.001) when cyclosporin A was administered under hyperoxaluric condition. On pretreatment with vitamin E the cyclosporin A-induced biochemical changes observed in the presence of hyperoxaluria were abolished.
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PMID:Effect of cyclosporin A on tissue lipid peroxidation and membrane bound phosphatases in hyperoxaluric rat and the protection by vitamin E pretreatment. 935 65

The preventive action of vitamin E (Vit. E)-containing liposomes on cataractogenesis was examined in male Wistar rats (five weeks old) fed a 25% galactose diet. Vit. E-containing liposomes prepared with dipalmitoylphosphatidylcholine were instilled into both eyes three times a day over a 45-day period. Cataract appeared at 18-day galactose feeding and developed gradually thereafter. Simultaneous Vit. E-containing liposome instillation delayed this cataractogenesis. Lenses of 18-day galactose-fed rats showed decreases in Vit. E and reduced glutathione (GSH) contents and Na+, K(+)-ATPase activity and increases in lipid peroxide (LPO), galactitol, and water contents. Lenses of 45-day galactose fed rats showed decreases in GSH content and Na+,K(+)-ATPase activity and increases in Vit. E, LPO, galactitol, and water contents. Serum Vit. E and cholesterol levels decreased in 18-day galactose-fed rats, while both levels increased in 45-day galactose-fed rats. Simultaneous Vit. E-containing liposome instillation prevented these changes except for the changes of lenticular galactitol and water contents and serum Vit. E and cholesterol levels. These results indicate that simultaneously instilled Vit. E-containing liposomes can delay cataractogenesis in young adult rats fed a 25% galactose diet mainly by the antioxidative action of Vit. E contained in the instilled liposomes.
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PMID:Preventive action of vitamin E-containing liposomes on cataractogenesis in young adult rats fed a 25% galactose diet. 943 57

Hyperglycemia is the major causal factor in the development of diabetic vascular complications and can mediate their adverse effects through multiple pathways. One of those mechanisms is the activation of protein kinase C (PKC) by hyperglycemia-induced increases in diacylglycerol (DAG) level, partly due to de novo synthesis. The activation of PKC regulates various vascular functions by modulating enzymatic activities such as cytosolic phospholipase A2 and Na+,K+-ATPase, and gene expressions including extracellular matrix components and contractile proteins. Some of the resulting vascular abnormalities include changes in retinal and renal blood flow, contractility, permeability, proliferation, and basement membrane. Among the various isoforms of PKC predominantly the beta isoforms are activated in cultured vascular cells exposed to high glucose and vascular tissues isolated from animal models of diabetes mellitus. Administration of vitamin E, which decreases DAG level possibly through the activation of DAG kinase, prevents hemodynamic changes in retina and renal glomeruli of diabetic rats. In addition, the inhibition of PKC beta isoforms by a specific inhibitor (LY333531) can normalize the changes in gene expression of cytokines, caldesmon, and hemodynamics. These results provide supportive evidence that the activation of PKC, especially the beta isoforms, is involved in the development of diabetic vascular complications, and that PKCbeta inhibitors can be used in the treatment of diabetic vascular complications.
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PMID:Protein kinase C activation and its role in the development of vascular complications in diabetes mellitus. 946 65

We showed before that in cardiac myocytes partial inhibition of Na+/K+-ATPase by nontoxic concentrations of ouabain causes hypertrophy and transcriptional regulations of growth-related marker genes through multiple Ca2+-dependent signal pathways many of which involve Ras and p42/44 mitogen-activated protein kinases. The aim of this work was to explore the roles of intracellular reactive oxygen species (ROS) in these ouabain-initiated pathways. Ouabain caused a rapid generation of ROS within the myocytes that was prevented by preexposure of cells to N-acetylcysteine (NAC) or vitamin E. These antioxidants also blocked or attenuated the following actions of ouabain: inductions of the genes of skeletal alpha-actin and atrial natriuretic factor, repression of the gene of the alpha3-subunit of Na+/K+-ATPase, activation of mitogen-activated protein kinases, activation of Ras-dependent protein synthesis, and activation of transcription factor NF-kappaB. Induction of c-fos and activation of AP-1 by ouabain were not sensitive to NAC. Ouabain-induced inhibition of active Rb+ uptake through Na+/K+-ATPase and the resulting rise in intracellular Ca2+ were also not prevented by NAC. A phorbol ester that also causes myocyte hypertrophy did not increase ROS generation, and its effects on marker genes and protein synthesis were not affected by NAC. We conclude the following: (a) ROS are essential second messengers within some but not all signal pathways that are activated by the effect of ouabain on Na+/K+-ATPase; (b) the ROS-dependent pathways are involved in ouabain-induced hypertrophy; (c) increased ROS generation is not a common response of the myocyte to all hypertrophic stimuli; and (d) it may be possible to dissociate the positive inotropic effect of ouabain from its growth-related effects by alteration of the redox state of the cardiac myocyte.
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PMID:Intracellular reactive oxygen species mediate the linkage of Na+/K+-ATPase to hypertrophy and its marker genes in cardiac myocytes. 1038 43


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