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)

Sodium selenite has been shown to inhibit Na,K-ATPase. Glutathione, at sufficient excess, is able to prevent or reverse the inhibition. Dithiothreitol can also reverse much of the inhibition, but KCN cannot. Selenomethionine does not inhibit Na,K-ATPase. The interactions of sodium selenite with Na,K-ATPase and glutathione may aid in understanding the early events in selenium cataractogenesis.
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PMID:Inhibition of Na,K-ATPase by sodium selenite and reversal by glutathione. 302 32

Rabbit corneas were isolated, denuded of epithelium, and perfused on the anterior and posterior surfaces with Krebs Ringer-bicarbonate with additions of 50 microM H2O2, 125 microM BCNU, or 100 microM ouabain. The permeability of the corneal endothelium to labelled mannitol and inulin was determined by adding these compounds to the endothelial perfusate and measuring the rate of appearance of radioactivity in the anterior perfusate. Both H2O2 and BCNU increased the flux of mannitol and inulin across the endothelium in a time dependent manner, but ouabain had no effect. Additions of glucose with H2O2 or of GSH with BCNU prevented the observed changes in permeability. ATPase activities in the endothelia of intact, isolated corneas were also determined following incubation in the same media. The only observable effects of H2O2 and BCNU were slight reductions in the activity of Na+ + K+ ATPase. It is concluded that permeability changes, the leak, are more critical than active transport processes, the pump, in determining the rate and extent of swelling that results from exposure of the cornea to these agents.
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PMID:Pump and leak in regulation of fluid transport in rabbit cornea. 316 May 43

The protective effect of geraniin (tannin from Geranium thunbergii) against oxidative damage was examined in the mouse ocular lens. Oxidative damage in the lens was induced by diamide, diazene dicarboxylic acid bis (N,N-dimethylamide); diamide oxidized the sulfhydryl groups in both the membrane and cytoplasm but did not increase lipid peroxide. Geraniin showed protective effects on the changes in the Na+/K+ ratio, GSH level, Na,K-ATPase activity, GSH reductase activity and the sulfhydryl level of the membranous protein in the diamide-treated lens, but such protective effects of geraniin were not observed in the cell-free system of the lens. In addition, geraniin itself was unable to reduce GSSG to GSH and also unable to inhibit the oxidative reaction of the sulfhydryl group to diamide. These results suggest that in the intact lens geraniin would act primarily on the lens cell membrane surface to inhibit an influx of diamide into the inner part of the plasma membrane and the cytoplasm, and consequently that geraniin may protect sulfhydryl groups in the cell membrane and cytoplasm from their oxidation by diamide and keep the redox system of the lens in a normal state.
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PMID:Effect of tannin on oxidative damage of ocular lens. 318 50

The role of reduced glutathione (GSH) in lens membrane function was studied by depleting GSH with 1-chloro-2,4-dinitrobenzene (CDNB), a reaction catalyzed by GSH-S-transferase. Depletion of GSH in the lens epithelium by 70-90% led to a decrease in uptake and increase in efflux of 86Rb. ATP levels and Na+/K+-ATPase activity were normal while there was a slight decrease in lactate production. The results provide the first direct evidence that depletion of endogenous GSH per se does not lead to inactivation of Na+/K+-ATPase. However, lenses deficient in GSH when challenged with a normally tolerated level of H2O2 showed significant inactivation of membrane ATPase without a further increase in membrane permeability. Pretreatment with CDNB resulted in a 3-fold stimulation of the hexose monophosphate shunt activity which is attributed to the unexpected finding of a significant increase in the level of oxidized glutathione in the lens. It is concluded that deficiency of GSH causes a marked increase in membrane permeability and such lenses are susceptible to oxidative damage resulting in inactivation of the Na+/K+ pump, thus leading to ionic changes and cataract development.
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PMID:Effect of glutathione depletion on cation transport and metabolism in the rabbit lens. 318 92

The presence of glutathione was demonstrated histochemically in livers of rats treated with diethylnitrosamine or N-nitrosomorpholine. Glutathione content was markedly elevated in adenosine triphosphatase-deficient, gamma-glutamyltranspeptidase-positive hyperplastic cell islands. This finding may partly explain the increased resistance of hyperplastic cells to cytotoxic actions of hepatocarcinogens.
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PMID:Histochemical demonstration of enhanced glutathione content in enzyme-altered islands induced by carcinogens in rat liver. 610 9

The effects of the SH-groups binding agent p-chloromercurybenzoate (rho CMB) and the SH-containing compounds dithiothreitol (DTT), beta-mercaptoethanol (ME) and reduced glutathione (GSH) on activation by Mg2+ and K+ of ATPase in plasma membrane preparations from corn sprout root cells were studied. Rho CMB inhibited the ATPase activity, the degree of inhibition being directly dependent on the increase of the inhibitor concentration (from 10(-6) up to 10(-4) M); the inhibition was eliminated by the SH-containing agents (25 mM). DTT and ME added to the homogenization medium and ME added to the reaction mixture produced different effects on the ATPase activity of the membranes depending on the nature of the cations added. In the absence of the additives the ATPase activity was somewhat decreased, showing a sharp rise in the presence of Mg2+; an addition of K+ to a Mg2+-containing medium further increased the enzyme activity. GSH had no effect on the ATPase activation by the cations.
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PMID:[The role of SH-groups in the development sensitivity of ATPase in plasma membranes of plant cells to ions]. 621 85

Intoxication of rats with paracetamol (2.0 g/kg, b. wt.,os) is not followed by peroxidative decomposition of liver microsomal lipids "in vivo" but seems to interfere with ATPase and 5'-Nucleotidase activity in isolated plasmamembranes. Treatment with reduced glutathione, cys=teine and 2. mercaptopropionylglycine results in partial protection against liver injury provoked by the toxin. However, these sulphydryl compounds are not able to prevent the fall of liver GSH content occurring after paracetamol.
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PMID:[Susceptibility of the liver to lipid peroxidation after treatment with paracetamol]. 626 99

Reduced glutathione (0.3 mM) stimulates the activity of sodium-potassium activated ATPase (Na+K+ATPase) by 54% in plasma membranes prepared from bovine corneal endothelial cells. Oxidized glutathione, however, has no effect on Na+K+ATPase activity in the same tissue, although it does inhibit magnesium activated ATPase (Mg++ATPase) by approximately 30%. Adenosine neither stimulates nor inhibits either Na+K+ATPase or Mg++ATPase in these plasma membranes. It is postulated that the stimulatory effect of glutathione on deturgescence stems from the direct reaction of the reduced form of the tripeptide on sulfhydryl groups located on plasma membranes of corneal endothelial cells. It is highly probable that these sulfhydryl groups are part of the Na+k+ATPase complex itself.
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PMID:The effects of glutathione and adenosine on plasma membrane ATPases of the corneal endothelium. An hypothesis on the stimulatory mechanism of perfused glutathione upon deturgescence. 627 70

Functional integrity of liver cell organelles in rats given the model abrupt cytotoxin 1,1-dichloroethylene (1,1-DCE) was examined by enzymatic histochemistry. Fasted 200-gm. male Sprague-Dawley rats were sacrificed 1, 2, 4, or 6 hours after an oral dose of 200 mg. of 1,1-DCE per kg. (in mineral oil) and 6 hours after 50, 100, or 150 mg. of 1,1-DCE per kg. Cubes of liver were quick frozen for histochemistry. Stage or degree of liver injury was assessed by histology and by measuring serum transaminase activities and liver ion levels. We found both early injury (2 hours following the 200-mg. per kg. dose) and slight injury (6 hours following the 50-mg. per kg. dose) characterized by: increases in liver sodium levels and striking decreases in the central area staining patterns of bile canaliculi membrane Mg++-ATPase, as well as of outer mitochondrial membrane monoamine oxidase and inner mitochondrial membrane succinate dehydrogenase and cytochrome oxidase. As injury progressed with time or increased in severity with dose, aberrations in the levels of other liver cell ions occurred, serum transaminase activities rose, and decreased staining of plasma membrane and mitochondrial membrane components were evident in progressively wider areas around the central vein. Glutathione depletion was panlobular. In contrast, only at later times (4 and 6 hours) and after the larger doses did alterations to functional components of the mitochondrial matrix, endoplasmic reticulum, lysosomes, and cytosol become evident in a narrow area around the central vein, which became necrotic. We consider these later appearing alterations secondary consequences of the midzonal necrosis and sinusoidal congestion produced by 1,1-DCE, whereas the plasma membranes and mitochondrial membranes appear to be primary foci of injury.
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PMID:Histochemical evidence that plasma and mitochondrial membranes are primary foci of hepatocellular injury caused by 1,1-dichloroethylene. 646 95

The mammalian lens contains an unusually high concentration of glutathione (GSH), the highest level being in the epithelium. GSH is present largely in the reduced state. The high concentration of GSH in a normal lens and the decreased concentration in most types of cataracts have led to many hypotheses on its role in cataract formation. These hypotheses are considered in the light of current evidence. GSH is synthesized and degraded in the lens. Both processes require ATP, derived largely from glycolysis. Carbohydrate metabolism is also involved in the maintenance of GSH in the reduced state. There is a direct link between the rate of formation of oxidized glutathione (GSSG) and the stimulation of the hexose monophosphate shunt through the generation of NADPH. One possible function of GSH in the lens is to maintain the thiol (SH) groups of proteins in the reduced state, thus preventing formation of high molecular weight (HMW) protein aggregates. The formation of HMW proteins in X-ray-induced cataracts through disulphide bond formation and the involvement of SH oxidation in HMW proteins isolated from human cataractous lenses suggest a role for GSH in protecting protein SH groups. GSH in the lens may also protect critical SH groups involved in regulating cation transport and permeability. Studies with mammalian lenses indicate that lowering the lens GSH concentration leads to increased permeability to cations and inactivation of Na+,K+-ATPase. A consequence of the changes in ion distribution is the inhibition of protein synthesis, which may explain the cessation of growth in cataractous lenses. GSH may also protect against oxidative damage to the lens. GSH metabolism is intimately involved in detoxification of H2O2, normally present in the aqueous humour. Lenses with impaired shunt activity or inhibited glutathione reductase are more susceptible to oxidative damage by peroxide. This may contribute to the formation of cataract.
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PMID:Metabolism and function of glutathione in the lens. 656 81


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