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)

Chronic ethanol exposure causes alterations in biologic membranes of different cell types. (Na + K) adenosine triphosphatase (ATPase), a membrane-bound enzyme inhibited by the acute presence of ethanol, increases its activity in rat kidney after chronic ethanol consumption. The aim of this investigation was to evaluate the effect of ethanol on the modulation of (Na + K)-ATPase by glucocorticoids and mineralocorticoids in renal papillary collecting duct cells. Cultured renal papillary collecting duct cells were exposed to a medium containing 150 mM ethanol plus either 100 nM aldosterone or 10 nM dexamethasone. Control groups were cultured in the absence of ethanol and/or the hormones. Mg(2+)-ATPase was used as control enzyme. The activity of ATPases was measured by ATP hydrolysis. Ethanol increased the activities of (Na + K)-ATPase and Mg(2+)- ATPase in 29 and 33% of controls, respectively; only (Na + K)-ATPase activity was elevated in the presence of aldosterone or dexamethasone, whereas Mg(2+)-ATPase was unaltered by these hormones. The effects of aldosterone and dexamethasone on (Na + K)-ATPase activity were augmented by ethanol in 50 and 19% of controls, respectively. These results suggest that ethanol treatment enhances the upregulation of (Na + K)-ATPase activity by both aldosterone and dexamethasone, in cultured renal papillary collecting duct cells.
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PMID:Effect of ethanol on regulation of (Na + K)-adenosine triphosphatase by aldosterone and dexamethasone in cultured renal papillary collecting duct cells. 1262 30

The study investigates the effect of aqueous extract of fenugreek seeds (Trigonella foenum graecum) on lipid peroxidation and antioxidant status in experimental ethanol toxicity in rats. The ability of the seed extract to prevent iron-induced lipid peroxidation in vitro was also investigated. Ethanol feeding for 60 days resulted in significant increases in the activities of serum aspartate transaminase, alanine transaminase and alkaline phosphatase. The levels of serum lipid hydroperoxides and thiobarbituric acid reactive substances in liver and brain were also significantly elevated. Significantly lower activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase and glutathione reductase were observed in liver and brain accompanied by depletion in glutathione, ascorbic acid and alpha-tocopherol concentrations. Activity of Ca(2+) ATPase in brain was significantly lowered. Simultaneous administration of aqueous extract of fenugreek seeds with ethanol prevented the enzymatic leakage and the rise in lipid peroxidation and enhanced the antioxidant potential. The seeds exhibited appreciable antioxidant property in vitro which was comparable with that of reduced glutathione and alpha-tocopherol. Further, histopathological examination of liver and brain revealed that, aqueous extract of fenugreek seeds could offer a significant protection against ethanol toxicity.
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PMID:Protective effect of fenugreek (Trigonella foenum graecum) seeds in experimental ethanol toxicity. 1291 70

The study investigates the cytoprotective effect of taurine on ethanol-induced alterations in lipids and enzymes involved in ion-transport in rat tissues. Male albino rats were divided into 4 groups (n = 8) and maintained for 28 days as follows: control group, ethanol (6 g/kg/day) group, ethanol plus taurine (10 g/kg diet/day) group and control plus taurine group. Ethanol administration caused significant increases in the lipids in plasma and tissues, such as liver, kidney and brain, together with reductions in the activities of ATPases in tissues as compared to control animals. Histological studies revealed lipid accumulation and inflammatory cell infiltrates in the liver and kidney while edematous changes were observed in the brain. Simultaneous administration of taurine along with alcohol attenuated the rise in lipid levels and normalized ATPase activities. Histological changes were alleviated on treatment with taurine. The study suggests a bioprotective effect of taurine in ethanol intoxication.
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PMID:Taurine prevents ethanol-induced alterations in lipids and ATPases in rat tissues. 1622 40

A possible involvement of two different systems in proton translocation was investigated by simultaneous measurement of transmembrane electron flow and proton secretion in a pH-stat combined with a redoxstat. The pH gradient between cytoplasm and apoplast is probably maintained by an H(+) -pumping ATPase and by a second proton extrusion system, which seems to be linked to a redox chain with NAD(P)H as electron donor. Indole acetic acid inhibits both e(-) and H(+) efflux, but only if the ;electron draw' from the outside is not too high. The electron draw depends on the hexacyanoferrate level at the plasmalemma surface and on the Ca(2+) concentration. The inhibiting effect of auxin on e(-) and H(+) efflux in the presence of hexacyanoferrate can be only detected at low levels of bivalent cations and of the artificial electron acceptor. The inhibition of e(-) and H(+) efflux by auxin requires high oxygen levels. The influence of auxin on both e(-) and H(+) transfer disappears below 2 kilopascals O(2), a level which does not influence respiration. Ethanol and fusicoccin do not increase the e(-) flux, probably because the electron transfer from the plasma membrane to HCF III is the limiting step. If electron transfer is reduced by IAA pretreatment, ethanol increases e(-) flux. Fusicoccin decreases e(-) and increases H(+) efflux if the rates have been lowered previously by indole acetic acid pretreatment. This effect depends on high oxygen levels and is reversible by lowering oxygen pressure. Auxin and Ca(2+) change e(-) flow and H(+) ejection in a 1:1 ratio.
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PMID:Hormone action on transmembrane electron and h transport. 1666 28

Ethanol tolerance, ATPase activity and the lipid composition of the plasma membrane to study potential relationship among them were examined in five different wine yeast strains. Yeast cells were subjected to ethanol stress (4% v/v). Principal component analysis of the results revealed that the wine yeasts studied can be distinguished in terms of ATPase activity and oleic acid (C18:1), and palmitoleic acid (C16:1), in plasma membrane. Multiple regression analysis was used to identify a potential influence of some components of the plasma membrane on ethanol tolerance and ATPase activity. Based on the results, the ergosterol, oleic acid and palmitoleic acid are highly correlated with ATPase activity and ethanol tolerance. Ethanol tolerance and the ATPase activity of the plasma membrane were correlated at the 96.64% level with the oleic acid and ergosterol in plasma membrane. The Saccharomyces cerevisiae var. capensis flor yeast strain, which exhibited the highest ergosterol concentration in plasma membrane when grown in the presence of 4% v/v ethanol, was found to be the most ethanol-tolerant.
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PMID:Relationship between ethanol tolerance, H+ -ATPase activity and the lipid composition of the plasma membrane in different wine yeast strains. 1669 Jan 48

Hepatic injury elicits intracellular stress that leads to peroxidation of membrane lipids accompanied by alteration of structural and functional characteristics of the membrane, which affects the activity of membrane-bound ATPases. We have explored the effect of leptin on hepatic marker enzyme and membrane-bound adenosine triphosphatases in ethanol-induced liver toxicity in mice. The experimental groups were control, leptin (230 microg kg(-1), i.p. every alternate day for last 15 days), alcohol (6.32 g kg(-1), by intragastric intubation for 45 days), and alcohol plus leptin. Ethanol feeding to mice significantly (P < 0.05) elevated the plasma leptin, alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT) and hepatic lipid hydroperoxides (LOOH), and plasma and hepatic total ATPases, Na(+), K(+)-ATPase and Mg(2+)-ATPase. There was a significant decrease in Ca(2+)-ATPase and reduced glutathione (GSH). Leptin injections to ethanol-fed animals further elevated the levels of hepatic LOOH, plasma and hepatic total ATPases, Na(+), K(+)-ATPase and Mg(2+)-ATPase, while the Ca(2)-ATPase and GSH were decreased significantly. In addition, leptin administration was found to increase the plasma levels of leptin, ALT, ALP, GGT, Na(+) and inorganic phosphorous, and decrease the levels of K(+) and Ca(2+) in ethanol-fed mice. These findings were consistent with our histological observations, confirming that leptin enhanced liver ailments in ethanol-supplemented mice.
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PMID:Effect of leptin administration on membrane-bound adenosine triphosphatase activity in ethanol-induced experimental liver toxicity. 1687 59

The pathologic activation of proteases within the pancreatic acinar cell is a key initiating event in acute pancreatitis. Past studies have suggested that the generation of a low-pH environment is critical to this process. Vacuolar adenosine triphosphatase (vATPase) is a multiprotein complex that transports protons across cellular membranes. Activation of the vATPase requires assembly of the soluble (V(1)) subunits on the membrane subunits (V(0)). It is found that conditions that cause protease activation in the acinar cell also cause assembly of V(1) on V(0). Further, inhibitors of vATPase block this protease activation. Ethanol and butanol sensitize the acinar cell to cholecystokinin-induced zymogen activation; vATPase inhibitors also blocked this activation. Activation of the vATPase may be central to the pathologic activation of proteases in the acinar cell and may also modulate the sensitizing effects of alcohols.
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PMID:Vacuolar adenosine triphosphatase and pancreatic acinar cell function. 1695 63

An endogenous natriuretic and vasoconstrictor Na/K-ATPase inhibitor, marinobufagenin (MBG), is implicated in NaCl-induced hypertension and in ethanol addiction. In rats, MBG suppresses voluntary alcohol intake, while immunization against MBG induces alcohol-seeking behavior. Since alcohol withdrawal is associated with elevation of blood pressure (BP) and renal sodium retention, we hypothesized that MBG mediates pressor response to ethanol withdrawal. In male Sprague-Dawley rats, forced ethanol intake (20% v/v, 2.8+/-0.2 g/day for 7 days) did not affect BP and MBG excretion. Ethanol withdrawal was associated with a 21 mm Hg increase in BP, a 10% decrease in hematocrit, and a three-fold increase in renal MBG excretion. In vivo administration of anti-MBG antibody to rats prevented withdrawal-induced BP elevation. Therefore, MBG mediates pressor response to ethanol withdrawal, and may link mechanisms of ethanol dependence and hypertension.
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PMID:Endogenous bufadienolide mediates pressor response to ethanol withdrawal in rats. 1768 16

Ethanol (164 mm) produced reproducible relaxations in isolated mouse esophageal strips. Hexamethonium (10-500 microm), a ganglionic blocking agent, and lidocaine (10-100 microm), a local anesthetic agent, failed to affect the relaxations induced by ethanol in the mouse esophagus. Although verapamil (10-500 microm), a selective blocker of L-type Ca(2+) channels, failed to affect the relaxations to ethanol, ruthenium red (10-100 microm), a selective blocker of ryanodine receptors (intracellular Ca(2+) channels), and cyclopiazonic acid (1-10 microm), a selective blocker of sarcoplasmic reticulum Ca(2+) ATPase (SERCA), significantly inhibited these relaxations. In addition, tetraethylammonium (10-100 microm), a potassium-selective ion channel blocker and N(omega)-nitro-l-arginine (l-NOARG; 10-500 microm), a specific inhibitor of nitric oxide synthase (NOS), neomycin (10-500 microm), a phospholipase C inhibitor and indomethacine (1-10 microm), a non-selective COX inhibitor, significantly inhibited the relaxations induced by ethanol. In contrast ouabain (10-100 microm), an inhibitor of Na(+)-K(+)-ATPase, failed to cause significant alteration on these relaxations in the same tissue. The results of the present study suggest that the inhibitory effect of ethanol on the mouse esophagus may be direct effect of ethanol on the muscle tissue rather than neuronal effect. In addition, intracellular but not extracellular Ca(2+) may have a role on ethanol-induced relaxations in isolated mouse esophageal strips. Potassium channels and nitric oxide may also have a role on these relaxations. Similarly, phospholypase C and arachidonic acid pathways may contribute the relaxations to ethanol. However Na(+)-K(+)-ATPase may not have a role on relaxations induced by ethanol in the mouse esophagus.
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PMID:Ethanol-induced relaxation of mouse esophagus: subcellular mechanisms. 1973 2

Ethanol intoxication resulted in high extent of lipid peroxidation, and reduction in antioxidant defenses (decreased GSH, GSH/GSSG ratio, and catalase, SOD and GPx activities) and (Na+/K+)-ATPase activity in kidney. Alpha-tocopherol treatment effectively protected kidney from ethanol induced oxidative challenge and improved renal (Na+/K+)-ATPase activity. Ethanol induced oxidative stress in the kidney and decreased (Na+/K+)-ATPase activity could be reversed by treatment with ascorbic acid.
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PMID:Effect of alpha-tocopherol supplementation on renal oxidative stress and Na+/K+ -adenosine triphosphatase in ethanol treated Wistar rats. 1976 Oct 47


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