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 Na(+)-K+ ATPase activity and SH group content were decreased whereas malondialdehyde (MDA) content was increased upon treating the porcine cardiac sarcolemma with xanthine plus xanthine oxidase, which is known to generate superoxide and other oxyradicals. Superoxide dismutase either alone or in combination with catalase and mannitol fully prevented changes in SH group content but the xanthine plus xanthine oxidase-induced depression in Na(+)-K+ ATPase activity as well as increase in MDA content were prevented partially. The Lineweaver-Burk plot analysis of the data for Na(+)-K+ ATPase activity in the presence of different concentrations of MgATP or Na+ revealed that the xanthine plus xanthine oxidase-induced depression in the enzyme activity was associated with a decrease in Vmax and an increase in Km for MgATP; however, Ka value for Na+ was decreased. Treatment of sarcolemma with H2O2 plus Fe2+, an hydroxyl and other radical generating system, increased MDA content but decreased both Na(+)-K+ ATPase activity and SH group content; mannitol alone or in combination with catalase prevented changes in SH group content fully but the depression in Na(+)-K+ ATPase activity and increase in MDA content were prevented partially. The depression in the enzyme activity by H2O2 plus Fe2+ was associated with a decrease in Vmax and an increase in Km for MgATP. These results indicate that the depressant effect of xanthine plus xanthine oxidase on sarcolemmal Na(+)-K+ ATPase may be due to the formation of superoxide, hydroxyl and other radicals. Furthermore, the oxyradical-induced depression in Na(+)-K+ ATPase may be due to the formation of superoxide, hydroxyl and other radicals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of cardiac sarcolemma Na(+)-K+ ATPase by oxyradical generating systems. 749 43

The present paper shows that cultured bovine endothelial cells can be labeled with 3H-carnitine by incubation. This process is slow and is uphill, requiring Na+/K+ ATPase activity. After 3 days incubation isotopic equilibrium is reached, when the cells contain about 0.5 mM (total) carnitine at a medium concentration of about 3 microM. The plasmamembrane barrier is rather resistant to acidosis and oxygen free radicals (OFR). The rate of carnitine release increases significantly only at pH below 5.8. At pH 6.0 the release of stored carnitine can be initiated by the addition of D- or L-lactate. OFR, generated by the addition of xanthine and xanthine oxidase, did not affect carnitine release. Both mild acidosis and OFR left plasmamembranes of endothelial cells intact as judged by the absence of lactate dehydrogenase loss from the cells. Therefore, the known increase of capillary permeability during ischemia and reperfusion may not be due to plasmalemmal disruption of individual endothelial cells, but to increase of inter-endothelial spaces.
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PMID:Uptake and release of carnitine by vascular endothelium in culture; effects of protons and oxygen free radicals. 777 71

Formation of reactive oxygen species and disfunction of the excitatory amino acid (EAA) system are thought to be key events in the development of neuronal injury in several acute and long-term neurodegenerative diseases. Recent evidence suggests that the two phenomena may be interdependent. The present study is aimed at exploring possible molecular mechanisms underlying oxygen radical-EAA interaction. Exposure of cortical astrocytic cultures to either xanthine + xanthine oxidase (X/XO), a free radical-generating system, or hydrogen peroxide (H2O2) results in a marked decrease of high-affinity glutamate transport. Within 10 min of X/XO application, uptake falls to approximately 60% of its control value. In parallel no detectable release of lactate dehydrogenase occurs. X/XO effect is abolished in the presence of a mixture of scavenger enzymes (superoxide dismutase+catalase) or by the disulfide-reducing agents glutathione and dithiothreitol (DTT), but not by lipophilic antioxidants or ascorbate. The time course of inhibition shows an almost linear decline of glutamate transport during cell exposure to free radicals, while upon their inactivation the decline stops but established inhibition persists for at least 1 hr. In this situation, application of DTT significantly restores transport function. These data suggest that free radicals inhibit glutamate uptake primarily by long-lasting oxidation of protein sulfhydryl (SH) groups. Chemical modifiers of free SH groups, such as p-chloromercuribenzoate and N-ethylmaleimide, also induce uptake inhibition. Na+/K+ ATPase is a known target of oxygen radicals and may be involved in glutamate uptake inhibition. Indeed, ouabain, a blocker of the pump, reduces uptake in astrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glutamate uptake inhibition by oxygen free radicals in rat cortical astrocytes. 791 Feb 3

Oxygen-free radicals generated by xanthine oxidase during hypoxia-ischemia may result in cellular injury through harmful effects on membrane phospholipids. The present study investigated the effect of administration of allopurinol, an inhibitor of xanthine oxidase, on free-radical generation and brain cell membrane injury during hypoxia by inhibiting the breakdown of hypoxanthine to uric acid. Brain cell membrane Na+,K(+)-ATPase activity and lipid peroxidation products (conjugated dienes and fluorescent compounds) were determined as indices of brain membrane function and structure. Cerebral oxygenation was continuously monitored during hypoxia by 31P-NMR spectroscopy. Plasma and brain tissue levels of uric acid were measured to evaluate xanthine oxidase activity and purine degradation. Na+,K(+)-ATPase activity decreased significantly in both hypoxic groups; however, the allopurinol-treated hypoxic group showed a smaller decrease than the untreated hypoxic group (47.3 +/- 4.9 vs. 42.0 +/- 2.7 mumol Pi/mg protein/h, P < 0.05), respectively. Conjugated dienes increased significantly in the untreated hypoxic compared to control animals (0.070 +/- 0.045 vs. 0.004 +/- 0.006 mumol/g brain, P < 0.05), with the allopurinol-treated animals having intermediate values (0.053 +/- 0.039 mumol/g brain). Fluorescent compounds were lower in the allopurinol-treated hypoxic group compared to the untreated hypoxic group (0.79 +/- 0.19 vs. 1.06 +/- 0.60 micrograms/quinine sulfate/g brain, P < 0.05). Measurements of serum and brain tissue uric acid were significantly lower during hypoxia in the allopurinol-treated compared to the untreated group (30.3 +/- 15.6 vs. 45.7 +/- 10.6 microM (P < 0.05) and 1.69 +/- 0.97 vs. 4.27 +/- 2.37 nmol/g (P < 0.05), respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of allopurinol on uric acid levels and brain cell membrane Na+,K(+)-ATPase activity during hypoxia in newborn piglets. 795 82

Active sodium (Na+) transport by alveolar type II (ATII) cells plays an important role in limiting the volume of alveolar fluid. Reactive oxygen and nitrogen species, released in the epithelial lining fluid by activated inflammatory cells or present in inspired gases, may damage Na+ transporters and decrease fluid reabsorption. To test this hypothesis we exposed ATII cells to xanthine and xanthine oxidase (1 or 10 mU/ml), or to boluses of peroxynitrite (0.1-1 mM final concentration) for 15 min and measured 1) cellular oxygen consumption (VO2); 2) amiloride-inhibitable 22Na+ uptake, as an index of Na+ movement through apically located Na+ channels; and 3) ouabain-sensitive 86Rb+ uptake, as an index of the activity of the basolaterally located Na(+)-K(+)-ATPase. After exposure of ATII cells to 0.5 or 1 mM peroxynitrite, amiloride-inhibitable 22Na+ uptake decreased to 68 +/- 7 and 56 +/- 11 of their control values, respectively (mean +/- SE; n > or = 6). Exposure to 0.5 mM peroxynitrite decreased ATII cell VO2 from 76 +/- 6 to 25 +/- 5 microM.h-1 x 10(6) cells-1 (mean +/- SE; n = 5). Cell viability and ouabain-sensitive 86Rb+ uptake remained at control levels for either peroxynitrite concentration. Exposure of ATII cells to 10 mU/ml xanthine oxidase decreased their VO2 from 94 +/- 8 to 63 +/- 6 (mean +/- SE; n = 5), but did not alter amiloride-inhibitable 22Na+ uptake. These findings indicate that physiological concentrations of peroxynitrite, but not of reactive oxygen species, decrease ATII cell Na+ transport by damaging apically located amiloride-sensitive Na+ channels.
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PMID:Peroxynitrite inhibition of oxygen consumption and sodium transport in alveolar type II cells. 802 51

The biochemical effects of the non-12-0-tetradecanoylphorbol-13-acetate (TPA)-type tumor promoter thapsigargin (TG), which does not bind to the phorbol-ester receptor, or activate protein kinase C (PKC) or increase inositol polyphosphates, were characterized in mouse epidermis in vivo. The cold scraping method is required to detect the induction of ornithine decarboxylase (ODC) activity by TG, a response much smaller than that caused by TPA and with a different time course. TG pre-treatments do not alter or cause a refractory state against ODC induction by TPA. But TG stimulates hydroperoxide (HPx) production and RNA, protein, and DNA synthesis almost as much as TPA. Moreover, the sequential effects of TG and TPA on DNA synthesis are identical: early inhibition at 8 hr followed by maximal stimulation at 16-32 hr. TG-stimulated HPx production requires protein synthesis and xanthine oxidase, phospholipase A2, and lipoxygenase activities but not RNA and DNA synthesis, and cyclooxygenase and protease activities. The HPx response to TG is not mimicked by the PKC activator prostratin or inhibited by pre-treatments with prostratin or specific PKC inhibitors. However, the Ca(2+)-ATPase inhibitor cyclopiazonic acid and the Ca2+ ionophore and weak ODC inducer A23187 mimic remarkably the HPx responses to TG and TPA. Since TG and A23187 are known to be, respectively, weak and incomplete tumor promoters as compared with TPA, the present results suggest that the HPx responses common to Ca(2+)-mobilizing and TPA- or non-TPA-type agents are insufficient to achieve tumor promotion in the absence of major ODC induction.
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PMID:Ability of the non-phorbol ester-type tumor-promoter thapsigargin to mimic the stimulatory effects of 12-0-tetradecanoylphorbol-13-acetate on ornithine decarboxylase activity, hydroperoxide production, and macromolecule synthesis in mouse epidermis in vivo. 825 22

The effects of ischemia and reperfusion with and without oxygen radical scavengers and xanthine oxidase inhibitors on Ca(2+)-ATPase activity were examined in the rat liver of 5 min ischemia followed by 5 and 10 min reperfusion. Ischemia was produced by the ligation of right hepatic artery and right portal vein. Superoxide dismutase, catalase and allopurinol were administered by subcutaneous injection of 60,000U/kg, 90,000U/kg and 200mg/kg, respectively before ligation. Reaction products of Ca(2+)-ATPase were morphometrically analyzed by RUZEX IIIU. Histochemically, Ca(2+)-ATPase activities were demonstrated on plasma membrane of liver cells, bile canaliculi and Kupffer cells involving mitochondria in liver cells of control rats. Ca(2+)-ATPase activities were depressed in the central lobes of liver after 5 min ischemia followed by 5 and 10min reperfusion. However, the activities of Ca(2+)-ATPase were not depressed by addition of oxygen radical scavengers and xanthine oxidase inhibitor before ischemia. These results suggest that oxygen free radicals may influence Ca(2+)-ATPase activity and contribute to liver cell damage due to ischemia-reperfusion.
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PMID:[The role of Ca(2+)-ATPase and oxygen radical in reperfusion injury of rat liver]. 827 65

In an attempt to elucidate the physiological activities of (6E,12E)-tetradecadiene-8,10-diyne-1,3-diol diacetate (TDEYA), which was detected as a hydrolysis form (TDEY) in the plasma after oral administration of a decoction of Atractylodes rhizome in rats, we examined the inhibitory effects of various enzymes which are considered to participate in the regulation of body fluid levels and inflammatory reactions. TDEY and TDEYA did not show inhibitory effects on carbonic anhydrase (CA) or angiotensin converting enzyme (ACE) at concentrations less than 1.0 x 10(-3) M. However, both acetylene compounds inhibited Na+,K+ adenosine triphosphatase (Na+,K(+)-ATPase) weakly and xanthine oxidase (XO) strongly. From the results of several acetylene compounds examined on XO inhibition, it is clear that the active structure of the compounds is due to the presence of conjugated triple and double bonds. In the in vivo experiment of TDEYA, urine volume, urinary electrolytes and uric acid excretion showed no significant differences from the control. However, the administration of TDEYA to rats tended to increase xanthine excretion.
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PMID:Enzyme inhibitory activities of acetylene and sesquiterpene compounds in atractylodes rhizome. 839 28

To understand the influence of oxidant stress on the barrier function of airway epithelium, we conducted studies to determine the effects of chemically generated reactive oxygen species on permeability, permselectivity, and active ion transport of ferret trachea. We examined the consequences of oxidant injury using ferret trachea mounted in Ussing-type chambers and bathed with a modified Krebs-Henseleit solution containing mannitol and xanthine. We added xanthine oxidase to the luminal bathing solution, which reacted with the xanthine to generate reactive oxygen species. Tissue electrical conductance and short-circuit current were significantly increased after the addition of xanthine oxidase. Simultaneous measurement of mannitol flux (as a marker of paracellular conductance) and the backflux of chloride (lumen to submucosa) demonstrated a significant oxidant-induced increase in mannitol flux and backflux of chloride. Mannitol flux and the backflux of sodium (submucosa to lumen) also increased after oxidant stress. Comparison of the diffusion of sodium relative to the diffusion of chloride in relation to predicted diffusion in free solution indicated that the paracellular pathway was cation selective after oxidant stress. Active ion transport, as reflected by the short-circuit current, was significantly increased transiently after oxidant stress. Studies with furosemide, amiloride, and diphenylamine-2-carboxylate are suggestive that oxidant stress transiently stimulates the Na-K-ATPase. These studies demonstrated that exposure to reactive oxygen species significantly altered the permeability of the tracheal epithelium as well as active ion transport.
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PMID:Oxidant injury alters barrier function of ferret tracheal epithelium. 844 29

This study was investigated to clarify the role of intracellular Ca2+ following endotoxin treatment (1 mg/kg, intraperitoneally) to D-galactosamine-sensitized mice (400 mg/kg, intraperitoneally), and to observe lipid peroxide levels, an index of hepatotoxicity, in endotoxin/galactosamine (Ga1N)-challenged mice under activation of macrophages, especially Kupffer cells, by zymosan. The liver lipid peroxide level and serum glutamic pyruvic transminase activity in mice 18 hr after administration of endotoxin/Ga1N were markedly higher than those in mice treated only with endotoxin. In spite of an increase in lipid peroxide formation, there was little or no effect of Ga1N administration on xanthine oxidase and superoxide dismutase activities in mice given endotoxin. However, the injection of verapamil (10 mg/kg, subcutaneously) markedly decreased lipid peroxide levels in liver of endotoxin/Ga1N-injected mice. In the mice given a Ca(2+)-deficient diet, lipid peroxide level in liver after endotoxin/Ga1N injection was markedly decreased compared to that in mice fed a normal diet. Administration of dexamethasone (200 micrograms/kg, intraperitoneally) in mice 1 hr before treatment with endotoxin/Ga1N did not induce lipid peroxide formation. Administration of endotoxin to Ga1N-treated mice resulted in a higher level of liver cytosolic free Ca2+ ([Ca2+]i) than that in endotoxin-treated mice. On the other hand, Ca(2+)-ATPase activity in liver plasma membrane in the endotoxin/Ga1N-treated mice was markedly decreased as compared with endotoxin alone. On the contrary, the Ca(2+)-ATPase activity in liver mitochondria was higher in endotoxaemic mice treated with GA1N than in mice given endotoxin alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of Ca2+ on endotoxin-sensitivity by galactosamine challenge: lipid peroxide formation and hepatotoxicity in zymosan-primed mice. 858 8


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