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)

Single cell suspensions of epidermal cells from guinea pigs were analyzed histochemically for the presence of the following enzymes: 5'-adenosine triphosphatase, nonspecific esterase, specific esterase, myeloperoxidase and leukocyte alkaline phosphatase. A population of cells was positive for nonspecific esterase, leukocyte alkaline phosphatase, and 5'-adenosine triphosphatase. This population was identified as Langerhans' cells because the number of cells stained for these enzymes paralleled the number of Langerhans' cells in the suspension. These same enzymes were shown to be present in guinea pig leukocytes of the mononuclear-phagocytic series, suggesting that they and Langerhans' cells may have a precursor in common.
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PMID:Histochemical analysis of Langerhans' cells. 23 76

To examine the effects of activated neutrophils (PMNs) on Na(+)-K(+)-ATPase, phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs were incubated with canine renal cortical basolateral membrane (BLM), and BLM ouabain-sensitive Na(+)-K(+)-ATPase activity was subsequently quantified. Na(+)-K(+)-ATPase activity decreased to 40.0 +/- 8.7% (SE) of control in the presence of activated PMNs, from 0.89 +/- 0.12 to 0.34 +/- 0.05 mumol Pi.mg protein-1.min-1. This inhibition coincided with a decrease in the apparent Michaelis constant (Km) for ATP from 0.18 +/- 0.02 to 0.05 +/- 0.01 mM. Inclusion of catalase (CAT) and superoxide dismutase (SOD) in the BLM/PMN/PMA incubation mixture resulted in partial preservation of enzyme activity, with an increase to 57.0 +/- 4.6% of control with CAT alone and to 70.0 +/- 5.3% with both CAT and SOD. SOD alone had no protective effect. Neither the myeloperoxidase inhibitor azide nor the hypochlorous acid scavenger L-methionine preserved enzyme activity. Hydroxyl radical scavengers and iron chelators were also ineffective in attenuating Na(+)-K(+)-ATPase inhibition by activated PMNs. These results indicate that activated PMNs mediate a decrease in BLM Na(+)-K(+)-ATPase activity characterized by a reduction in maximum velocity and Km for ATP that appears to be mediated in part by reactive oxygen metabolites.
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PMID:Activated neutrophils inhibit Na(+)-K(+)-ATPase in canine renal basolateral membrane. 131 73

A human megakaryoblastic cell line, designated CHRF-288-11, has been established in vitro through the use of adherent stromal cells in long-term human bone marrow culture. Long-term bone marrow cultures were required for the initial adaptation of the megakaryoblastic cells to culture conditions; however, once adapted, the cells were weaned from the stromal layer until they proliferated in the complete absence of any feeder layers. The seed cells for the establishment of this line were derived from a solid tumor; the cloned cell line derived from this tumor exhibits markers characteristic of megakaryocytes and platelets. Specifically, the cells express platelet peroxidase, platelet factor 4, and platelet Ca+(+)-adenosine triphosphatase (ATPase), glycoprotein IIb-IIIa (CDw41), factor VIII antigen, and the MY7 (CD13) and MY9 (CD33) antigens. The cells do not express the erythroid markers glycophorin A and hemoglobin, the myeloid marker myeloperoxidase, nor markers specific for T and/or B cells. The established cell line produces both basic fibroblast growth factor and transforming growth factor-beta, properties demonstrated previously for the solid tumor. The clonal cell population exhibited a unique, singular karyotype, indicating cellular homogeneity. The cells display a doubling time of approximately 33 hours in either 25% horse or calf serum. Treatment of the cells with 1 X 10(-8) mol/L phorbol 12-myristate 13-acetate (PMA) leads to the induction of multi-nucleation and hyperploidy in the cells, with approximately 35% of the cells exhibiting two or more nuclei per cell, and greater than 80% of the cells enlarging in size. The establishment of this unique cell line under defined culture conditions will be beneficial for the future study of megakaryocytic properties expressed by this cell line.
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PMID:In vitro establishment and characterization of a human megakaryoblastic cell line. 231 Aug 25

The purpose of this investigation was to determine which enzyme activities are true canine neutrophil plasma membrane markers. Three enzymes thought to be present on plasma membranes were chosen for study: 5'-nucleotidase, magnesium-dependent adenosine triphosphatase (Mg2+-ATPase), and leucine aminopeptidase. Both 5'-nucleotidase and Mg2+-ATPase were found to be ectoenzymes in the canine neutrophil but additional Mg2+-ATPase activity was located intracellularly. An endogenous inhibitor of 5'-nucleotidase was found in the cytosol of canine neutrophils. The specific 5'-nucleotidase inhibitor, adenosine 5'-[alpha, beta-methylene] diphosphate also inhibited the canine enzyme in intact cells. Leucine aminopeptidase was located solely in the myeloperoxidase-containing granules of the canine neutrophil. Plasma membrane, as identified by the presence of Mg2+-ATPase and 5'-nucleotidase activities, was separated from other cell organelles by Percoll-density gradient centrifugation of a 10 000 X g supernatant of nitrogen cavitated neutrophils.
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PMID:Canine neutrophil plasma membrane markers. 298 65

Alteration of the surface of human neutrophils with the nonpenetrating, protein-inactivating agent p-diazobenzenesulfonic acid (DASA) was found to prevent activation of the respiratory burst by some stimuli, but not others. Production of superoxide anion (O2-) stimulated by concanavalin A or the chemotactic peptide formyl-methionyl-leucyl-phenylalanine FMLP was inhibited by DASA pretreatment, whereas O2- production stimulated by phorbol myristate acetate (PMA), sodium fluoride. or the ionophore A23187 was not inhibited by DASA. Pretreatment with DASA inhibited oxygen uptake stimulated by FMLP, but not oxygen uptake stimulated by PMA. DASA reproducibly inhibited activities of two known surface enzymes Mg++-ATPase and alkaline phosphatase, by 45-55% and 60-70%, respectively. The inhibition by DASA of O2- production did not appear to be caused by interference with binding of the affected stimuli, since pretreatment with DASA did not inhibit release of the lysosomal enzymes lysozyme and myeloperoxidase induced by concanavalin A or FMLP. Membrane-rich particulate fractions from neutrophils have been shown to contain NADPH-dependent oxidative activity that is presumably responsible for the phagocytosis-associated respiratory burst of intact cells. The PMA-activated enzyme was susceptible to inhibition of directly exposed to DASA in this particulate fraction. These findings suggest that more than one mechanism exists for activation of the respiratory burst oxidase in human neutrophils, and that the neutrophil possesses at least one oxidase that is not an ectoenzyme.
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PMID:Respiratory burst enzyme in human neutrophils. Evidence for multiple mechanisms of activation. 625 8

Na(+)-K(+)-adenosinetriphosphatase (ATPase) plays a key role in the absorption of electrolytes, water, and nutrients from the small intestine. The expression of Na(+)-K(+)-ATPase was examined in isolated enterocytes during the course of the ileal inflammatory response elicited by intraluminal administration of 2,4,6-trinitrobenzenesulfonic acid. The ileal inflammatory response was characterized by a marked cellular infiltrate, villous atrophy, and crypt hyperplasia along with fibrosis and smooth muscle hypertrophy. Peak levels of myeloperoxidase were observed at day 7, and ileal mucosal injury was paralleled by increases in ileal mucosal permeability. Ileal enterocytes were harvested from days 3 to 30 after the induction of ileitis. Decreases in Na(+)-K(+)-ATPase functional activity were observed from days 3 to 21 and were accompanied by corresponding decreases in Na(+)-K(+)-ATPase pump abundance, alpha 1- and beta 1-protein expression, and mRNA abundance, whereas Na(+)-K(+)-ATPase turnover, Michaelis-Menten constant values, and inhibition constant values for Na+ and ouabain, respectively, were unaltered. Alterations in transcriptional and posttranscriptional events may determine the changes in Na(+)-K(+)-ATPase activity in this particular model. Additionally observed increases in thymidine kinase and ornithine decarboxylase activities appear to signify alterations in the state of differentiation of the ileal epithelium and may determine the phenotypic expression of enterocyte transporters and permeability in the setting of inflammation.
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PMID:Na(+)-K(+)-ATPase alpha 1- and beta 1-mRNA and protein levels in rat small intestine in experimental ileitis. 749 57

Sodium azide (AZ) is a nitrovasodilator with diverse biochemical properties. We found that low doses of AZ led to a profound protective effect against postischemic, acute renal failure (ARF) in rats. AZ, given at 250 micrograms/kg iv, before 25 min of renal artery occlusion (RAO) and again before reperfusion, conferred almost complete protection against loss of kidney function determined 18 h after RAO. The effect of AZ was evidenced by a higher creatinine clearance (+348%) and lower levels of blood urea nitrogen (-69%) and histological renal damage (-50%) compared with ischemic control animals. Indexes of kidney function in AZ-treated animals subjected to RAO were not significantly different from those of nonischemic control animals. Two other nitrovasodilators, sodium nitroprusside and hydralazine, at doses which produced decreases in blood pressure similar to that of AZ, were ineffective at preventing ARF. The beneficial effect of AZ may be due to its known ability to inhibit one or more enzymes including adenosinetriphosphatase, cytochrome-c oxidase, and myeloperoxidase.
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PMID:Sodium azide protects against ischemia-induced acute renal failure in rats. 834 10

We have assessed the effect of the oral ingestion of thioacetamide on small intestine structure and function. Thioacetamide-treated rats showed diminished mucosa weight; protein, DNA, and RNA content; and leucine aminopeptidase activity as compared to controls in both jejunum and ileum. In the jejunum, there was a reduction in the activities of alkaline phosphatase, ATPase, glucose-6-phosphatase, and myeloperoxidase, whereas in the ileum, maltase, lactase, and gamma-glutamyltranspeptidase were reduced. In both jejunum and ileum we found enlarged intercellular spaces, dark epithelial enterocytes, and lymphocyte infiltration. Enterocytes showed lobulated nuclei, deranged mitochondria with loss of their cristae, dilated rough endoplasmic reticulum containing dense material, and vesiculation of the smooth endoplasmic reticulum and the Golgi apparatus. Smooth muscle cells of the intestine exhibited ultrastructural alterations. These findings indicate that chronic oral intake of thioacetamide mimics not only hepatic alterations but also small intestine alterations normally associated with human cirrhosis.
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PMID:Hepatotoxic agent thioacetamide induces biochemical and histological alterations in rat small intestine. 928 39

The adhesion of human polymorphonuclear granulocytes (PMN) with confluent human endothelial cells (line EAhy926) and with solid substrate coated by collagen and fibronectin (Fn) was studied by phase contrast microscopy and by the measurement of myeloperoxidase activity. The ecto-ATPase inhibitors suramin and Reactive Blue 2 (RB2) more than doubled the adhesion of PMN to endothelial cells. The cells hydrolyzed added ATP and this reaction was inhibited by suramin and RB2. The degree of ATP hydrolysis during PMN adherence depended on solid substrata and decreased in the order: non-stimulated endothelial cells, TNF-stimulated endothelial cells, collagen-coated surface, Fn-coated surface. In the same order adherence increased. The endogenous level of extracellular ATP in the PMN-endothelial coculture was around 25 nM. We conclude that PMN-endothelial adhesion is counteracted by an ecto-ATPase or by ATP receptors with ATPase activity. Such interactions may play a role in PMN rolling and diapedesis as well as in the pathophysiology of PMN activation by an anergic endothelium.
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PMID:Involvement of ecto-ATPase and extracellular ATP in polymorphonuclear granulocyte-endothelial interactions. 951 66

Oxygen free radical generation contributes to the reinfusion damage after hemorrhagic shock. Taurine has been proposed to have radical scavenging properties under certain experimental conditions. Therefore the present study was undertaken to investigate if taurine would be able to attenuate adverse effects of shock/resuscitation in male rats (fasted over night). Under pentobarbital anesthesia, hemorrhagic shock (HS) was induced for 1 h by bleeding of the animal [mean arterial blood pressure (MAP) = 40 mm Hg] followed by shed blood reinfusion and another 1 h period of resuscitation. Rats were divided into two groups: Treated rats (n = 6) were injected with taurine (40 mg/kg body mass) prior to withdrawal of shed blood; untreated rats (n = 9) received respective volumes of a normal saline solution. In untreated animals, free radical induced lipid peroxidation was documented by an increase of malondialdehyde (MDA) in the systemic circulation (nmol/ml; HPLC measurement) from 1.06 +/- 0.08 during normotension (NT) to 1.35+/- 0.18** 1 h after resuscitation (RS). Accordingly, plasma levels of alanine aminotransferase (ALT) (11 +/- 2; 35 +/- 12; 94 +/- 44 U/l, NT; HS; RS) and ammonia (120 +/- 39; 532 +/- 161; 224 +/- 101 micrograms/dl) changed significantly during the experimental protocol. Hepatic ATPase-content as an indicator of energetic status of the liver fell from 4.8 +/- 0.83 to 0.56 +/- 0.27 after HS and recovered to only 2.7 +/- 1.6 mumol/g after RS. Leukocyte infiltration of the liver was followed by tissue levels of myeloperoxidase (MPO) which did not change during HS, but rose during RS (37.9 +/- 18.5; 38.6 +/- 16.4; 77.5 +/- 24; arbitrary units), documenting an inflammatory reaction after HS. Taurine treated rats showed levels of MDA not different from untreated rats after RS; also no differences were observed concerning enzyme concentrations and ammonia levels. The liver tissue levels of ATP and MPO revealed no differences between the two groups during the various periods of the experiment. Liver tissue perfusion, as measured by Laser Doppler flowmetry, also did not show significant differences between both groups. MAP was significantly higher in the taurine-treated rats during the first 40 min of resuscitation. It is concluded that even a relatively high dose of taurine failed to attenuate the impact of oxygen free radicals and did not improve the recovery of the rats during the early resuscitation period.
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PMID:No beneficial effects of taurine application on oxygen free radical production after hemorrhagic shock in rats. 963 32


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