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 adsorption to human erythrocytes of Escherichia coli lipopolysaccharide treated by mild alkaline hydrolysis (h-LPS) stimulated an increase in the intracellular Na+ concentration and a decrease in the intracellular K+ concentration of the erythrocytes. Erythrocytes treated by h-LPS remained responsive to the membrane adenosine triphosphatase inhibitors ouabain and ethacrynic acid, indicating that hLPS did not alter erythrocyte cations be depleting energy intermediates or uncoupling energy metabolism from active cation transport. The h-LPS-treated erythrocytes became non-agglutinable by the lectin concanavalin A prior to the development of changes in intracellular cations. In addition, h-LPS-treated erythrocytes demonstrated a three-fold greater cation response to ethacrynic acid than the untreated erythrocytes; this greater response was probably due to local membrane effects by h-LPS on the ethacrynic acid-sensitive adenosine triphosphatase. It is suggested that the h-LPS-induced alteration of erythrocyte cation content was secondary to an increase in ion permeability localized to the concanavalin A receptor regions of the erythrocyte membrane, possibly combined with indirect effects of membrane-bound h-LPS on ethacrynic acid-sensitive adenosine triphosphatase.
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PMID:Effect of alkali-treated lipopolysaccharide on the intracellular cations of human erythrocytes. 33 Apr 8

We investigated the effects of eserine and ouabain on the permeability of the blood-brain barrier (B.B.B.) as related to the febrile response induced with LPS in rabbit. Results are as follows; The febrile response induced by LPS (0.02 and 1.0 mug/kg) i.v. was suppressed by administration of ouabain (0.06 mg/kg, i.v.). Contrary to the febrile response of LPS given i.c. (10(-4) and 10(-3) mug/kg), the febrile response was not suppressed with the same dose of ouabain. The pyrogenicity of cerebrospinal fluid (CSF) withdrawn at two hours after rabbits had been injected with LPS (25 mug/kg) was suppressed by ouabain (0.06 mg/kg, i.v.). Pyrogenic response was enhanced by pretreatment with eserine (0.5 mg/kg, s.c.) given one hr before LPS (1 mug/kg, i.v.). The pyrogenicity of CSF was also potentiated to a greater extent by pretreatment of eserine than with LPS alone. In the eserinized rabbit (0.5 mg/kg, s.c.), the pyrogenicity of CSF was potentiated to a greater extent by ACh (10 mug/kg, i.v.) than by LPS (1 mug/kg, i.v.) alone. From these data, it is concluded that the inhibition of Na, K-ATPase by ouabain decreases the pyrogenicity of LPS, while the inhibition of cholinesterase by eserine enhances the pyrogenicity.
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PMID:[Effects of eserine and ouabain on the febrile reaction induced by lipopolysaccharide]. 103 14

p-Bromophenacyl bromide (PBPB), quinacrine and indomethacin, which inhibit phospholipase A2 (PLA2; EC 3.1.1.4) activity in several tissues, caused a dose-dependent inhibition of prelabelled [3H]noradrenaline ([3H]NA) release evoked by high concentrations of K+ from rat cerebral cortical synaptosomes. Release of prelabelled [3H]NA was caused by natural lysophosphatidic acid (LPA; 10(-6)-10(-5) g mL-1) and lysophosphatidylcholine (LPC; 10(-6)-10(-5) g mL-1) and synthetic LPA (6 x 10(-6), 2 x 10(-5) M) and LPC (6 x 10(-6), 2 x 10(-5) M), but not by natural lysophosphatidylserine (LPS; 10(-5) g mL-1), lysophosphatidylethanolamine (LPE; 10(-5) g mL-1) and lysophosphatidylinositol (LPI; 10(-5) g mL-1). The release evoked by natural LPA and LPC could be inhibited only marginally by PBPB and quinacrine. Phosphatidic acid (PA)-specific and phosphatidylcholine (PC)-specific PLA2 activities from rat cerebral cortical synaptosomes were stimulated in incubation medium containing high concentrations of K+ or calcium ionophore A23187. Low concentrations of PLA2 (10(-6)-10(-8) g mL-1, from bee venom) inhibited the synaptic membrane Na+,K+-ATPase activity in incubation media with intracellular levels of free Ca2+. Several lysophospholipids (LPLs), metabolites of the PLA2 type, also inhibited the synaptic membrane Na+,K+-ATPase activity in a dose-dependent manner. The minimum effective concentrations of natural LPA, LPC, LPS, LPI and LPE were 10(-6), 4.7 x 10(-6), 10(-5), 4.7 x 10(-5) and 4.7 x 10(-5) g mL-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of Na+,K+-ATPase activity by phospholipase A2 and several lysophospholipids: possible role of phospholipase A2 in noradrenaline release from cerebral cortical synaptosomes. 257 Aug 49

We report on an experimental model that permitted us to evaluate the biologic relevance of membrane-associated biochemical events with respect to cell proliferation and maturation, each induced by distinct sets of signals. Antigen-affinity-enriched murine B cells cultured in the presence of a proliferative signal induced by LPS showed activation of Na+/K+ ATPase and enhanced the uptake of proline, followed by RNA, protein, and DNA synthesis, without the generation of antibody. Stimulation with both the proliferative signal(s) and the maturation signal(s) derived from lymphokines of an EL-4 thymoma induced B cells to proliferate and synthesize mRNA encoding mu-chain of IgM and to mature into IgM-secreting cells. Most important, the secretory product of EL-4, in the absence of LPS, activated Na+/K+ ATPase but failed to stimulate uptake of proline and synthesis of DNA or mu-specific mRNA. A similar response was observed in splenocytes depleted of T cells and in unfractionated spleen cells. Thus a component secreted by EL-4 can induce some of the early molecular events characteristic of the proliferative response but lacks the ability to initiate blast transformation and DNA synthesis.
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PMID:Activation of cation transport by lymphokines in B cells without induction of DNA synthesis or immunoglobulin gene transcription. 300 Nov 79

This study addresses the role of intracellular calcium (Ca2+) in the expression of iNOS, an IL-1 inducible gene in human articular chondrocytes. The calcium ionophore A23187 and ionomycin did not induce NO release or iNOS expression but inhibited dose dependently IL-1-induced NO release with IC50 of 200 nM and 100 nM, respectively. Increased intracellular Ca2+ induced by thapsigargin or cyclopiazonic acid, inhibitors of the endoplasmic reticulum Ca2+ ATPase, had similar inhibitory effects with IC50 of 1 nM and 3 microM, respectively. LPS and TNF alpha induced NO production were also suppressed by these Ca2+ elevating drugs. Levels of IL-1-induced iNOS protein were reduced by A23187, thapsigargin, and cyclopiazonic acid. These drugs as well as Bay K 8644 and KCl inhibited IL-1-induced iNOS mRNA expression. To analyze the role of Ca2+ in the expression of other IL-1 responsive genes in chondrocytes, these Ca2+ modulating drugs were tested for effects on COXII. In contrast to the inhibitory effects on iNOS mRNA, these drugs induced COXII mRNA expression and in combination with IL-1, enhanced COXII mRNA levels. Ca2+ mediated increases in COXII mRNA expression were associated with an increase in COXII protein. The kinetics of Ca2+ effects on IL-1-induced iNOS mRNA levels suggested a posttranscriptional mechanism. Analysis of iNOS mRNA half life showed that it was 6-7 h in IL-1-stimulated cells and decreased by A23187 to 2-3 h. In conclusion, these results show that Ca2+ inhibits IL-1-induced NO release, iNOS protein, and mRNA expression in human articular chondrocytes by reducing iNOS mRNA stability. Under identical conditions increased Ca2+ enhances IL-1-induced COXII gene and protein expression.
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PMID:Increased intracellular Ca2+ selectively suppresses IL-1-induced NO production by reducing iNOS mRNA stability. 754 Jun 12

The ability of putative Ca(2+)-ATPase inhibitor of endoplasmic reticulum (ER), thapsigargin (TG), to induce nitric oxide (NO) synthesis in murine peritoneal macrophages was examined. TG alone had small effect on NO synthesis, whereas TG in combination with LPS markedly increased NO synthesis in a dose dependent manner. This increase in NO synthesis was reflected as increased amount of inducible NO synthase (iNOS) mRNA by Northern blotting. In addition, the ability of TG on NO synthesis could be mimicked by another chemically unrelated inhibitor of Ca(2+)-ATPase, 2,5-DI-(t-butyl)-1, 4-benzohydroquinone (tBuBHQ). Adding EGTA, a calcium chelator, to the incubation medium significantly reduced the ability of macrophages to induce NO synthesis in response to the optimal stimulation of TG or TG plus LPS. These results therefore demonstrate that intracellular Ca2+ pool depletion is linked to the induction of NO synthesis in murine peritoneal macrophages and further suggest that it is also related with interferon-gamma (IFN-gamma)-induced signaling.
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PMID:Intracellular Ca2+ pool depletion is linked to the induction of nitric oxide synthesis in murine peritoneal macrophages. 758 Oct 11

This study presents animal experiments on endotoxin (lipopolysaccharides: LPS) damage to the inner ear with special reference to the stria vascularis. The experimental group animals (albino guinea pigs) were injected with LPS into the perilymphatic space. Pyrogen-free saline (PFS) was injected into the control group. Strial structural evaluation and hearing tests were carried out before and one, three and five days after treatment. In PFS-treated (control) ears, no significant change was found either in hearing or structure. However, thresholds of N1/P1 were elevated and latencies prolonged in LPS-treated ears. They had severe strial damage mainly to the cellular organelles. The mitochondria became swollen with a disordered, broken, degenerated or absent crest. Secondary lysosomes and autophagosomes increased in number with the presence of medulative inclusions. Na(+)-K(+)-ATPase reactant was obviously diminished. It is concluded that LPS-induced strial ototoxicity produces ion imbalance, causing changes in endolymph composition and energy failure in the organ of Corti and is also responsible for the pathogenesis of inner ear sequelae secondary to otitis media.
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PMID:Endotoxic damage to the stria vascularis: the pathogenesis of sensorineural hearing loss secondary to otitis media? 818 16

Endotoxins (lipopolysaccharides; LPS) are known to cause multiple organ failure, including renal dysfunction. The present report elucidates LPS distribution and effect on renal proximal tubules in an attempt to gain a better understanding of the cellular mechanism underlying the pathogenesis of renal dysfunction in endotoxemia and sepsis. Rats were intravenously treated with biotin-linked or regular Escherichia coli (0111:B4) LPS (3 mg/kg) and sacrificed at different times. Kidneys were retrieved and examined for LPS localization, tubular permeability, ultracytochemical alterations, leukocyte sequestration, and ICAM-1 expression. The functional impact of endotoxemia was also assessed by monitoring the changes in urine levels of glucose in timed collections up to 6 h. LPS was localized on the plasma membranes of the apical microvilli, the labyrinth of the lateral intercellular spaces, in various organelles of epithelial cells, and in the endothelial cells of the peritubular capillaries. LPS caused structural damage and calcium accumulation in the mitochondria, leakage of tight junctions, widening of the basolateral intercellular spaces, intracellular and extracellular edema, leukocyte margination and accumulation, vascular expression of ICAM-1, and decrease of plasma membrane and mitochondrial Ca2(+)-ATPase. Physiological study showed that both urine volume and glucose were greatly increased after LPS infusion. The pathological alterations in the proximal tubules may directly contribute to the reduction in the reabsorption ability of the proximal tubules.
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PMID:Distribution and role of lipopolysaccharide in the pathogenesis of acute renal proximal tubule injury. 860 2

The Na+,K(+)-ATPase catalytic (alpha) subunit in sciatic nerve of lipopolysaccharide (endotoxin, LPS)-treated rat was investigated. Using Western blot to determine subunit isoform polypeptide levels in rat sciatic nerve, we found a substantial reduction in alpha 1 polypeptide, but not that of alpha 2 and alpha 3 polypeptides, after the administration of LPS. Moreover, when rats were treated with polymyxin B (a LPS neutralizer) and NG-nitro-L-arginine (an inhibitor of nitric oxide (NO) synthase), the effects of LPS were reversed. These results implicate a specific marked deficit in alpha 1 subunit isoform of Na+,K(+)-ATPase in the pathogenesis of neuropathy during endotoxemia, through, at least in part, the L-arginine/NO pathway.
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PMID:The in vivo effect of lipopolysaccharide on Na+,K(+)-ATPase catalytic (alpha) subunit isoforms in rat sciatic nerve. 936 23

In the present study we evaluated the effects of NO synthase (NOS) induction on the regulation of cytochrome c oxidase (CO) and F0F1-ATPase subunit expression in astroglial and mixed cortical cell cultures. In mixed cortical cell cultures, 18 h of treatment with lipopolysaccharide (LPS, 0.1 microgram/mL) plus interferon-gamma (INF-gamma, 10 U/mL) caused an increase of mRNAs for CO-I, F0F1-ATPase 6 and also for iNOS at 20 DIV. The induction of both CO-I and F0F1-ATPase 6 was abolished by the NOS inhibitor N-monomethyl-L-arginine (NMMA) or by the enzymatic scavenger superoxide dismutase/catalase (SOD/CAT). In primary astroglial cell cultures, treatment for 18 h with increasing concentrations of LPS and INF gamma, produced an increase in the amount of mitochondrial encoded CO-I and -II subunits, with no significant modifications of nuclear encoded subunit IV. An increase was also observed at level of transcription for CO-I and -II, and F0F1-ATPase 6 mRNAs. These effects were abolished by addition of NMMA or SOD/CAT. mRNA induction of CO-I was higher in mixed cortical than in astroglial cell cultures while that of F0F1-ATPase 6 was similar in both cell types. These results suggest that the expression of mitochondrial encoded subunits (CO-I, CO-II and F0F1-ATPase 6) is up-regulated in response to oxygen and NO reactive species. The activity of cytochrome c oxidase decreased after LPS/INF gamma treatment in both astroglial and mixed cortical cultures. The activity of ATP synthase was unmodified, while ATP content drastically decreased after LPS/INF gamma treatment, in both astroglial and mixed cortical cultures. The enzymatic activities of catalase and Mn-SOD (mitochondrial) showed a significant increase after LPS/INF gamma treatment, which was abolished by NMMA.
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PMID:Effect of nitric oxide synthase induction on the expression of mitochondrial respiratory chain enzyme subunits in mixed cortical and astroglial cell cultures. 989 46


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