Disease relevance of Edathamil

• Inefficacy of EDTA chelation therapy for coronary atherosclerosis [1].
• CONTEXT: Chelation therapy using EDTA is an unproven but widely used alternative therapy for ischemic heart disease [2].
• Both vaccine preparations (trichloroacetic acid and EDTA) were found to lack pyrogenicity and toxicity for experimental animals [3].
• One line, established in this laboratory from a metastatic solid tumor by repeated treatment of the primary outgrowth with 0.02 percent EDTA, allowed a continuous culture of melanoma cells free of fibroblasts [4].
• Outer membranes from two nontypable H. influenzae isolates that caused otitis media and pneumonia (middle ear and transtracheal aspirates) were prepared by shearing organisms in EDTA [5].

Psychiatry related information on Edathamil

• Here, we report that, following treatment with EDTA, Puralpha was released from polyribosomes in mRNA/protein complexes (mRNPs), which also contained mStaufen, Fragile X Mental Retardation Protein (FMRP), myosin Va, and other proteins with unknown functions [6].
• Also, the REM sleep deprivation induced increase in the enzyme activity was observed in lysed preparations and in the presence of EDTA only [7].
• Use of EDTA to remove endogenous zinc appears to offer a mechanism for study of the effects of short-term zinc supplementation at critical periods in the pregnant zinc-deficient rat [8].
• A low response time (<2 min) and a rapid recovery of response by EDTA seem the most interesting characteristics of the proposed biosensor at the present stage of development, along with the well known easy preparation of this kind of biosensors [9].
• Whole blood in EDTA and unstimulated saliva samples were collected from 37 HIV(+) patients, of whom 20 had a history of intravenous drug abuse (IVDA) [10].

High impact information on Edathamil

• The 100 kd protein also bound to native fibronectin receptor, and this binding could be reversed with EDTA [11].
• This interaction is inhibited by anti-PADGEM antibodies, PADGEM, and EDTA; anti-GPIIb-IIIa, anti-thrombospondin, anti-GPIV, and thrombospondin produce no effect [12].
• The mean (+/- SE) glomerular filtration rate, as measured by the clearance of 51Cr bound to EDTA, fell from 0.25 +/- 0.03 to 0.10 +/- 0.05 ml per second (P less than 0.01) in the group on the regular diet, whereas it fell from 0.23 +/- 0.04 to 0.20 +/- 0.05 ml per second (P not significant) in the group on the protein-restricted diet [13].
• During development of Dictyostelium discoideum, a surface glycoprotein of Mr 80,000 (gp80) is known to mediate EDTA-resistant cell-cell adhesion via homophilic interaction [14].
• However, treatment of the cytoskeletal fraction with EDTA or low levels of ribonuclease resulted in polysome degradation but no release [15].

Chemical compound and disease context of Edathamil

• The monocyte ACE from patients with sarcoidosis was activated by chloride ions and inhibited by EDTA, captopril, and rabbit antiserum to purified human plasma ACE, indicating that enzymatic activity was effected specifically by ACE [16].
• The elution profiles of the labeled amino acids obtained from preparations of Escherichia coli glutamine synthetase which had been oxidized by MCO systems comprised of either Fe(II)/O2 or ascorbate/Fe(II)/O2 both in the presence and absence of EDTA were qualitatively the same [17].
• Lipopolysaccharide (LPS) extracted from the deep rough mutant of Escherichia coli D31m4 was disaggregated with 0.1 M EDTA, pH 7.0, and fractionated on a diethylaminoethyl-cellulose column to yield the biphosphate form of LPS [18].
• Alkaline phosphatase (ALP) in human choriocarcinoma cells (malignant trophoblasts) was characterized by its greater sensitivity to EDTA and L-leucine inhibition as compared with the placental isozyme [19].
• The intravenous infusion of edetate disodium (disodium EDTA) showed a normal phosphaturic and cyclic adenosine monophosphate response, ruling out the diagnosis of pseudohypoparathyroidism [20].

Biological context of Edathamil

• Platelet aggregation was associated with adsorption of multimers of factor VIII/von Willebrand factor onto the platelets and was inhibited by EDTA [21].
• This protein has been implicated in the EDTA-stable (Ca2(+)-independent) type of cell adhesion of aggregating cells [22].
• Thus the ratio of protoporphyrin IX accumulation from ALA in cultures treated with CaMg EDTA compared with controls treated with ALA alone was greatest in normal cells, least in EPP cells, and intermediate in the heterozygote cells [23].
• Neither EDTA, phenylmethylsulfonylfluoride, nor epsilon-amino-N-caproic acid prevented platelet-initiated formation of C5-9, suggesting that the reaction may involve mechanisms of complement activation not previously described [24].
• After 1-2 h, the majority of the bound immune complexes were not released into the serum during blood clotting at either 37 degrees C or room temperature, but there was a considerably greater release of the immune complexes into the plasma of blood that was anticoagulated with EDTA [25].

Anatomical context of Edathamil

• Immunoblotting revealed an EDTA-dependent cosedimentation with ribosomes in sucrose gradients for 11 candidate translation-machinery-associated (TMA) proteins [26].
• The fixed islets were then dissociated with trypsin and EDTA to yield cell suspensions that contained mainly four cell types; beta-cells, capillary endothelial cells, acinar cells, and pancreatic duct epithelial cells [27].
• These platelet contaminants were removed by sequential incubations of monocytes in serum and EDTA followed by adherence and detachment from tissue culture vessels [28].
• We isolated cell envelopes by treating whole bacterial cells with lysozyme and EDTA to convert them to spheroplasts, then lysing the spheroplasts osmotically or sonically [29].
• Pulmonary macrophages of mice in the steady state were isolated by lavage with PBS containing EDTA and subsequent enzymatic digestion of tissue with pronase and DNA-ase [30].

Associations of Edathamil with other chemical compounds

• Conversion was less than 10% of normal when MPO-deficient PMNs were employed; formation by normal PMNs was inhibited by the peroxidase inhibitors, azide, and cyanide, and a model system consisting of MPO, H2O2, chloride (or bromide) and EDTA was found which shared many of the properties of the predominant PMN system [31].
• We found that antisera to H-2.7 immunoprecipitated C4 and no other protein from mouse EDTA-plasma [32].
• Addition of 1 mM Ca2+ to RPMI medium increased the binding of TSP to suspended U937 cells more than eightfold; the increase was blocked by EDTA but not by heparin [33].
• Cytoplasmic extracts of CML leukocytes prepared with ice-cold 0.34-M sucrose solutions containing Mg2+-ATP, dithiothreitol, and EDTA at pH 7.0 underwent rapid gelation when warmed to 25 degrees C. Initially, the gel could be liquified by cooling to ice-bath temperature [34].
• The consumption occurred in the absence of detectable anti-heart mitochondria autoantibody, was demonstrated to be calcium dependent, and was inhibited by either 0.01 M EDTA or ethylene glycol bis(bets-aminoethyl ether) N,N,N',N',-tetraacetic acid (EDTA) [35].

Gene context of Edathamil

• The MMP inhibitors, EDTA and 1,10-phenanthroline, as well as recombinant TIMP-1, reduced these activities which colocalized with regions of increased immunoreactive MMP expression, i.e., the shoulders, core, and microvasculature of the plaques [36].
• Immunoprecipitates of human C4 from EDTA-plasma were incubated with [14C]methylamine and analyzed by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis and fluorography [37].
• Incubation of these two preparations resulted in a Mg-ATP-dependent inactivation of NR that was reversed with EDTA [38].
• The catalytic properties of the Arg-35 mutant were changed so that PC activation by the mutant no longer required Ca2+ in the presence of TM, but, instead, it was accelerated by EDTA [39].
• The TC-B12 binding sites in the proximal tubule epithelium colocalized with megalin as shown by ligand binding to cryosections of rat kidney cortex, and the binding was inhibited by anti-megalin polyclonal antibody, EDTA, and RAP [40].

Analytical, diagnostic and therapeutic context of Edathamil

• The ligation reaction occurs rapidly on removal of Mg2+ by EDTA [41].
• Immunoprecipitation experiments showed the GR antigen to be 110-120 kD Mr. The binding of soluble GR antigen was inhibited by EDTA and O-sialoglycoprotease, but not neuraminidase treatment of the target cells [42].
• It was suggested that the C-C36 antigens responsible for tumor-rejection activity against the same tumor cells had a molecular weight range of approximately 150,000 to 250,000 (fraction II) in the presence of 5 mM EDTA and had been eluted into unbound fractions to lens culinaris lectin on affinity chromatography [43].
• In the radioimmunoassay, antibody-containing plasma (1:100) is incubated with 0.2 pmoles of [3H]serotonin, EDTA, and either serotonin standards or unknown samples (0.1 ml) [44].
• This 19S complex is of extraordinary stability: dissociated by 0.5 M KCl or EDTA from the (still repressed) core globin mRNP, it can be purified on gradients containing 1% Sarkosyl, and resists (unfixed) caesium sulphate-dimethylsulphoxide density centrifugation [45].

References