Disease relevance of Edathamil

• EDTA (calcium disodium edetate) lead mobilization and x-ray fluorescence (XRF) finger bone lead tests were done in 42 patients with chronic renal failure and without persisting lead intoxication [1].
• Thus a possible role of zinc in causing neuronal death in the brain needs to be fully investigated. intraventricular injections of calcium EDTA have already been shown to reduce neuronal death after a period of ischemia [2].
• Effects of calcium disodium versenate (CaNa2EDTA) chelation in moderate childhood lead poisoning [3].
• However, the toxicity was not blocked by the mercury chelator, 2,3-dimercaptopropane-1-sulphonate (DMPS), but was blocked by the metal chelator, calcium disodium ethylenediaminetetraacetate (CaEDTA) [4].
• To clarify the molecular mechanisms of this neuroprotective effect, we used a focused cDNA array of stress-response genes with zinc chelation (calcium EDTA) in our rat model of fluid percussion brain injury at 2 h, 24 h, and 7 days after injury [5].

High impact information on Edathamil

• The effects of calcium, EDTA, and temperature on the binding of lipoproteins to the hepatic membranes were also evaluated [6].
• Versene dissociation of the 13762 solid tumor produced better growth rates than did pronase-DNase, but the former decreased cell viability and yields [7].
• The effect of iron status on calcium disodium edetate (CaNa2EDTA)-induced lead diuresis was examined in 112 children with moderate lead intoxication [8].
• In parallel experiments, we compared neuronal cell death in TUNEL-stained brain sections in traumatized rats with and without calcium EDTA treatment [5].
• The membrane penetrating chelator diethyldithiocarbamate (DEDTC) was found to block the AMG staining whereas calcium-EDTA, known not to pass through cell membranes, did not influence the staining, proving that the detected zinc ions are intracellularly located [9].

Chemical compound and disease context of Edathamil

• Lead mobilization test in children with lead poisoning: validation of a 5-hour edetate calcium disodium provocation test [10].
• Chelation in metal intoxication XVIII: Combined effects of thiamine and calcium disodium versenate on lead toxicity [11].
• The aims of this study were to evaluate renal alterations produced during chronic lead poisoning and their progression when poisoning was over and to determine the efficiency of chelating treatment with calcium disodium ethylenediaminetetraacetate (EDTA) [12].

Biological context of Edathamil

• Lead-induced oxidative stress and hematological alterations and their response to combined administration of calcium disodium EDTA with a thiol chelator in rats [13].
• Chelatable lead body burden (by calcium-disodium EDTA) and blood lead concentration in man [14].
• A solution containing the same amount of disodium calcium EDTA as the CM solutions inhibited phagocytosis significantly, although less than the CM solution [15].
• Calcium EDTA therapy was initiated, followed by aggressive gastrointestinal decontamination [16].
• In a series of eight experiments attempts were made to change the levels of calcium in the blood of sheep by intravenous infusions of calcium, EDTA and thyrocalcitonin or changing the acid-base balance by various means [17].

Anatomical context of Edathamil

• Calcium-EDTA therapy had no influence on erythrocyte, serum, or urine chromium level [18].
• After sufficient outgrowth, cultures were dispersed with trypsin/versene and maintained as independent cell lines [19].
• These findings and the fact that calcium EDTA acid blocks the plasma and surface staining, but not the acrosomal and mitochondrial staining, suggest that chelatable zinc ions exist in two separate pools in human semen [20].
• Based on the experiments performed, chorionic villus cells are more sensitive to pronase, trypsin, and versene during subculture and have a higher DNA content per single cell and release more [125I]-Beta-human chorionic gonadotropin into culture medium than those found in amniotic fluid cells [21].
• When endothelial cells were induced to retract from their substrate by exposure to cold or versene and then incubated with PRP, platelets were observed adhering to endothelial cell processes and to an extracellular microfilamentous network, located beneath the cell [22].

Associations of Edathamil with other chemical compounds

• PLC/PRF/5 cells were not inhibited by maintenance in up to 60 microM of another chelating agent that has a similar affinity for iron, calcium disodium versenate (EDTA) [23].
• Combination therapy was also effective in potentiating the depletion of blood, hepatic and renal lead by calcium disodium EDTA and D-penicillamine (DPA), renal lead by DMSA and reversal of inhibited blood delta-aminolevulinic acid dehydratase (ALAD) activity by calcium disodium EDTA and DPA [24].
• A lead-intoxicated patient with extremely high blood lead levels and unexpectedly mild symptoms was studied prior to and following treatment with calcium disodium edetate (ethylenediaminetetraacetic acid) and then prior to and following oral administration of zinc sulfate [25].
• The kinetics of Yttrium-90 (Y-90) in bone of mice was investigated in combination with edetate calcium disodium (CaNa2EDTA) [26].
• The recommended management is immediate gastric lavage and subsequent chelation therapy with calcium EDTA and dimercaprol [27].

Gene context of Edathamil

• Short-term administration of dimercaptopropanol (BAL) and calcium disodium edetate (EDTA) for diagnostic and therapeutic lead mobilization [28].

Analytical, diagnostic and therapeutic context of Edathamil

• Chelation therapy was not administered because all the children had negative lead mobilization tests indicating limited response to the chelating agent, calcium disodium edetate (CaNa2EDTA) [29].
• In this study a close correlation [correlation coefficient (r) = 0.86, P less than 0.001] was found between the blood lead level of 20 lead workers and their urinary excretion of lead for 24 h after intravenous infusion with 1 g of the chelating agent calcium disodium edetate [30].
• Lead burdens were similar in both the study and control groups as assessed by 72-h chelatable urinary lead excretion after intramuscular injection of calcium disodium EDTA (0.74 +/- 0.63 vs. 0.61 +/- 0.40 mumol per 72 h, respectively), and by blood lead (0.35 +/- 0.23 vs. 0.35 +/- 0.20 mumol/l) [31].
• When copper was given in the form of copper calcium EDTA (B), deaths occurred within 48 hours of the subcutaneous injection of 3 or 4 mg copper per kg body-weight [32].
• INTERVENTION AND OUTCOME: The patient required narcotic analgesia for abdominal pain and was treated with chelation therapy with calcium ethylenediaminetetra-acetate (calcium EDTA) for five days which resulted in a high urinary excretion of lead and resolution of his symptoms over a period of several days [33].

References