Calcium Ethylenediaminetetraacetate Research Articles

Preparation of cellulose nanofiber/polyvinyl alcohol-based composite films for metal ion detection by starch/disodium calcium ethylenediaminetetraacetate synergistic complexation effect

Heavy metal pollution causes irreversible damage to plants, animals, and humans. Therefore, it is meaningful to develop facile, fast, and efficient strategies for heavy metal ion (HMI) detection. Here, a portable composite film (CPSE) was designed for HMI detection with high sensitivity and wide detection range. The CPSE was prepared by using cellulose nanofibers (CNF)/polyvinyl alcohol (PVA) as the matrix and utilizing modified starch (HPS) to assist disodium calcium ethylenediaminetetraacetate (EDTA-Ca) to form stable complexes with HMI. The R, G and B values (the three primary colors of light) were captured using an image acquisition system to produce an HMI standard color card successfully. Specifically, the composite film can effectively distinguish Cu2+, Pb2+ and Fe3+. The response time of the composite film to HMI was 2–4 s, and the detection ranges of Cu2+ and Fe3+ were 5–700 ppm and 10–1000 ppm, respectively. Additionally, the synergistic effect of HPS and EDTA-Ca led to the increase in tensile strength (1.59–1.71 times), tear strength (3.29–3.57 times), and glass transition temperature (~ 6 °C) compared to CNF/PVA/HPS and CNF/PVA/EDTA-Ca films. This study confirms the value of CPSE films as materials for HMI detection and suggests innovative ideas for designing similar biomass detection materials in the future.

Lead Levels in the Eggs of a Chicken With Lead Toxicosis

A 1.5-year-old Polish hen was presented with a history of watery droppings and poor vent tone. Results of diagnostic tests revealed blood lead at levels considered to be toxic. Chelation therapy was started with calcium ethylenediaminetetraacetate. The hen was laying eggs before, during, and after chelation therapy. Eggs were tested for the presence of lead by combining yolk and albumen together. Before chelation therapy, the level of lead in the egg tested was 14 μg. Two days after the end of chelation therapy, results of a second blood lead test revealed a drop to nontoxic levels. No lead was detected in the combined yolks and albumen of eggs collected 7-11 days after the end of chelation therapy. Four weeks after the end of chelation therapy, no lead was identified in the shells of tested eggs.

Uncommon Sources and Some Unsual Manifestations of Lead Poisoning in a Tropical Developing Country

Lead-containing cooking utensils, sometimes used in South Indian homes, and indigenous medications, widely used in India and increasingly in developed countries, may be responsible for lead intoxication in adults. We report chronic lead poisoning in five adult patients. Not all patients had abdominal colic, while dramatic weight loss, depression and encephalopathy were seen. Once recognized, lead poisoning is treatable and sometimes preventable. Response to chelation therapy with agents such as calcium ethylenediaminetetraacetate (CaEDTA) is impressive, although several courses of therapy may be necessary.

Deposition of Carbonated Hydroxyapatite (CO3HAp) on Poly(Methylmethacrylate) Surfaces by Decomposition of Calcium–EDTA Chelate

Inspired from the nature, the development of organic–inorganic composites between polymers and hydroxyapatite (HAp) has been investigated extensively. In this study, bone‐like apatite (carbonated hydroxyapatite, CO3HAp) was precipitated on poly(methylmethacrylate) (PMMA) films by the oxidative decomposition of Ca–EDTA (calcium–ethylenediamine tetraacetate) chelates. Corona‐treated PMMA films were soaked in a Ca–EDTA–PO4–H2O2 solution and aged at 63°C and pH∼9 for times ranging from 1 to 24 h. Apatite formed on PMMA films was characterized by X‐ray diffraction, Fourier transform infrared (FTIR), Scanning electron microscope, energy‐dipersive X‐ray spectroscopy, and carbon analysis. The apatite was found to be CO3HAp with Ca/P atomic ratio ranging between 1.3 and 1.9. Elemental analyses indicated that the carbonate content of the apatite phase was around 6.5 wt% after 24 h of aging time. Lattice parameters were estimated using a Rietveld profile‐analysis and found to be a=0.9438 nm and c=0.6901 nm. Furthermore, FTIR spectra indicated that the apatite deposited on PMMA was B‐type CO3HAp, in which carbonate ions occupy the phosphate sites. In the first 3 h of aging, isolated rod‐like HAp particles were observed. With time, the needle‐like crystallites radiate from a nucleus to form double‐spherulite shape particles. The crystallites grew into a continuous layer with a thickness of ∼15 μm after 24‐h aging. The adhesive strength between the PMMA substrate and the apatite layer was determined to be around 1.7 MPa.

Effects of acute and chronic oval exposure of lead on blood pressure and bone mineral density in rats

The immediate and late deleterious effects of early lead (Pb) exposure on human health are major challenges to the health professionals. Therefore, a major underlying contribution of Pb accumulated earlier in life to chronic disorders such as hypertension and osteopenia, commonly found in the elderly, cannot be definitively excluded. Using Sprague–Dawley rats, we examined the effects of drinking 1% Pb acetate on very young rats for 40 days on Pb kinetics, body weight (BW), systolic blood pressure (SBP) and bone mineral density (BMD) over a year-long period. We also examined the effects of early and later chelation using disodium calcium ethylenediaminetetraacetate (Na 2CaEDTA). The early ingestion and accumulation of Pb was associated with an increased SBP acutely that returned to control levels with continuing challenge and later rose above control months later after the Pb challenge had been halted. Early accumulation of Pb over a short period was also associated with decreased BMD at the end of one year. Chelation after the initial Pb challenge at various times favorably influenced the SBP but could not prevent the lowering of BMD.

Zinc in the extracellular area of the central nervous system is necessary for the development of kainic acid-induced persistent hyperalgesia in mice

Kainic acid produces a persistent hyperalgesia when injected intraperitoneally (i.p.) in the rat or mouse. At higher doses than those needed to influence nociception, kainic acid induces seizures and translocation of histologically reactive zinc in the hippocampus. We tested the hypothesis that zinc, localized in a population of small diameter primary afferent neurons, plays a role in kainic acid-induced hyperalgesia similar to that in the hippocampus where zinc translocation accompanies kainic acid-induced seizures. The importance of zinc in the extracellular area was assessed by the influence of compounds that chelate divalent cations (disodium calcium ethylene diaminetetraacetate (CaEDTA)) or zinc (dipicolinic acid (DPA)) on kainic acid-induced hyperalgesia. When measured using the tail flick assay, thermal hyperalgesia was blocked by pretreatment intrathecally (i.t.) with either 10 nmol of NaCaEDTA or 1 nmol of DPA, drugs whose distribution is limited to the extracellular area. Injection of 10 ng zinc chloride i.t. had no long-term effect on nociception or on kainic acid-induced hyperalgesia. Whether zinc is translocated in response to a hyperalgesic dose of kainic acid was determined using the zinc-selective dye, N-(6-methoxy-8-quinolyl)-para-toluenensulfonamide (TSQ), which produces a delicate stain in the neuropil of the mouse spinal cord as well as a dense stain in the hippocampus. Injection of a hyperalgesic dose of kainic acid failed to alter TSQ fluorescence in either the spinal cord or hippocampus, in contrast to the distinct bleaching of TSQ in the hippocampus 24 h after a convulsant dose of kainic acid. Together these data suggest that, while not translocated, zinc in the extracellular area is necessary but not sufficient for the development of kainic acid-induced hyperalgesia.

Erythrocyte ALA-d activity in experimentally lead-poisoned ducks and its change during treatment with disodium calcium EDTA

To determine useful procedures for the diagnosis and prognosis of lead poisoning in waterfowl caused by ingestion of lead pellets, erythrocyte delta-aminolevulinic acid dehydratase ( ALA-d) was investigated in experimentally lead-poisoned ducks. A highly positive correlation was observed between the concentration of blood lead and the ALA-d activity ratio (the ratio of activated:non-activated enzyme activity) in those birds given seven lead pellets (3 mm diameter). The ALA-d activity ratio rapidly increased after the administration of lead pellets, but began to fall immediately after the initiation of disodium calcium ethylenediamine tetra-acetate ( CaEDTA) therapy which resulted in a rapid decrease in the concentration of lead in the blood of these birds. In contrast, the ALA-d activity remained inhibited even after blood lead levels began to decrease following treatment. These results demonstrated that the ALA-d activity ratio is a very useful and sensitive indicator for the diagnosis and evaluation of therapeutic effects after lead poisoning in waterfowl.

Lead poisoning from Indian herbal medicine (Ayurveda)

To present a case of lead poisoning following ingestion of Indian herbal medicine. A 37-year-old man presented with a history of abdominal pain, anorexia and malaise. He had recently returned from a trip to India where he had been taking two different herbal tonics. Investigation revealed low-grade hepatitis and normocytic anaemia with prominent basophilic stippling. The blood lead concentration was high, and analysis of the herbal tablets revealed a very high lead content. 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. Lead poisoning in Australia is usually the result of chronic industrial exposure, but practitioners should be aware of the possibility of poisoning from other domestic sources such as unglazed pottery, cosmetics and herbal remedies, especially those from Asia and India, in which lead may be present in high concentration. Patients from Asia who present with unexplained anaemia or abdominal symptoms should be asked about exposure to such sources.

Permeability of fetal microvessels in the perfused term human placenta

The toxicity of calcium ethylenediaminetetraacetate (CaEDTA) resulting from sustained iv infusion was studied in dogs. Signs of toxicity included vomiting, depression, and, occasionally, bloody diarrhea. The dogs were in a shocklike state terminally. Because of the reported nephrotoxicity of the drug, parameters of renal function were measured using conventional steady-state techniques. Glomerular filtration rate, renal plasma flow, and tubular maxima for glucose and PAH were decreased 8–22% following CaEDTA infusion; acetate enhancement of TmPAH was substantially reduced. Essentially no changes occurred in blood urea nitrogen, plasma electrolyte concentrations, or urinary excretion rates of sodium, potassium, or chloride. Histopathologic changes included hemorrhage and necrosis of intestinal epithelium with loss of villous structure and a necrotizing nephrosis of the proximal convoluted tubules.Evaluation of intestinal function revealed a marked depression of glucose absorption but no significant changes in the net fluxes of sodium, potassium, or chloride from the duodenum as toxicity developed. The permeability of the intestine to a volume marker was greatly increased. Studies of the intestinal diffusion ratios of solutes of various molecular sizes indicated the permeability increase was limited to the relatively large molecules.The results indicate CaEDTA is not primarily nephrotoxic in the dog and, therefore, renal failure probably is not the cause of death. The infusion of a very stable chelate, CrEDTA, was nontoxic. This suggested that CaEDTA toxicity is due to its chelative properties rather than some nonspecific action of the EDTA moiety.

Treatment of lead poisoning in wild geese

Summary Twenty-seven wild geese (Anser albifrons) suffering from lead poisoning caused by ingestion of lead shot were treated with disodium calcium ethylenediaminetetraacetate. The concentration of lead in blood ranged from 0.4 to 23.0 μg/ml, with a mean concentration of 5.6 μg/ml. In 22 of the birds, 1 to 48 lead pellets (mean, 10.5 pellets/bird) were seen on radiographs of their gizzards. Eleven of 27 birds recovered 3 to 8 weeks after the initiation of treatment. In the birds that recovered, the lead pellets were rapidly eroded as the birds recovered their appetites in response to treatment, and disappeared radiographically between treatment days 17 and 52. The birds that did not survive died within 4 weeks, despite decreased concentrations of lead in blood. Of these 16 birds, 15 had radiographic evidence of impaction of the proventriculus at the first examination and no evidence of resolution of the impaction at the time of death. In contrast, only 2 of the 11 geese that recovered had impaction of the proventriculus at the time of admission. Thus, the condition of the proventriculus seems to be the first consideration to evaluate in the prognosis of lead poisoning in geese.

鉛中毒に罹患したハクチョウとマガンの治療

During the period from April to May 1990, 18 swans (Cygnus spp.) and 80 wild geese (Anser albifrons) were found emaciated or dead because of lead-poisoning caused by ingestion of lead shots at Lake Miyajima in Hokkaido. Twenty-seven wild geese, four Whooper Swans (C. cygnus cygnus), and two Bewick's swans (C. cygnus bewickii) were treated using disodium calcium ethylenediaminetetraacetate (CaEDTA). The concentration of blood lead at the time of admission averaged 4.6, ranging from 3.2 to 8.0μg/ml in swans, and averaged 5.6, ranging from 0.4 to 23.0μg/ml in wildgeese. In all of the swans 4 to 40 lead pellets, with an average of 17 were seen on radiographs of their gizzards. In 22 of the geese 1 to 48 lead pellets, with an average of 10.5 per bird, were seen. The blood lead levels decreased to about 1/2 to 1/5 of the initial values one week after the institution of the therapy in all the bird treated. Eleven of 27 birds recovered 3 to 8 weeks after the therapy. These lead shots were rapidly eroded as the birds recovered their appetite in re-sponse to the treatment and disappeared no radiographs during treatment days 17 to 52. Sixteen geese and all the swans failed to recover their apPetite and died within 4 weeks in spite of a decrease in the concentra-tion of blood lead.

Comparative mobilization of lead by chelating agents

The relative abilities of approximately 20 chelating agents to act as antagonists for acute and chronic lead poisoning have been examined in the mouse. The acute LD 50 for lead acetate trihydrate was determined and found to be 135.3 mg Pb/kg for i.p. injection with a 95% confidence interval of 87.1–210.3 mg Pb/kg. The relative efficacy of chelating agents to reduce liver, kidney, spleen, bone and brain levels of lead was determined. The movement of lead from the liver to the bone was followed during the first 7 days post injection and was found to result in appreciable changes in the lead levels of these organs from day to day during this entire period. Of the compounds examined, the ones which were most effective in mobilizing lead under various conditions included meso-2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercaptopropane-1-sulfonate (DPMS), disodium calcium ethylenediaminetetraacetate (Na 2CaEDTA), trisodium zinc triethlenetetraminehexaacetate, dicalcium ethylenediaminetetra(methylenephosphonate) (Ca 2EDTPO) and diethyl dimercaptosuccinate (DEMSA) and 2,3-dimercapto-1-propanol (BAL).

Calcium ethylenediaminetetraacetate toxicity in the rat: Ultrastructural effects on skin collagen

The effect of calcium ethylenediaminetetraacetate (CaEDTA) i.v. infusion on skin ultrastructure was studied in the rat with the aid of transmission electron microscopy. High magnification electron micrographs of collagen fibrils were analysed with a computer aided image analyser, in terms of the Gaussian distribution of fibril diameter and the distance between cross striations of collagen fibrils (D-spacing). CaEDTA caused marked depletion of collagen fibrils in the skin. The collagen fibrils from CaEDTA treated rats exhibited significant increases in D-spacing (about 30%) and diameter (about 40%) compared to saline treated controls. These findings are consistent with earlier published biochemical data indicating that CaEDTA enhances collagen degradation in the rat.

Rapid separation of linear and cyclic glucooligosaccharides on a cation-exchange resin using a calcium ethylenediaminetetraacetate solution as eluent

Rapid separation of linear and cyclic glucooligosaccharides on a cation-exchange resin using a calcium ethylenediaminetetraacetate solution as eluent

Effect of chronic lead on the haematology, blood glutathione and bone marrow non-haeme iron of dogs.

Ten clinically normal male beagle dogs were used in the study. Two dogs served as control, 4 received 2 mg lead/kg daily and 4 received 5 mg lead/kg/daily. Lead was administered for 13 weeks, after which one-half of each experimental group was treated with calcium ethylene diaminetetraacetate (CaEDTA) for 5 days. All animals were then monitored for another 4 weeks. Blood lead levels, haematology, blood glutathione concentration, and the number of bone marrow cells with stainable iron granules were measured weekly during the 18-week experimental period. Clinical signs of poisoning were observed only in one dog in the high dose group after 6 weeks. The signed included emaciation, anorexia, muscular weakness, evidence of abdominal pain and depression. These signs were reversed with cessation of lead dosing and CaEDTA treatment. Blood lead levels and the number of marrow cells with non-haeme iron increased in both lead-dosed groups; nucleated red blood cells increased only in high lead dosed group. There was a trend for an increased packed cell volume in all groups; however, the high lead dosed group did not increase as fast. No significant changes were observed in blood glutathione concentration and in other haematologic parameters. There were no differences in the parameters studied between the dogs treated with CaEDTA and those not so treated. Blood lead levels and the number of nucleated red blood cells decreased after cessation of lead administration and the number of marrow cells with iron also tended to decrease after lead removal.

EDTA and the rat intestine: Rosenblatt, D. E. & Aronson, A. L. (1978). Calcium ethylenediaminetetraacetate (CaEDTA) toxicity: time-and dose-response studies on intestinal DNA synthesis in the rat. Expl mol. Path.28, 202. Rosenblatt, D. E., Doyle, D. G. & Aronson, A. L. (1978). Calcium ethylenediaminetetraacetate (CaEDTA) toxicity: time- and dose-response studies on intestinal morphology in the rat. Expl mol. Path.28, 215

EDTA and the rat intestine: Rosenblatt, D. E. & Aronson, A. L. (1978). Calcium ethylenediaminetetraacetate (CaEDTA) toxicity: time-and dose-response studies on intestinal DNA synthesis in the rat. Expl mol. Path.28, 202. Rosenblatt, D. E., Doyle, D. G. & Aronson, A. L. (1978). Calcium ethylenediaminetetraacetate (CaEDTA) toxicity: time- and dose-response studies on intestinal morphology in the rat. Expl mol. Path.28, 215

Renal ultrastructural changes induced by calcium EDTA in rats

Calcium ethylenediaminetetraacetate (CaEDTA) was found to induce definite ultrastructural changes in the rat kidney, when infused intravenously at toxic doses (6 mmoles/kg/24 h). These changes consisted of increased vacuolation and lysosomal activity in the proximal tubular epithelium and decreased electron density of the glomerular basement membrane. No abnormalities were seen in the mitochondria.

Calcium ethylenediaminetetraacetate (CaEDTA) toxicity—Effect of lysosomal stabilizers and labilizers on CaEDTA-induced collagen degradation in the rat

Degradation of collagen accompanies the progression of CaEDTA toxicity in the rat. After the parenteral administration of CaEDTA (6 m-moles/kg/24 hr, constant i.v. infusion for 48 hr), the urinary excretion of hydroxyproline is markedly increased. Radioisotope studies indicated that the source of this enhanced urinary hydroxyproline is the degradation of both mature and immature collagen. The present study was concerned with the effect of known lysosomal stabilizers and labilizers on CaEDTA-induced collagen breakdown. Massive doses of cortisol (50 mg/kg/8 hr, i.m.), as well as other anti-inflammatory agents believed to stabilize lysosomal membranes, were administered together with CaEDTA to rats. The concurrent administration of cortisol partially antagonized the degradative action of CaEDTA as evidenced by a significant reduction in urinary hydroxyproline excretion. Radioisotope labeling experiments traced this reduction in urinary hydroxyproline to inhibition of CaEDTA-induced degradation of mature (insoluble) collagen. In contrast, the concurrent administration of CaEDTA and vitamin A palmitate (250,000 I.U./kg/12 hr, s.c.), a lysosomal labilizer, produced a synergistic increase in urinary hydroxyproline excretion which was the result of increased breakdown of newly formed (soluble, immature) collagen. These results suggest that lysosomal mechanisms play a role in the degradation of collagen produced by CaEDTA.

Calcium ethylenediaminetetraacetate (CaEDTA) toxicity: Studies on the mechanism of CaEDTA potentiation of pentobarbital anesthesia in the rat

Rats which received an iv infusion of CaEDTA (6 mmol/kg/24 hr for 36 and 48 hr) were more susceptible to the anesthetic effect of pentobarbital Na than rats similarly infused with 0.9% NaCl solution. Less mg/kg pentobarbital Na, administered iv, were required to induce a state of surgical anesthesia. The data indicated that the potentiative action of CaEDTA probably was due to an effect on central neurones rather than enhanced distribution of the anesthetic to the brain. This contention was based upon the following findings in CaEDTA-treated rats relative to controls: lower pentobarbital concentrations in the brain at the onset of anesthesia, no difference in brain/plasma concentration ratios of anesthetic when appropriate corrections were made for binding to plasma proteins and pH-p K A relationships in blood, and no difference in brain/plasma concentration ratios of a normally nonpermeating solute. Moreover, when standard doses of pentobarbital Na were given ip, CaEDTA-treated rats slept significantly longer and concentrations of pentobarbital in plasma and brain were significantly less than controls on arousal. Dexamethasone antagonized the potentiative effect of CaEDTA on pentobarbital anesthesia. The occurrence of higher concentrations of pentobarbital in brain and a lower brain/plasma concentration ratio at the onset of anesthesia suggested the steroid acted to stabilize cerebral neurones to the effect of the anesthetic as well as impede the distribution of pentobarbital to the brain. Serotonin concentrations were found to be significantly decreased in brain, duodenum, and kidney, but not the liver, consequent to CaEDTA administration. The iv infusion of calcium acetate, equimolar to CaEDTA, also potentiated barbiturate anesthesia.

Effects of ethylenediaminetetraacetate (EDTA) on urinary excretion of hydroxyproline, calcium and phosphorus in the rat.

The effects of ethylenediaminetetraacetate (EDTA) were studied in rats. Intravenous infusion of 4.84 mM Na2EDTA increased the urinary excretion of calcium six-fold, phosphorus three-fold and hydroxyproline 55% in 158 g thyroparathyroidectomized (TPTXed) rats. Calcitonin (25 MRC mU/rat/h) abolished the sodium EDTA-induced increase in hydroxyproline excretion, presumptive evidence that sodium EDTA was acting on bone. To determine whether the changes induced by sodium EDTA are due to lowering of plasma calcium, rats were infused with 4.84 mM ethylenebis(oxyethylenenitrilo)tetraacetic acid (EGTA), a more specific calcium chelator. EGTA increased the urinary excretion of calcium and phosphorus (P<0.001) but not hydroxyproline in thyroparathyroidectomized rats. Furthermore, when TPTXed rats were infused with calcium EDTA (4.84 mM Ca2EDTA) in order that ionic calcium concentration would not be altered, hydroxyproline excretion was again markedly increased but phosphorus excretion was decreased by 26%. Since the displacement of the sodium ions in Na2EDTA by calciumin vivo is instantaneous, and since calcium EDTA itself induces collagenolysis, the increase in urinary hydroxyproline excretion due to sodium EDTA cannot be attributed solely to lowering of plasma calcium. From these data two conclusions are drawn. First, sodium EDTA enhances bone breakdown independently of its effect on parathyroid hormone secretion. Second, since bone plays a major role in the maintenance of plasma calcium, interpretation of results should be made with caution in those investigations in which EDTA is used to study calcium homeostasis.