Disease relevance of NITRILOTRIACETIC ACID

• The two best characterised obligately aerobic NTA-utilising genera (Chelatobacter and Chelatococcus) are members of the alpha-subgroup of Proteobacteria [1].
• Subacute nephrotoxicity and induction of renal cell carcinoma in mice treated with ferric nitrilotriacetate [2].
• Iron, as ferric nitrilotriacetate or ferric ammonium citrate, was administered to rat hepatoma cells (H4AZC2) that were grown in serum-containing media or in hormone-supplemented defined media on collagen matrices [3].
• An experimental model of copper toxicosis in terms of copper-induced cirrhosis of the liver was established with exogenous copper chelated by nitrilotriacetate [4].
• Rats and rabbits parenterally treated with a large daily dose of ferric nitrilotriacetate manifested diabetic symptoms such as hypergycemia, glycosuria, ketonemia, and ketonuria after approximately 60 days fo treatment [5].

High impact information on NITRILOTRIACETIC ACID

• It has been proposed that nitrilotriacetic acid be substituted for trisodium polyphosphates in detergents as a way to reduce the rate of eutrophication in the Great Lake Basin. The reaction of nitrilotriacetic acid with chlorine-containing solutions produces a hitherto unknown degradation production, N-formyliminodiacetic acid, in high yield [6].
• The effect of chloroquine was reversed by iron nitriloacetate, an iron compound that is soluble at neutral to alkaline pH, but not by holotransferrin, which releases iron only in an acidic environment [7].
• Chloroquine had no major direct effect on L. pneumophila multiplication in artificial media except at extremely high concentrations (15,000-fold that which inhibited L. pneumophila multiplication in mononuclear phagocytes), and inhibition at such concentrations was not reversed by iron nitrilotriacetate [8].
• In contrast to results in fetal calf serum (FCS), soluble Fe (ferric nitriloacetate) reversed 42/6 growth inhibition of serum-free HL60 cells [9].
• The intestinal fate of two tripeptides (triglycine and trileucine), which differ markedly in solubility and molecular weight, have been investigated by jejunal perfusion in healthy human volunteers [10].

Chemical compound and disease context of NITRILOTRIACETIC ACID

• The hydrophobic segment of the b subunit from E. coli F(1)F(0)-ATP synthase was modified with a histidine tag at the carbonyl terminus and was aggregated selectively by using a series of multivalent, dendritic chelating agents with nitrilotriacetic acid functional groups [11].
• Fe(III) bound to a chelator, nitrilotriacetate (NTA), has been reported to induce a high frequency of adenocarcinoma localized to the proximal tubules of the kidney in rodents [12].
• The chelating agents EDTA, o-phenanthroline, nitrilotriacetic acid (NTA), ethylenediamine-bis(o-hydroxyphenylacetic acid) (EDDA) or dimethylglyoxime prevented the expression of hydrogenase activity in batch cultures of nitrogen-fixing Azotobacter chroococcum, but did not inhibit preformed enzyme [13].
• Analysis of a clinical isolate of Acinetobacter baumannii showed that this bacterium was able to grow under iron-limiting conditions, using chemically defined growth media containing different iron chelators such as human transferrin, ethylenediaminedi-(o-hydroxyphenyl)acetic acid, nitrilotriacetic acid, and 2,2'-bipyridyl [14].
• The influence of nitrilotriacetic acid trisodium salt (NTA) on the mutagenic and clastogenic activity of several water-insoluble or poorly soluble chromium compounds was determined by means of the Salmonella/microsome assay (plate test on TA100 strain) and the sister-chromatid exchange (SCE) test in mammalian cell cultures (CHO line) [15].

Biological context of NITRILOTRIACETIC ACID

• Combined histochemical and biochemical analysis of sex hormone dependence of ferric nitrilotriacetate-induced renal lipid peroxidation in ddY mice [16].
• Hydroxyl radical production and human DNA damage induced by ferric nitrilotriacetate and hydrogen peroxide [17].
• Formation of this adduct under oxidative stress in vivo was immunohistochemically examined in rats exposed to ferric nitrilotriacetate, a carcinogenic iron chelate that specifically induces oxidative stress in the kidneys of rodents [18].
• There is, however, no clear interaction between the nitrilotriacetate anion and the synergistic anion binding site, Arg121 [19].
• Renal cortical genomic DNA derived from 10- to 12-week-old male C57BL/6 mice, of untreated control or 6 hours after intraperitoneal injection of 3 mg iron/kg ferric nitrilotriacetate, was enzyme digested, immunoprecipitated, cloned, and mapped to each chromosome [20].

Anatomical context of NITRILOTRIACETIC ACID

• Complexes of 111In3+ and nitrilotriacetate were encapsulated in ghosts made from human, rabbit, rat, and mouse erythrocytes, and their leakage was monitored by both methods [21].
• Triton-solubilized membranes were equilibrated with an affinity matrix consisting of the amiloride analogue A35 (5-N-(3-aminophenyl)amiloride) covalently coupled to Sepharose CL-4B beads through a triglycine spacer arm [22].
• The iron chelates of ethylenediaminetetraacetic acid (EDTA) and nitrilotriacetic acid were very active at promoting the hydrogen peroxide-dependent oxidation of porphyrinogens, and a similar role of iron was found for the NADPH-dependent oxidation of porphyrinogens by liver microsomes in vitro [23].
• Cultured chick embryo hepatocytes were iron-loaded with ferric nitrilotriacetate [24].
• Streptozotocin (STZ), a renal carcinogen, and trisodium nitrilotriacetate monohydrate (NTANa3), a renal carcinogen and tumor promoter, showed mild growth-enhancing effects on both cell lines, as determined by significant increases in SA, but not in cloning efficiency (CE) [25].

Associations of NITRILOTRIACETIC ACID with other chemical compounds

• The U1 snRNP, containing a histidine-tagged 70K protein, was isolated from cell extracts by anti m3G-cap immunoaffinity and subsequent nickel nitrilotriacetic acid chromatography [26].
• Distinct polyphosphoinositide binding selectivities for pleckstrin homology domains of GRP1-like proteins based on diglycine versus triglycine motifs [27].
• Metal dissociation constants for glyoxalase I from human erythrocytes were determined by use of nitrilotriacetic acid as a metal buffer [28].
• This previously inaccessible human P450 was purified to electrophoretic homogeneity (10.7 nmol of P450/mg) from solubilized bacterial membranes using two sequential chromatographic steps, nickel nitrilotriacetate followed by hydroxylapatite [29].
• Classical trajectory simulations are performed to study energy transfer in collisions of protonated triglycine (Gly)(3) and pentaglycine (Gly)(5) ions with n-hexyl thiolate self-assembled monolayer (SAM) and diamond [111] surfaces, for a collision energy E(i) in the range of 10-110 eV and a collision angle of 45 degrees [30].

Gene context of NITRILOTRIACETIC ACID

• The combined results demonstrate that cytohesin-1 triglycine participates in a major phosphatidylinositol 3-kinase-independent pathway linking cell-surface receptors to Arf1 activation and translocation in human granulocytes [31].
• Me2SO-differentiated HL-60 cells expressed ARNO and cytohesin-1 isoforms with a diglycine and a triglycine motif in their PH domains, respectively [31].
• Exposure of the cells to iron (200 micromol/L ferric nitrilotriacetic acid for 72 h) significantly decreased transferrin receptor mRNA (80%), DMT1 mRNA (57%) and IREG1 mRNA (52%) [32].
• To examine whether this effect is due to iron depletion we added iron chelates (ferric citrate, FeCi; ferric nitrilotriacetic acid, FeNTA) which can be internalized by cells without the requirement for Tf [33].
• We have used a combination of ammonium sulphate fractionation, nickel nitrilotriacetate affinity purification, ATP Sepharose affinity chromatography and Resource Q ion exchange chromatography to purify two different Cdc28p kinase complexes [34].

Analytical, diagnostic and therapeutic context of NITRILOTRIACETIC ACID

• Recombinant LHCII was isolated by detergent-mediated monomerization of pure trimers followed by affinity-chromatography on Ni(2+)-NTA-agarose (NTA is nitrilotriacetic acid) [35].
• The presence of (R)-HNE and (S)-HNE epitopes in vivo was immunohistochemically examined in the kidney of rats exposed to the renal carcinogen, ferric nitrilotriacetate, by which nuclear and cytosolic stainings with mAbR310 and mAbS412, respectively, were detected [36].
• We have measured the polarized visible Raman and FTIR spectra of trialanine and triglycine in D(2)O at acid, neutral, and alkaline pD [37].
• The stability of this complex is investigated here by using two concordant nanotechniques (surface forces apparatus and vesicle micromanipulation) that allow direct measurements of adhesion energies due to the chelation of nickel ions by nitrilotriacetate (NTA) groups grafted on surfaces [38].
• Induction of a wide range of C(2-12) aldehydes and C(7-12) acyloins in the kidney of Wistar rats after treatment with a renal carcinogen, ferric nitrilotriacetate [39].

References