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PubMed2001

In-situ separation of chromium(III) and chromium(VI) and sequential ETV-ICP-AES determination using acetylacetone and PTFE as chemical modifiers.

Electrothermal vaporization-inductively coupled plasma-atomic emission spectrometry (ETV-ICP-ES) has been used for the sequential determination of Cr(III) and Cr(VI). The method is based on the difference between the chelate reactions of the two Cr species and acetylacetone. Cr(III) chelate was separated from Cr(VI) and determined with use of acetylacetone as chemical modifier. The retained Cr(VI) in graphite tube was analyzed subsequently, after addition of polytetrafluoroethylene (PTFE) as chemical modifier. The different factors affecting the vaporization behavior of Cr(III) acetylacetonate were investigated in detail. The detection limits for Cr (III) and Cr(VI) were 0.56 and 1.4 ng mL(-1), respectively, and relative standard deviations for 0.1 microg mL(-1) Cr(III) and 0.1 microg mL(-1) Cr(VI) were 2.5% (n = 6) and 4.8% (n = 6), respectively. The linear ranges of the calibration curve for both Cr(IIl) and Cr(VI) covered three orders of magnitude. The proposed method was used to analyze water samples with satisfactory results.

Calibration↗
PubMed2005

Binding of chromium(VI) to histones: implications for chromium(VI)-induced genotoxicity.

The first evidence has been obtained for Cr(VI) (chromate) binding to isolated calf thymus (CT) histones under physiological conditions (pH 7.4, Cl(-) concentration 152 mM, 310 K). No significant Cr(VI) binding under the same conditions was observed for other extracellular and intracellular proteins, including albumin, apo-transferrin and G-actin, as well as for CT DNA. The mode of Cr(VI) binding to histones was studied by vibrational, electronic and X-ray absorption (X-ray absorption near-edge structure and X-ray absorption fine structure) spectroscopies and molecular mechanics calculations. A proposed binding mechanism includes electrostatic interactions of CrO(4) (2-) with protonated Lys and Arg residues of histones, as well as the formation of hydrogen bonds with the protein backbone. Similarly, Cr(VI) can bind to nuclear localization signals (typically, Lys- and Arg-rich fragments) of other nuclear proteins. Selective binding of Cr(VI) to newly synthesized nuclear proteins (including histones) in the cytoplasm is likely to be responsible for the active transport of Cr(VI) into the nuclei of living cells.

Animals↗
PubMed1989

Chromium (V) and hydroxyl radical formation during the glutathione reductase-catalyzed reduction of chromium (VI).

Electron spin resonance measurements provide evidence for the formation of long-lived Cr(V) intermediates in the reduction of Cr(VI) by glutathione reductase in the presence of NADPH and for the hydroxyl radical formation during the glutathione reductase catalyzed reduction of Cr(VI). Hydrogen peroxide suppresses Cr(V) and enhances the formation of hydroxyl radicals. Thus Cr(V) intermediates catalyze generation of hydroxyl radicals from hydrogen peroxide through a Fenton-like reaction. Thus the mechanism of Cr(VI) toxicity might involve the interaction between macromolecules and the hydroxyl radicals.

Animals↗
PubMed1996

Role of chromium(IV) in the chromium(VI)-related free radical formation, dG hydroxylation, and DNA damage.

A reactive Cr(IV) ester was synthesized from a reaction of CrO3 with 2,4-dimethyl-2,4-pentanediol as verified by electron spin resonance (ESR) and magnetic susceptibility measurements. ESR spin trapping studies demonstrate that the Cr(IV) ester is capable of generating hydroxyl free radical (.OH) through a Fenton-like mechanism (Cr(IV)+H2O2-->Cr(V)+.OH+OH-) with a concomitant generation of Cr(V) species (g = 1.9787). Cr(IV) caused DNA strand breaks as measured by electrophoretic assays. H2O2 enhanced the DNA strand breaks via .OH formation by a Cr(IV)-mediated Fenton-like reaction. In the Cr(IV)/H2O2 system, formate did not block Cr(V) formation, but prevented DNA damage, indicating that .OH radicals, and not Cr(V), caused the DNA damage. Reaction of Cr(VI) with ascorbate was also used as a source of Cr(IV). Incubation of Cr(VI), ascorbate, and DNA caused DNA strand breaks. A free radical trap, 5,5-dimethyl-1-pyrroline (DMPO), only slightly inhibited the DNA damage. Addition of Mn(II), which inhibited Cr(IV), caused significant protection. H2O2 enhanced the DNA damage via Cr(IV)-mediated .OH radical generation and Mn(II) inhibited the damage, again showing that Cr(IV) and its related .OH generation caused DNA strand breaks. HPLC measurements showed that .OH radicals generated by a Cr(IV)-mediated Fenton-like reaction generated 8-hydroxy-2'-deoxyguanosine from 2'-deoxyguanosine. The results demonstrate that Cr(IV) and its generated .OH radicals are capable of damaging DNA. Moreover, in comparison with Cr(V), Cr(IV) is a more potent DNA damaging agent.

Chromium↗
PubMed1984

Disposition of intratracheally administered chromium(III) and chromium(VI) in rabbits.

Intratracheal instillation of 51CrCl3 in anaesthetized rabbits resulted in partial absorption. In blood, the absorbed material was entirely confined to the plasma compartment. Only trace amounts were deposited in liver and kidney. By contrast, after similar application of Na(2)51CrO4 the bulk of blood radioactivity was present in erythrocytes. Substantial deposition occurred in liver and kidneys. It is concluded that Cr(VI) may enter the body unreduced via the lung and is partly deposited in cells over a prolonged period of time.

Animals↗
PubMed2005

Toxicity of chromium(III) and chromium(VI) to the earthworm Eisenia fetida.

The effects of Cr(III) and Cr(VI) on the survival, behavior, and morphology of the earthworm, Eisenia fetida, in water at pH 6, 7, and 8 and their toxicity in 10 different soils and an organic substrate have been assessed. A decrease in the pH of water resulted in increased toxicity of Cr to the earthworm. In water, both Cr species produced behavioral changes and morphological symptoms. The 48-h LC(50) values of Cr(III) at pH 6, 7, and 8 were 1.93, 2.55, and 2.78 mg/L, and those of Cr(VI) were 0.47, 0.61, and 0.63 mg/L, respectively. The 14-day median lethal concentrations (LC(50)) of Cr(III) and Cr(VI) for earthworm range from 1656 to 1902 mg/kg for Cr(III) and from 222 to 257 mg/kg for Cr(VI) in soil. In the organic substrate, the LC(50) values of Cr(III) and Cr(VI) were 1635 and 219 mg/kg, respectively. Stepwise multiple regression analysis predicted that clay content of soils accounted for 92% and 88% of the variation in the LC(50) values of Cr(III) and Cr(VI), respectively.

Animals↗
PubMed2006

Chromium fractionation in semi-arid soils amended with chromium and tannery sludge.

We studied Cr fractionation in three semi-arid soils (cultivated, under-the-canopy, and outside-the-canopy soils). The soils were amended with: Cr3+, Cr6+, tannery sludge, Cr3++tannery sludge, and Cr6++tannery sludge and all soils were incubated for 30 and 120 days at 25 degrees C. The Cr in three semi-arid soils was fractionated using sequential extraction (Tessier scheme). Data of Cr fractionation were used to find the correlations with microbial activities determined in previous work. The microbial activities: CO2-C evolved, dehydrogenase activity and nitrification were determined in the same soils amended with the same treatments. Tannery sludge was added at 0.0125 g g(-1) soil and Cr3+ or Cr6+ at 250 microg g(-1) soils. After 120 days of incubation, higher values of concentration of Cr were found in the residual fraction in the three soils amended with all the treatments, except cultivated and outside-the-canopy soils amended with Cr6++tannery. The non-residual fraction tended to decrease with time except in cultivated and outside-the-canopy soils amended with Cr6++tannery sludge. CO2-C evolved was significantly correlated (p<0.05 and p<0.001) with fractions bound to: Mn oxides, Fe oxides organic matter at 30 and 120 days of incubation (from r=0.827 to 0.979). Dehydrogenase activity was correlated with fractions bound to Fe oxides and bound to organic matter, and nitrification with fraction bound to organic matter at 30 days of incubation (r=0.874, 0.959, and 0.803, respectively). These results suggest that even in a sparingly available Cr fraction in semi-arid soils has effect on microbial activities.

Carbon Dioxide↗
PubMed2001

Separation of chromium (III) and chromium (VI) by capillary electrophoresis using 2,6-pyridinedicarboxylic acid as a pre-column complexation agent.

A simple method was developed for the simultaneous determination of Cr(III) and Cr(VI) by capillary zone electrophoresis (CZE), where Cr(III) was chelated with ligands to form anionic complexes. Nitrilotriacetic acid, N-2-hydroxyethylenediaminetriacetic acid, ethylenediaminetetraacetic acid, diethylenetriaminepentaacetic acid, and 2,6-pyridinedicarboxylic acid (PDCA) were investigated as Cr(III) complexing ligands. Of all the ligands studied, 2,6-PDCA with Cr(III) gave the largest UV response and high selectivity for Cr(III). In addition, the condition for pre-column derivatization, including pH, concentration ratio [Cr(III)/2,6-PDCA] and the stability of Cr(III) complexes were also examined. The separation of anionic forms of Cr(III) and Cr(VI) was achieved using co-CZE with UV detection at 185 nm. The electrolyte contained 30 mM phosphate, 0.5 mM tetradecyltrimethylammonium bromide, 0.1 mM 2,6-PDCA and 15% (v/v) acetonitrile at pH 6.4. The detection limits were 2 microM for Cr(III) and 3 microM for Cr(VI) and linear plots were obtained in a concentration range of 5-200 microM. The utility of the method was demonstrated for the determination of Cr(III) and Cr(VI) in contaminated soils.

Chromium↗
PubMed2001

Hydrogen peroxide effects on chromium oxidation state and solubility in four diverse, chromium-enriched soils.

High concentrations of H2O2 are being tested for in situ oxidation and remediation of buried organic contaminants in soils and groundwater. Peroxide is being considered as a direct chemical oxidant in Fenton-type reactions or as a source of oxidizing equivalents in bioremediation schemes. How H2O2 affects the oxidation state and solubility of Cr(III) and Cr(VI), common co-contaminants with organic chemicals, is explored here in four chemically diverse soils containing elevated levels of Cr. Soil contaminated with soluble Cr(VI) from chromite ore processing residue and soil containing high levels of recently reduced Cr (III) from electroplating waste both released dissolved Cr(VI) after single applications of up to 24 mM H2O2. In no case was there evidence that H202 reduced preexisting Cr(VI) to Cr(III), even though this would be allowed thermodynamically. Chromate in the leachates exceeded the U.S. EPA drinking water standard for total dissolved Cr (2 microM) by a factor of 10-1000. Anaerobic conditions in an organic-rich, tannery waste-contaminated soil protected Cr(III) from oxidation and mobilization. Mineral forms of Cr in serpentinitic soil near a former chromite mine also resisted oxidation on the time scale of days. Mobilization of Cr(VI) could be a hazardous consequence of using H2O2 for in situ remediation of chemically complex wastes, but H2O2 could prove attractive for ex situ treatment (i.e., soil washing). This paper demonstrates marked differences among Cr-contaminated soils in their capacity to release Cr(VI) upon chemical treatment with H2O2.

Carcinogens, Environmental↗
PubMed2003

Chromium remediation or release? Effect of iron(II) sulfate addition on chromium(VI) leaching from columns of chromite ore processing residue.

Chromite ore processing residue (COPR), derived from the so-called high lime processing of chromite ore, contains high levels of Cr(III) and Cr(VI) and has a pH between 11 and 12. Ferrous sulfate, which is used for remediation of Cr(VI) contamination in wastewater and soils via reduction to Cr(III) and subsequent precipitation of iron(III)/chromium(III) hydroxide, has also been proposed for remediation of Cr(VI) in COPR. Instead, however, addition of FeSO4 to the infiltrating solution in column experiments with COPR greatly increased leaching of Cr(VI). Leached Cr(VI) increased from 3.8 to 12.3 mmol kg(-1) COPR in 25 pore volumes with 20 mM FeSO4, reaching solution concentrations as high as 1.6 mM. Fe(II) was ineffective in reducing Cr(VI) to Cr(III) because it precipitated when it entered the column due to the high pH of COPR, while Cr(VI) in solution was transported away with the infiltrating solution. The large increase in leaching of Cr(VI) upon infiltration of sulfate, either as FeSO4 or Na2SO4, was caused by anion exchange of sulfate for chromate in the layered double hydroxide mineral hydrocalumite, a process for which scanning electron microscopy with energy-dispersive X-ray microanalysis provided direct evidence.

Anions↗
PubMed2001

EPR spectroscopic studies of the reduction of chromium(VI) by methanol in the presence of peptides. Formation of long-lived chromium(V) peptide complexes.

The synthesis and characterization of the first Cr(V) complexes with non-sulfur-containing peptides, which may mimic the chemistry of the intermediates in the formation of Cr-induced peptide-DNA cross-links in vivo, are reported. The reduction of Cr(VI) with methanol in the presence of a number of non-sulfur-containing peptides produced relatively stable Cr(V)-peptide complexes, which were characterized by EPR spectroscopy and electrospray mass spectrometry. The reaction of Cr(VI) with methanol alone (in the absence of peptide ligands) resulted in the formation of two Cr(V)-methanol intermediates, with giso values of 1.9765 and 1.9687. The methanol reduction of Cr(VI) in the presence of the glycine peptides, triglycine, tetraglycine, and pentaglycine resulted in the formation of both Cr(V)-methanol and Cr(V)-peptide intermediates, while only the Cr(V)-peptide complexes were detected in the reactions with the alanine peptides trialanine, tetraalanine, and pentaalanine. Similar EPR signals were observed for all of the Cr(V)-peptide complexes with giso values between approximately 1.986 and approximately 1.979, and AN values of (2.1-2.6) x 10(-4) cm-1.

Alanine↗
PubMed2004

Synthesis and characterization of a chromium(V) cis-dioxo bis(1,10-phenanthroline) complex and crystal and molecular structures of its chromium(III) precursor.

The first structurally characterized Cr(V) dioxo complex, cis-[CrV(O)2(phen)2](BF4) (2, phen=1,10-phenanthroline) has been synthesized by the oxidation of a related Cr(III) complex, cis-[Cr(III)(phen)2(OH2)2](NO3)3.2.5H2O (1, characterized by X-ray crystallography), with NaOCl in aqueous solutions in the presence of excess NaBF4, and its purity has been confirmed by electrospray mass spectrometry (ESMS), EPR spectroscopy, and analytical techniques. Previously reported methods for the generation of Cr(V)-phen complexes, such as the oxidation of 1 with PbO2 or PhIO, have been shown by ESMS to lead to mixtures of Cr(III), Cr(V), Cr(VI), and in some cases Cr(IV) species, 3. Species 3 was assigned as [CrIV(O)(OH)(phen)2]+, based on ESMS and X-ray absorption spectroscopy measurements. A distorted octahedral structure for 2 (CrO, 1.63 A; Cr-N, 2.04 and 2.16 A) was established by multiple-scattering (MS) modeling of XAFS spectra (solid, 10 K). The validity of the model was verified by a good agreement between the results of MS XAFS fitting and X-ray crystallography for 1 (distorted octahedron; Cr-O, 1.95 A; Cr-N, 2.06 A). Unlike for the well-studied Cr(V) 2-hydroxycarboxylato complexes, 2 was equally or more stable in aqueous media (hours at pH=1-13 and 25 degrees C) compared with polar aprotic solvents. A stable Cr(III)-Cr(VI) dimer, [Cr(III)(Cr(VI)O4)(phen)2]+ (detected by ESMS), is formed during the decomposition of 2 in nonaqueous media. Comparative studies of the oxidation of 1 by NaOCl or PbO2 have shown that [Cr(V)(O)2(phen)2]+ was the active species responsible for the previously reported oxidative DNA damage, bacterial mutagenicity, and increased incidence of micronuclei in mammalian cells, caused by the oxidation products of 1 with PbO2. Efficient oxidation of 1 to a genotoxic species, [Cr(V)(O)2(phen)2]+, in neutral aqueous media by a biological oxidant, hypochlorite, supports the hypothesis on a significant role of reoxidation of Cr(III) complexes, formed during the intracellular reduction of Cr(VI), in Cr(VI)-induced carcinogenicity. Similar oxidation reactions may contribute to the reported adverse effects of a popular nutritional supplement, Cr(III) picolinate.

Chromium↗