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PubMed2001

Ferrate treatment for removing chromium from high-level radioactive tank waste.

A method has been developed for removing chromium from alkaline high-level radioactive tank waste. Removing chromium from these wastes is critical in reducing the volume of waste requiring expensive immobilization and deep geologic disposition. The method developed is based on the oxidation of insoluble chromium(III) compounds to soluble chromate using ferrate. This method could be generally applicable to removing chromium from chromium-contaminated solids, when coupled with a subsequent reduction of the separated chromate back to chromium(III). The tests conducted with a simulated Hanford tank sludge indicate that the chromium removal with ferrate is more efficient at 5 M NaOH than at 3 M NaOH. Chromium removal increases with increasing Fe(VI)/Cr(II) molar ratio, but the chromium removal tends to level out for Fe(VI)/ Cr(III) greaterthan 10. Increasingtemperature leadsto better chromium removal, but higher temperatures also led to more rapid ferrate decomposition. Tests with radioactive Hanford tank waste generally confirmed the simulant results. In all cases examined, ferrate enhanced the chromium removal, with a typical removal of around 60-70% of the total chromium present in the washed sludge solids. The ferrate leachate solutions did not contain significant concentrations of transuranic elements, so these solutions could be disposed as low-activity waste.

Chromium↗
PubMed1993

Transformation of immortal, non-tumorigenic osteoblast-like human osteosarcoma cells to the tumorigenic phenotype by nickel sulfate.

Epidemiological studies have indirectly linked compounds of chromium, nickel and arsenic to human carcinogenesis. However, there is no evidence that metal compounds can transform human cells to the tumorigenic phenotype in culture. We show here that exposure to 36 microM NiSO4 for 48-96 h results in transformation of an immortal, nontumorigenic, osteoblast-like cell line, HOS TE85, to the tumorigenic phenotype. Continuous passaging following treatment leads to the formation of a few dense foci. The cells isolated and expanded from the foci are morphologically transformed, and form anchorage-independent colonies of the size and abundance comparable to that formed by Kirsten murine sarcoma virus transformed HOS TE85 cells. The transformed cells from tumors in nude mice, have enhanced levels of plasminogen activators and have lost the ability to form model bone matrix on extended culture in the presence of ascorbic acid and beta-glycerophosphate. A number of cell lines have been established from nude mouse tumors. Cytogenetic analysis reveals 16 marker chromosomes and an aberrant chromosome 16. This is the first report of the transformation of a human cell line to tumorigenic phenotype by a metal carcinogen.

Animals↗
PubMed1988

[Methodology and evaluation of exposure to fumes formed during welding of chromium-nickel steel].

Using various methods for determination of welding fumes components and taking into account a simultaneous determination of soluble compounds of chromium III and IV, hygienic evaluation in two working places employing different systems of MMA/SS welding, TIG/SS welding and padding was carried out. As it is indicated by the results, proper hygienic evaluation of working conditions is possible owing to the measurements of individual exposure of workers in the breathing zone, allowing for determination of chromium manganese, nickel, and, while applying low-hydrogen electrodes, also fluorides, in every test.

Air Pollutants, Occupational↗
PubMed1989

Molecular basis of hexavalent chromium carcinogenicity: effect on gene expression.

The carcinogenicity of chromium(VI) compounds is explained in terms of the "uptake-reduction" model. According to this model, chromium (VI) enters cells as the anionic tetrahedral species chromate, CrO4(2-), using normal cellular anion transport systems, such as the sulfate transport system. Redox-active enzymes and small molecules reduce chromium (VI) intracellularly and produce "reactive intermediates" capable of damaging cellular constituents. DNA is presumed to be a critical target within the cell; however, chromium (VI) itself is unreactive toward DNA under physiological conditions in vitro. Thus, the ability of chromium(VI) to damage DNA depends on the presence of cellular components capable of producing putative DNA-damaging agents, such as chromium(VI) thioester, chromium(V), chromium(IV), chromium(III), thiyl radical and hydroxyl radical, upon reaction with the chromium(VI). The exact nature of the DNA damage will be strongly dependent on the reactive intermediates produced by cellular components and systems active in chromium(VI) metabolism. The chromium(VI)-induced DNA damage disrupts the normal functioning of DNA in critical cellular processes, including transcription and replication. The effect of chromium(VI)-induced DNA damage on the function of DNA as a template for transcription has been examined in chick embryo liver in vivo. Chromium(VI) induced DNA-protein and DNA interstrand cross-links and suppressed the induction of 5-aminolevulinic acid synthase and cytochrome P-450 mRNA by porphyrinogenic drugs. In contrast, chromium(VI) increased the basal steady-state mRNA levels of these two inducible genes, but had no effect on the steady-state mRNA levels of the constitutive genes, beta-actin, conalbumin and albumin. Nuclear "run-off" transcription experiments showed that the effect of chromium(VI) on the steady-state levels of basal and drug-inducible 5-aminolevulinic acid synthase mRNA was principally the result of changes in the transcription rate of the 5-aminolevulinic acid synthase gene. Chromium(VI)-induced changes in gene expression correlated with the presence of DNA interstrand and DNA-protein cross-links, suggesting that chromium(VI)-induced DNA lesions lead to changes in expression of the targeted genes.

Animals↗
PubMed2005

Mutagenicity of chromium picolinate and its components in Salmonella typhimurium and L5178Y mouse lymphoma cells.

Chromium picolinate is one of the most commonly used chromium dietary supplements available in the United States, and it has been marketed to consumers for use in weight loss, increasing muscle mass, and lowering serum cholesterol. Chromium picolinate is a synthetic compound that provides a bioavailable form of Cr(III) that is absorbed better than dietary chromium. However, there are several reports that it can have adverse effects. In order to study the mechanism of observed cellular toxicity and mutagenicity, chromium picolinate and its component compounds, chromium (III) chloride and picolinic acid, were evaluated in Salmonella typhimurium and L5178Y mouse lymphoma cells. Neither chromium picolinate nor chromium chloride induced a mutagenic response in S. typhimurium. However, in the L5178Y mouse lymphoma mutation assay, chromium picolinate induced mutagenic responses without and with the addition of S9.

Animals↗
PubMed1989

Generation of PM2 DNA breaks in the course of reduction of chromium(VI) by glutathione.

The carcinogen chromate is efficiently taken up and reduced to chromium(III) compounds by various biological systems. To test the possible DNA damage induced in the course of chromium(VI) reduction, we used a combination of chromate with the reductant glutathione (GSH) as well as a green complex of chromium(V), which is formed in the reaction of chromate with GSH. The combination of chromate and glutathione was found to cause single-strand breaks in supercoiled circular DNA of the bacteriophage PM2. The green chromium(V) complex Na4(GSH)4Cr(V).8H2O, prepared from chromate and glutathione, also cleaved supercoiled PM2 DNA. No DNA-degrading effects were observed with either chromate or the final product of the reaction with GSH, a purple anionic chromium(III) GSH complex. The nature of the buffering agents revealed a strong influence on the extent of DNA strand breaks produced by chromate and GSH. A variation of the GSH concentration in the reaction with chromate and PM2 DNA, performed in sodium phosphate-buffered solutions showed an initial increase in the number of strand breaks at GSH concentrations up to 1 mM followed by a decline at higher GSH concentrations. Since neither chromate, when administered individually, nor the final product of chromium(VI) reduction, the purple chromium(III) GSH complex, produced any detectable DNA cleavage, the critical steps leading to DNA strand breaks occur in the course of the conversion of chromium(VI) to chromium(III) by GSH, the most abundant intracellular low molecular thiol. Moreover, the demonstration that DNA cleavage is induced in the presence of the chromium(V) complex identifies chromium(V) as the oxidation state of the metal, which is involved in the steps leading to DNA-damaging effects of chromate.

Bacteriophages↗
PubMed1991

Differential DNA-protein crosslinking in lymphocytes and liver following chronic drinking water exposure of rats to potassium chromate.

Carcinogenic chromium (VI) compounds are persistent environmental contaminants with potential for human exposure through drinking water. One lesion associated with chromium (VI) exposure is the formation of DNA-protein crosslinks (DPC). In an attempt to develop markers of chromium exposure, the formation of DPC in lymphocytes was investigated. Fisher 344 rats were exposed to K2CrO4 in their drinking water for 3 and 6 weeks at concentrations of 100 and 200 ppm chromium. No DPC could be detected in isolated splenic lymphocytes using the alkaline elution technique or by using a polyclonal antibody to chromate-induced DPC. However, increased complexing of proteins with DNA was demonstrated in liver following 3 weeks of exposure at both 100 and 200 ppm chromium. Intraperitoneal administration of potassium chromate did not induce detectable DPC in lymphocytes; however, an increased association of proteins with isolated DNA was detected in the liver. DPC were also induced in isolated splenic lymphocytes following a 2-hr exposure in vitro to 100 microM K2CrO4 in a salts-glucose medium. Although chromium was detected in blood, liver, and kidney, blood levels were comparatively much lower. A comparison of chromium levels required to induce DPC in lymphocytes in vitro and the amount absorbed orally suggests that the white blood cell chromium levels following oral exposure may be too low to induce measurable DNA-protein crosslinks in lymphocytes.

Animals↗
PubMed1991

Chromium(III) bound to DNA templates promotes increased polymerase processivity and decreased fidelity during replication in vitro.

Carcinogenic chromium [Cr(VI)] compounds are reduced intracellularly to DNA- and protein-reactive chromium(III) species. However, the role of Cr(III) ions in chromium-induced genotoxicity remains unclear. We have investigated the effects of chromium(III) binding on DNA replication and polymerase processivity in vitro. Chromium ions bind slowly and in a dose-dependent manner to DNA. Micromolar concentrations of free chromium inhibit DNA replication, but if the unbound chromium is removed by gel filtration, the rate of DNA replication by polymerase I (Klenow fragment) on the chromium-bound template is increased greater than 6-fold relative to the control. This increase is paralleled by as much as a 4-fold increase in processivity and a 2-fold decrease in replication fidelity. These effects are optimum when very low concentrations of chromium ions are bound to the DNA [3-4 Cr(III) ions per 1000 nucleotide phosphates]. Increased concentrations of chromium lead to the production of DNA-DNA cross-links and inhibition of polymerase activity. These results suggest that low levels of DNA-bound chromium(III) ions may contribute to chromium mutagenesis and carcinogenesis by altering the kinetics and fidelity of DNA replication.

Binding Sites↗
PubMed1989

Analyses of chromium and nickel in human pulmonary tissue. Investigations in lung cancer patients and a control population under special consideration of medical expertise aspects.

After inhalative occupational exposure to certain compounds containing nickel and chromium (mostly over many years), an accumulation of these metals may occur in the lung tissue. This is of particular importance, both from a toxicological point of view and with regard to expert reports, since certain nickel and chromium compounds may induce lung cancers. In the context of this study, samples of pulmonary tissue from 34 deceased persons from the Bergen area (Norway) were analysed by atomic absorption spectrometry with regard to their content of chromium and nickel. The deceased comprised 21 men and 13 women. In 15 cases, death resulted from lung cancer; in the other 19 deceased, there was no indication of a malignant disease of the airways. The concentrations of nickel found in the lung tissue do not differ between patients with lung cancer and patients with healthy lungs. On the other hand, the concentration of chromium in the pulmonary tissue in the patients who had died of lung cancer and who had all been inhalative smokers, are higher (statistically significant) than in the nonsmokers or in those with healthy lungs. An accumulation of these two metals in the tumor matrix could not be detected. Both the average nickel and the average chromium concentrations were higher in the persons who had probably been exposed occupationally. Considering the present state of scientific knowledge, the aspects relevant to expert reports which result from the analyses of metals in the pulmonary tissue are discussed.

Adult↗
PubMed1996

A role for molecular oxygen in the formation of DNA damage during the reduction of the carcinogen chromium (VI) by glutathione.

Although well-established as carcinogens, the way in which chromium (VI) compounds exert their carcinogenic, mutagenic, and DNA-damaging potential remains obscure. It is clear that inside cells chromium(VI) is activated to its ultimate carcinogenic form by reducing agents including glutathione (GSH). The present study is intended to clarify if Fenton mechanisms are likely to be important in the formation of DNA lesions by chromium(VI) in combination with GSH. In buffer solutions which were treated to remove Fenton-active metal ions as well as in those not further purified, chromate and GSH induced similar numbers of single-strand breaks (SSB) in isolated PM2 DNA. Molecular oxygen was found to be essential for the formation of SSB, but chromium(V) species arising from chromate/GSH, unless activated by oxygen, appeared to be unreactive toward DNA. Upon addition of Mn(II) to solutions of chromium(VI) and GSH a diminution of Mn(II) ESR signals was observed, good evidence for the presence of chromium(IV) species. Using gas chromatography/mass spectrometry in selective ion-monitoring mode and high-performance liquid chromatography with electrochemical detection, we were able to show that Cr(VI)/GSH failed to induce base modifications typical of hydroxyl radical attack on DNA. Experimental conditions which readily induced SSB gave rise to the formation of chromium-DNA adducts, clearly demonstrating that the generation of these two DNA lesions is not mutually exclusive. We conclude that models which ascribe the induction of chromium-DNA adducts to chromium(V) and the generation of oxidative DNA damage including SSB to hydrogen peroxide are oversimplistic. It is not necessary to invoke a mechanism requiring the presence of added hydrogen peroxide to account for the ability of Cr(VI)/GSH to cause SSB. Our findings suggest that the combination of GSH, molecular oxygen, and chromium(VI) can damage DNA via non-Fenton pathways.

Carcinogens, Environmental↗