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At least 1,171 records · Page 65Linked to original sources
PubMed1994

Chromate-mediated free radical generation from cysteine, penicillamine, hydrogen peroxide, and lipid hydroperoxides.

The Cr(VI)-mediated free radical generation from cysteine, penicillamine, hydrogen peroxide, and model lipid hydroperoxides was investigated utilizing the electron spin resonance (ESR) spin trapping technique. Incubation of Cr(VI) with cysteine (Cys) generated cysteinyl radical. Radical yield depended on the relative concentrations of Cr(VI) and Cys. The radical generation became detectable at a cysteine:Cr(VI) ratio of about 5, reached its highest level at a ratio of 30, and declined thereafter. Cr(VI) or Cys alone did not generate a detectable amount of free radicals. Similar results were obtained with penicillamine. Incubation of Cr(VI), Cys or penicillamine and H2O2 led to hydroxyl (.OH) radical generation, which was verified by quantitative competition experiments utilizing ethanol. The mechanism for .OH radical generation is considered to be a Cr(VI)-mediated Fenton-like reaction. When model lipid hydroperoxides such as t-butyl hydroperoxide and cumene hydroperoxide were used in place of H2O2, hydroperoxide-derived free radicals were produced. Since thiols, such as Cys, exist in cellular systems at relatively high concentrations, Cr(VI)-mediated free radical generation in the presence of thiols may participate in the mechanisms of Cr(VI)-induced toxicity and carcinogenesis.

Chromates↗
PubMed2006

Isolation and characterization of Cr(VI) reducing Cellulomonas spp. from subsurface soils: implications for long-term chromate reduction.

Microbial enrichments from Cr(VI) contaminated and uncontaminated US Department of Energy Hanford Site sediments produced Cr(VI) reducing consortia when grown in the presence of Cr(VI) with acetate, D-xylose or glycerol as a carbon and energy source. Eight of the nine isolates from the consortia were Gram positive and four of these were identified by 16S rRNA sequence homology and membrane fatty acid composition as belonging to the genus Cellulomonas. Two strains, ES6 and WS01, were further examined for their ability to reduce Cr(VI) under growth and non-growth conditions. During fermentative growth on D-xylose, ES6 and WS01 decreased aqueous Cr(VI) concentrations from 0.04 mM Cr(VI) to below the detection limit (0.002 mM Cr(VI)) in less than three days and retained their ability to reduce Cr(VI) even after four months of incubation. Washed ES6 and WS01 cells also reduced Cr(VI) under non-growth conditions for over four months, both with and without the presence of an exogenous electron donor. K-edge XANES spectroscopy confirmed the reduction of Cr(VI) to Cr(III). The ability to reduce Cr(VI) after growth had stopped and in the absence of an external electron donor, suggests that stimulation of these types of organisms may lead to effective long-term, in situ passive reactive barriers for Cr(VI) removal. Our results indicate that Cr(VI) reduction by indigenous Cellulomonas spp. may be a potential method of in situ bioremediation of Cr(VI) contaminated sediment and groundwater.

Cellulomonas↗
PubMed2003

Potential hazards of hexavalent chromate in our drinking water.

A consideration of the consequences of human exposure to hexavalent Cr in the drinking water has been compiled. Since there is an absence of adequate human data on this subject the problem has been analyzed not only from human and animal studies but also from a mechanistic point of view. This treatise has been inspired by recent reviews and speculations that suggest that we may safely drink hexavalent Cr in great excess of the current EPA and states drinking water standards of 50-100 ppb.

Absorption↗
PubMed2003

Reduction of chromate (CrO4(2-)) by an enrichment consortium and an isolate of marine sulfate-reducing bacteria.

An enrichment consortium and an isolate (isolate TKW) of sulfate-reducing bacteria (SRB) have been obtained from metal-contaminated marine sediments of Tokwawan, Hong Kong SAR. These bacteria are capable of reducing highly toxic and soluble hexavalent chromium (Cr6+) enzymatically into less toxic and insoluble trivalent chromium (Cr3+) under anaerobic conditions. The enrichment consortium almost completely (98.5%) reduced 0.6 mM Cr6+ in 168 h and the rate of reduction was 0.5 g (Cr6+) g(protein)(-1)h(-1). In comparison, with Cr6+ as the sole electron acceptor (as a surrogate for SO4(2-)), isolate TKW reduced 94.5% of the initially added Cr6+ (0.36 mM) in 288 h, with the rate of 0.26 g (Cr6+) g(protein)(-1)h(-1). Adsorption by these bacteria was not the major mechanism contributing to the transformation or removal of Cr6+. The biomass and Cr3+ in the cultures increased simultaneously with the reduction of Cr6+. These indigenous SRB might have potential application in bioremediation of metal contaminated sediments.

Adsorption↗
PubMed2000

Vibrational anharmonicity and vibrational Stark effect of sulfate ions trapped in potassium, rubidium and cesium chromate.

Room and low temperature (approximately 100 K) FT-IR and Raman spectra of the sulfate doped K2CrO4, Rb2CrO4 and Cs2CrO4 were recorded. The positions of the nu1, nu3, and nu4 fundamental mode components of the dopant anions were measured. Nine (out of possible ten) second-order stretch-stretch vibrational transitions of the dopant anions were detected. On the basis of these data, the anharmonicity constants and the corresponding harmonic eigenvalues were calculated for several vibrational transitions using second-order perturbation theory expressions. The anharmonicity of the studied second-order transitions of the type nu1 + nu3i increases in the order (SO4/K2CrO4) < (SO4/Rb2CrO4) < (SO4/Cs2CrO4), while for those of the type nu3j + nu3i it basically follows the trend: (SO4/K2CrO4) > (SO4/Rb2CrO4) < (SO4/Cs2CrO4). The measured relative Stark splittings of the nu3 and nu4 mode components of the dopant SO4(2-) anions, as well as the average X13i/3i3j values decrease in the order (SO4/K2CrO4) > (SO4/Rb2CrO4) > (SO4/Cs2CrO4). In all cases, the splitting is larger for nu3 than for nu4 modes, indicating a smaller angular than the bond length distortion. The theory of vibrational Stark effect suggests that the observed frequency shifts of the nu1, nu3 and nu4 mode components may be attributed to the increase of the field strength at the doped anion site going from K2CrO4 to Cs2CrO4. The Stark splitting of these modes, on the other hand, implies that the internal crystalline field vector is almost parallel to the (hypothetical) C2 axis of the slightly distorted dopant tetrahedral anions.

Anions↗
PubMed2005

Formation of soluble organo-chromium(III) complexes after chromate reduction in the presence of cellular organics.

Microbial reduction of hexavalent chromium [Cr(VI)] to trivalent chromium [Cr(III)] has been investigated as a method for bioremediation of Cr(VI) contaminated environments. The produced Cr(III) is thought to be insoluble Cr(OH)3; however, recent reports suggested a more complex fate of Cr(III). A bacterial enzyme system, using NADH as the reductant, converts Cr(VI)to a soluble NAD+-Cr(III) complex, and cytochrome c-mediated Cr(VI) reduction produces cytochrome c-Cr(III) adducts. In this study, Cr(VI) reduction in the presence of cellular organic metabolites formed both soluble and insoluble organo-Cr(III) end-products. Several soluble end-products were characterized by absorbance spectroscopy and electron paramagnetic resonance spectrometry as organo-Cr(III) complexes, similar to the known ascorbate-Cr(III) complex. The complexes remained soluble and stable upon dialysis against distilled H20 and over a broad pH range. The ready formation of stable organo-Cr(III) complexes suggests that organo-Cr(III) complexes are rather common, likely representing an integral part of the natural cycling of chromium. Thus, organo-Cr(III) complexes may account for the mobile form of Cr(II) detected in the environment.

Ascorbic Acid↗
PubMed1989

Studies with nonradioisotopic sodium chromate. II. Single- and double-label 52Cr/51Cr posttransfusion recovery estimations.

A recently developed nonradioisotopic 52Cr technique was used to measure either red cell volume or posttransfusion recovery of stored red cells. The experimental method uses Zeeman electrothermal atomic absorption spectrophotometry to measure red cell chromium. Results from the 52Cr method were compared with those from 51Cr single-label and 125I-albumin/51Cr double-label procedures using 49-day AS-1 red cell concentrates drawn and prepared according to standard procedures. In the first group of five donors, red cell volume was estimated concurrently with both 52Cr-labeled fresh red cells and 125I-albumin. The latter measured plasma volume from which red cell volume was estimated on the basis of the hematocrit (125I red cell volume). 51Cr-labeled stored red cells were transfused to measure posttransfusion recoveries. The correlation between 52Cr and 125I red cell volumes was significant (r = 0.68, p less than 0.01), and, in this group, the differences were not significant (p less than 0.05). Twenty-four-hour posttransfusion recoveries of 51Cr-labeled stored red cells averaged 66 +/- 5 percent when measured with the 125I/51Cr technique and 69 +/- 8 percent when measured with the 52Cr/51Cr method. In the second group of five donors, red cell volume was estimated by the 125I-albumin technique, and the posttransfusion recovery of stored red cells was quantitated by 51Cr- and 52Cr-labeled stored cells simultaneously. In this group, posttransfusion recoveries with 125I/51Cr averaged 73 +/- 7 percent; with 125I/52Cr, they averaged 75 +/- 10 percent. Using the single-label method of calculation, recoveries averaged 76 +/- 7 and 75 +/- 10 percent for the 51Cr and 52Cr methods, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Transfusion↗
PubMed2004

Human nucleotide excision repair efficiently removes chromium-DNA phosphate adducts and protects cells against chromate toxicity.

Intracellular reduction of carcinogenic Cr(VI) leads to the extensive formation of Cr(III)-DNA phosphate adducts. Repair mechanisms for chromium and other DNA phosphate-based adducts are currently unknown in human cells. We found that nucleotide excision repair (NER)-proficient human cells rapidly removed chromium-DNA adducts, with an average t((1/2)) of 7.1 h, whereas NER-deficient XP-A, XP-C, and XP-F cells were severely compromised in their ability to repair chromium-DNA lesions. Activation of NER in Cr(VI)-treated human fibroblasts or lung epithelial H460 cells was manifested by XPC-dependent binding of the XPA protein to the nuclear matrix, which was also observed in UV light-treated (but not oxidant-stressed) cells. Intracellular replication of chromium-modified plasmids demonstrated increased mutagenicity of binary Cr(III)-DNA and ternary cysteine-Cr(III)-DNA adducts in cells with inactive NER. NER deficiency created by the loss of XPA in fibroblasts or by knockdown of this protein by stable expression of small interfering RNA in H460 cells increased apoptosis and clonogenic death by Cr(VI), providing genetic evidence for the role of monofunctional chromium-DNA adducts in the toxic effects of this metal. The rate of NER of chromium-DNA adducts under saturating conditions was calculated to be approximately 50,000 lesions/min/cell. Because chromium-DNA adducts cause only small changes in the DNA helix, rapid repair of these modifications in human cells indicates that the presence of major structural distortions in DNA is not required for the efficient detection of the damaged sites by NER proteins in vivo.

Cell Line↗
PubMed1992

Transformation of non-tumorigenic osteoblast-like human osteosarcoma cells by hexavalent chromates: alteration of morphology, induction of anchorage-independence and proteolytic function.

Soluble chromium (VI) compounds either alone or in combination with 3-methylcholanthrene (MC) were used to transform non-tumorigenic osteoblast-like human osteosarcoma cells (HOS TE85). The Cr(VI) compounds were highly toxic to these cells with LC50 values in the range of approximately 0.5-1.0 microM. Continuous passaging of the treated cells resulted in sustained increase in anchorage-independent (AI) colony formation. Treatment with Cr(VI) and MC resulted in substantial increase in AI growth. At the XVth passage, a number of individual AI colonies were expanded in culture and used for further studies. The cells are refractory in appearance and grow as 'nests' rather than as monolayers. The cell lines have relatively high plating efficiency (PE) in soft agar and respond to promotional effect of phorbol-12-myristate-13-acetate by an increase in PE and in the size and number of AI colonies. While the isolated cells are not tumorigenic when tested in athymic nude mice, most of the lines possess higher levels of plasminogen activator (PA) activity, considered as one of the markers of transformation. This is also reflected in the increase in the steady state level of urokinase type PA mRNA. These results show that Cr(VI) compounds are capable of promoting human cells to an altered phenotype characteristic of a stage in the carcinogenesis cascade.

Animals↗
PubMed1984

Analysis of the induction of alkali sensitive sites in the DNA by chromate and other agents that induce single strand breaks.

CaCrO4 was shown to induce alkali labile sites in the DNA of Chinese hamster ovary cells by analysis of the lack of linearity in the alkaline elution curves, and by a study of the dependence upon pH in the elution of DNA from filters. The effect of CaCrO4 on these parameters was compared with N-methyl-N-nitrosourea, an agent known to produce alkali labile sites. Based upon the aforementioned parameters HgCl2, formaldehyde and X-rays caused the formation of frank single strand breaks with little or no induction of alkaline labile sites. These findings demonstrate differences in the production of alkali sensitive sites by agents that cause DNA single strand breaks.

Alkalies↗
PubMed2006

Lower mutagenicity but higher stability of Cr-DNA adducts formed during gradual chromate activation with ascorbate.

Recent epidemiological and risk assessment studies have found a very high risk of lung cancer among chromium(VI)-exposed workers even at permissible levels of exposure. However, mechanistic views on the key genotoxic role of transient Cr(V) intermediates were more consistent with the threshold or highly non-linear (heavy dose) models of genetic damage by intracellular Cr(VI). In this work, we examined the production of mutagenic DNA lesions during metabolism of Cr(VI) by its dominant reducer ascorbate (vitamin C) under conditions promoting increased yield of transient Cr forms. We found that slow reductive activation of Cr(VI) by limited concentrations of ascorbate resulted in a greater yield of DCFH-oxidizing Cr intermediates but these species were unable to cause DNA strand breaks. Cr(VI)-ascorbate reactions generated a high number of Cr-DNA adducts that were responsible for all mutagenic responses detected in Cr(VI)-treated pSP189 shuttle plasmids following their replication in human cells. Mutagenicity of DNA damage resulting from the reactions with increased stability of Cr intermediates was approximately four times lower relative to the conditions lacking detectable Cr(V) formation. Unlike other reactions, slow reduction of Cr(VI) with ascorbate produced Cr-DNA adducts that were more resistant to dissociation by chelators, suggesting multicoordinate binding of Cr(III) to DNA. Overall, our findings do not support the possibility that increased Cr(V) formation at depleted ascorbate levels modeling heavy dose exposures causes higher levels of mutagenic DNA damage.

Ascorbic Acid↗