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PubMed2006

Incision of trivalent chromium [Cr(III)]-induced DNA damage by Bacillus caldotenax UvrABC endonuclease.

Some hexavalent chromium [Cr(VI)]-containing compounds are lung carcinogens. Once within cells, Cr(VI) is reduced to trivalent chromium [Cr(III)] which displays an affinity for both DNA bases and the phosphate backbone. A diverse array of genetic lesions is produced by Cr including Cr-DNA monoadducts, DNA interstrand crosslinks (ICLs), DNA-Cr-protein crosslinks (DPCs), abasic sites, DNA strand breaks and oxidized bases. Despite the large amount of information available on the genotoxicity of Cr, little is known regarding the molecular mechanisms involved in the removal of these lesions from damaged DNA. Recent work indicates that nucleotide excision repair (NER) is involved in the processing of Cr-DNA adducts in human and rodent cells. In order to better understand this process at the molecular level and begin to identify the Cr-DNA adducts processed by NER, the incision of CrCl(3) [Cr(III)]-damaged plasmid DNA was studied using a thermal-resistant UvrABC NER endonuclease from Bacillus caldotenax (Bca). Treatment of plasmid DNA with Cr(III) (as CrCl(3)) increased DNA binding as a function of dose. For example, at a Cr(III) concentration of 1 microM we observed approximately 2 Cr(III)-DNA adducts per plasmid. At this same concentration of Cr(III) we found that approximately 17% of the plasmid DNA contained ICLs ( approximately 0.2 ICLs/plasmid). When plasmid DNA treated with Cr(III) (1 microM) was incubated with Bca UvrABC we observed approximately 0.8 incisions/plasmid. The formation of endonuclease IV-sensitive abasic lesions or Fpg-sensitive oxidized DNA bases was not detected suggesting that the incision of Cr(III)-damaged plasmid DNA by UvrABC was not related to the generation of oxidized DNA damage. Taken together, our data suggest that a sub-fraction of Cr(III)-DNA adducts is recognized and processed by the prokaryotic NER machinery and that ICLs are not necessarily the sole lesions generated by Cr(III) that are substrates for NER.

Bacillus↗
PubMed1999

[Plasmid DNA breakage caused by reaction of intracellular redox compound with potassium dichromate].

OBJECTIVE: To study plasmid DNA breakage induced by hexavalent chromium (Cr(VI +)) compound in vitro. METHODS: DNA breakage was observed using plasmid relaxation method. RESULTS: pUC 118 plasmid DNA single strand breakage can not be caused by either ascorbic acid (1 mmol/L), or glutathione (5 mmol/L), or hydrogen peroxide (H(2)O(2), 17 mmol/L) or potassium dichromate (K(2)Cr(2)O(7), 0.5 mmol/L) alone. But, if DNA was incubated warmly with K(2)Cr(2)O(7) and intracellular redox compound, pUC118 plasmid DNA single strand breakage could be induced by K(2)Cr(2)O(7), ascorbic acid, or glutathione, or products of peroxidation reaction. K(2)Cr(2)O(7) (0.5 mmol/L) and H(2)O(2) (17 mmol/L) also could cause some double-strand breakage in plasmid. CONCLUSION: It suggests that ascorbic acid, glutathione and H(2)O(2) can play an important role in carcinogenicity of K(2)Cr(2)O(7).

Antioxidants↗
PubMed1986

Current concepts in occupational health: metals-chromium.

Chromium and its compounds have long been generally recognized as having potentially severe occupational health hazards. A brief review of the historical perspectives is provided. Failure to properly differentiate between the various valence states, which exhibit different toxicological properties and the physical state (solubility, particle size, etc.) as well as poor quantitation and characterization of exposure has led to confusion and potential error in estimating the risk inherent in working with chromium and its compounds. An overview is provided of the most recent and available data which address these issues in light of current concepts of scientific evaluation.

Carcinogens↗
PubMed1988

[The occupational risk in the manufacture of mineral pigments and iron oxide dyes].

The mineral pigments and ferric oxide dyes are used on a large scale in the paint and varnish industry, in building, chemical industry, polygraphy etc. For their production as basic raw materials are used lead, chromium and iron compounds. The concentrations of the toxic and accummulating lead and chromium in the air of the work environment surpass MAC and create most frequently "especially unfavourable" conditions of work. In all industrial processes the leading unfavourable factor is the chemical combined with unfavourable physical factors and overstress on the locomotor system. Changes were established in the organism of examined workers as result from the chronic effect of the factors of the work environment of the peripheral blood, digestive, nervous system and the skin. In view of reducing the risk of exposure to the toxic chemical factor it is imposed to take measures for sanitation of the work environment.

Absenteeism↗
PubMed2003

Complexities of chromium carcinogenesis: role of cellular response, repair and recovery mechanisms.

Certain hexavalent chromium (Cr(VI))-containing compounds are recognized occupational human lung carcinogens and may pose an environmental health risk. The carcinogenicity of Cr(VI) is targeted to particulate forms of moderate to low solubility. Soluble Cr(VI) oxyanions in the immediate cellular microenvironment traverse the cell membrane by non-specific anionic transporters. Cr(VI) is reductively metabolized within cells by agents including ascorbic acid (Asc), glutathione (GSH) and cysteine (Cys). During Cr(VI) reduction, a diverse range of genetic lesions are generated including Cr-DNA binary (mono) adducts, Cr-DNA ternary adducts, DNA protein crosslinks (DPCs), bi-functional (DNA interstrand crosslinks (ICLs)) adducts, single-strand breaks (SSBs) and oxidized bases. Some forms of Cr damage, such as ICLs, present physical barriers to DNA replication/transcription and, thus, likely promote a terminal cell fate such as apoptosis or terminal growth arrest. Other lesions, such as ternary DNA adducts, are potentially pre-mutagenic. Cr(VI) exposure elicits a classical DNA damage response within cells including activation of the p53 signaling pathway and cell cycle arrest or apoptosis. Moreover, Cr(VI) also induces the ATM-dependent DNA damage response pathway which is paradoxically required for both apoptosis and survival after Cr(VI) insult. In yeast, moderately cytotoxic concentrations of Cr(VI) result in an initial G1 arrest and delayed S phase progression, whereas less toxic levels of Cr(VI) induce G2 arrest, which requires homologous recombination for exit and survival. The past several years has witnessed many important advances in our understanding of the genetic/cellular damage produced by exposure to Cr(VI). Further information is needed regarding the potential involvement of oxygen radicals in Cr genotoxicity, the specific DNA repair pathways activated by Cr and the complex signaling mechanisms involved in the cellular response to Cr(VI). These pertinent issues must be considered in relation to the potential role that each plays in the induction of human respiratory tract cancer by particulate Cr(VI) compounds.

Air Pollutants, Occupational↗
PubMed2003

Barium chromate is cytotoxic and genotoxic to human lung cells.

Hexavalent chromium (Cr(VI)) compounds are widely accepted as human lung carcinogens. However, there have been few investigations of the genotoxicity of Cr(VI) in human lung cells. Moreover, our knowledge of the effects of Cr(VI) in human lung cells is further limited because the available data generally focus on the effects of only lead chromate (PbCrO(4)) and sodium chromate (Na(2)CrO(4)). To fully understand these carcinogenic compounds, the genotoxic effects to its target cells need to be evaluated for additional Cr(VI) salts. Accordingly, we investigated the cytotoxicity and clastogenicity of barium chromate (BC) in a human lung cell culture model (WTHBF-6 cells). We found that BC induced concentration-dependent cytotoxicity in WTHBF-6 cells, with relative survival of 88%, 74%, 67%, 12%, 3%, and 0.1% after exposure to 0.01, 0.05, 0.1, 0.5, 1, and 5 microg/cm(2) BC, respectively. Similarly, the amount of chromosomal damage also increased with concentration after a 24-h exposure. Specifically, 0.01, 0.05, 0.1, and 0.5 microg/cm(2) BaCrO(4) damaged 5%, 9%, 22%, and 49% of metaphase cells, with the total damage reaching 5, 10, 28, and 65 aberrations per 100 metaphases, respectively. Concentrations of 1 and 5 microg/cm(2) BC induced a profound cell cycle delay, and no metaphases were observed. The spectrum of damage included chromatid and chromosome-type lesions consistent with mechanistic events associated with the activation of oncogenes and inactivation of tumor suppressor genes. Overall the data indicate that BC is cytotoxic and genotoxic to human lung cells.

Barium↗
PubMed1981

Sources, transport and alterations of metal compounds: an overview. I. Arsenic, beryllium, cadmium, chromium, and nickel.

An overview is presented of the current state of knowledge of the salient aspects of the sources, transport, and alterations of arsenic, beryllium, cadmium, chromium, and nickel. This information is considered vital for a better assessment of the scope of potential human hazard to these ubiquitous toxicants and their compounds. Stress is focused on both natural and industrial activities, particularly on the latter's projected trends. Increasing use patterns per se of most of these metals, as well as aspects of waste disposal and the anticipated increased combustion of fossil fuels for power generation and space heating (particularly in the United States), are major causes of potential health concern. Additionally, attention is drawn to the need for increased research to fill the gaps in our knowledge in these vital areas, all in the hope of permitting a more facile identification and quantification of the potential hazard to exposure to these agents.

Air Pollutants↗
PubMed2005

Lead ions do not cause human lung cells to escape chromate-induced cytotoxicity.

Hexavalent chromium (Cr (VI)) compounds are established human lung carcinogens. Solubility plays a key role in Cr (VI) carcinogenicity, with the most potent carcinogens being water-insoluble or 'particulate'. Lead chromate is used as the prototypical particulate Cr (VI) compound since it is the most insoluble of these compounds. Previous work in our laboratory showed that lead chromate particles dissolve outside cells to produce chromium (Cr) and lead (Pb) ions and that the Cr ions were genotoxic. Pb has been hypothesized to play an epigenetic role in the carcinogenic activity of lead chromate, perhaps by allowing Cr-damaged cells to survive, however, this possibility has not been investigated. Accordingly, we determined the functional role of Pb and Cr ions in lead chromate-induced clonogenic survival. We found that vitamin C co-treatment eliminated Cr ion uptake, had only a slight effect on Pb ion levels, and eliminated lead chromate cytotoxicity. These data indicate that Cr ions caused the cytotoxicity. We found that lead chromate and soluble Cr (VI) induced similar amounts of cytotoxicity indicating that Pb does not play an epigenetic role and cause Cr-damaged cells to survive.

Ascorbic Acid↗
PubMed2003

Kinetics of an intratracheally administered chromium catalyst in rats.

Chromium-based catalysts are used for the synthesis of polyethylene, but little is known about the hazard and biomonitoring possibilities of this type of chromium for workers who may be occupationally exposed to such compounds. Therefore, the bioavailability and toxicokinetics of chromium were studied in male Wistar rats after a single intratracheal instillation (2 ml/kg body weight) of various doses (1, 5, or 25 mg/kg body weight) of the catalyst (approximately 1% chromium bound to an amorphous silica matrix), either before (CAT-Cr[III]) or after (CAT-Cr[VI]) heat treatment. The results were compared with those of equivalent amounts of two chromium salts (CrCl(3) and K(2) Cr(2) O (7). Each dose group was composed of three rats. The concentration of chromium was determined by atomic absorption spectrometry in urine (collected daily for 7 d) and in plasma, erythrocytes, lung, and liver tissue obtained 2 d (only highest concentration) and 7 d after dosing. On d 2, a significant increase in lung weight was found in the animals treated with the highest dose of the hexavalent Cr products. On d 7, on the basis of body weights, lung weights, and lung histology, there was no overt toxicity, except after the highest dose of CAT-Cr(VI). The elimination of all forms of chromium was apparently monoexponential, with calculated half-life elimination times in urine of 4-11 h for Cr(III) (CAT-Cr[III] and CrCl3 ) and 8-21 h for Cr(VI) (CAT-Cr[VI] and K(2) Cr(2) O(7). On d 2, the erythro-cytes Cr concentrations were significantly higher for the hexavalent Cr products than for the trivalent Cr products. After 7 d, the erythrocytes Cr concentrations were significantly increased above control values (3 microg/L) only in rats treated with the 2 highest doses of Cr( VI) compounds (12 and 64 microg/L for K(2) Cr(2) O(7), and 14 and 79 microg/L for CAT-Cr[VI]). The present study shows that intratracheally instilled Cr(VI) and Cr(III) have different toxicokinetic profiles and that the Cr(VI) catalyst has the same bioavailability and excretion kinetics as a water-soluble Cr(VI) salt. Exposure to chromium compounds could be monitored by measuring Cr concen-trations in urine (shortly after exposure) and in erythrocytes (also at later time points after high Cr[VI] exposure).

Animals↗
PubMed2003

[Chromium as an essential element].

Chromium was known for many years to be an element causing allergic reactions and having neurotoxic and carcinogenic effects. These effects can be observed especially in the case of hexavalent chromium. Only a little more than four decades ago trivalent chromium has been known as an essential element with relation to glycide and lipid metabolism. And only during several last years this chromium function has been revealed on a molecular level. After absorption in the gastrointestinal tract, chromium is most likely transported to cells bound to the plasma protein transferrin. Insulin initiates chromium transport into the cells where it is bound to the oligopeptide apochromodulin. This oligopeptide combined with four chromium(III) atoms forms chromodulin, which is important for amplifying the insulin signalling effect. After binding to insulin-activated receptor, chromodulin increases tyrosine kinase activity by one order. This enzyme forms a part of intracellular portion of insulin receptor. Chromium supplementation in people with chromium deficiency can improve glucose tolerance and some lipid metabolism parameters. The supplementation is indicated in persons with impaired glucose tolerance both in preclinical and manifested stadium of type 2 diabetes mellitus where increased lost of chromium in urine was documented. In these patients, chromium deficiency can participate in insulin resistance and hyperlipidaemia. Chromium is usually applied in the form of organic compounds: yeast extract or chromium(III) picolinate. Cr(III) picolinate can be reduced to compounds of Cr(II) in the cells which can then produce free hydroxyl radical in the so called Fenton reaction.

Animals↗
PubMed1976

A study on the clinical application of a direct leukocyte migration test in chromium contact allergy.

A capillary tube leukocyte migration inhibition assay has been adopted as an in vitro method for the demonstration of chromium hypersensitivity in twenty-two subjects with clinically proven or suspected chromium allergy. Two complexes of trivalent chromium and human serum albumin, exerting different migration inhibitory effects, have been prepared and used as the antigen. In the presence of the chromium-albumin complex with strong inhibitory activity, sensitivity to chromium was demonstrated independent of the clinical condition of the skin in all the patch test positive subjects. An additional positive response to the second chromium-albumin complex was observed only in those patients who were clinically in a state of exacerbation of an allergic contact dermatitis in which chromium allergy was an active causative factor. The results were not influenced by skin allergic reactivity to compounds other than chromium and the method was found to be of practical clinical value for diagnosing chromium allergy.

Albumins↗
PubMed1986

Abnormal deposits of chromium in the pathological human brain.

Three patients presented with encephalopathies: an undiagnosed degenerative disease of the brain, a degenerative cerebral disease in a patient with a myeloma but without a myelomatous deposit in the CNS and a malignant astrocytoma. Perivascular pallidal deposits (vascular siderosis) containing chromium, phosphorus and calcium plus sometimes traces of other elements were present in the three cases. Such deposits were present in the pallidal parenchyma and around vessels in the cerebellum in one case. Calcium and phosphorus are always present in any CNS calcification but the presence of chromium has not been reported. Chromium and its compounds (ingested, injected or inhaled) are toxic to humans and animals in trace doses. Approximately 900 cases of chromium intoxication have been reported and usually have had dermatological or pulmonary lesions (including cancer) but there is no report of involvement of the CNS. Sublethal doses of chromium nitrate injected intraperitoneally in rats and rabbits results in the presence of chromium in the brain. A thorough investigation was made to find the source of the chromium in these patients. Chromium was found to be present in trace amounts in the radiological contrast agents administered to these patients and in the KCl replacement solution and in mylanta, an antacid, given to one case. The evidence that chromium induced pathological changes in these three brains is circumstantial but shows that chromium can penetrate the human brain. This study indicates that vascular siderosis found in the brains of the majority of middle-aged and elderly humans is not simply an anecdotal pathological curiosity, but that it can serve as a route of entry for toxic products into the brain.

Aged↗
PubMed2001

Water quality analysis of mixtures obtained from tannery waste effluents.

In this study, the mixing of waste solution obtained from chrome tanning process and waste solution derived from liming of bovine leather was investigated. The liming process of bovine leather was performed using calcium carbonate and sodium sulfide, and the tanning process was performed using alkaline chromium sulfate. The analyses of waste solutions and sediments formed during the mixing process include pH values, the concentration of sulfides, the concentration of chromium(III) oxide, and parameters such as chemical oxygen demand and biochemical oxygen demand. All measurements were carried out before and after the mixing process. Results indicate that the mixing of the corresponding waste solutions yields the mixture effluents that are ecologically acceptable.

Animals↗
PubMed2004

Effects of taurine on oxidative stress parameters and chromium levels altered by acute hexavalent chromium exposure in mice kidney tissue.

The kidney has been regarded as a critical organ of toxicity induced by acute exposure to hexavalent chromium [Cr(VI)] compounds. Reactive intermediates and free radicals generated during reduction process might be responsible for Cr(VI) toxicity. In this study, the effects of pretreatment or posttreatment of taurine on Cr(VI)-induced oxidative stress and chromium accumulation in kidney tissue of Swiss albino mice were investigated. Single intraperitoneal (ip) potassium dichromate treatment (20 mgCr/kg), as Cr(VI) compound, significantly elevated the level of lipid peroxidation as compared with the control group (p<0.05). This was accompanied by significant decreases in nonprotein sulfhydryls (NPSH) level, superoxide dismutase (SOD), and catalase (CAT) enzyme activities as well as a significant chromium accumulation (p<0.05). Taurine administration (1 g/kg, ip) before or after Cr(VI) exposure resulted in reduction of lipid peroxidation levels and improvement in SOD enzyme activity (p<0.05). On the other hand, administration of the antioxidant before Cr(VI) exposure restored the NPSH level and CAT enzyme activity and also reduced tissue chromium levels (p<0.05), whereas posttreatment had only slight effects on these parameters. In view of the results, taurine seems to exert some beneficial effects against Cr(VI)-induced oxidative stress and chromium accumulation in mice kidney tissue.

Animals↗
PubMed1987

Effects of aluminum(III), chromium(III), and iron(III) on the rate of dissolution of calcium hydroxyapatite crystals in the absence and presence of the chelating agent desferrioxamine.

Aluminum ions (Al) and chromium (III) ions (Cr), as they exist in aqueous solution at neutral pH, adsorb onto calcium hydroxyapatite crystals (HAP) and severely inhibit their dissolution process, when present in concentrations less than 1 microM. Iron (III) ions (Fe), at concentrations up to 10 microM, have no effect on the dissolution process of HAP. The Fe-chelating agent desferrioxamine also forms strong complexes with Al but not with Cr. Desferrioxamine prevents the adsorption of Al to HAP and removes pre-adsorbed Al from the HAP surface, although not instantaneously, but has no significant effect on the adsorption of Cr to HAP. Desferrioxamine is also found to be capable of removing Al preadsorbed to bone powder.

Adsorption↗
PubMed2003

Effects of steric constraint on chromium(III) complexes of tetraazamacrocycles. Chemistry and excited-state behavior of 1,4-C2-cyclam complexes.

The synthesis and characterization of several Cr(III) complexes of the constrained macrocyclic ligand 1,4-C(2)-cyclam = 1,4,8,11-tetraazabicyclo[10.2.2]hexadecane is reported. The ligand appears to form only trans complexes, and the structure of trans-[Cr(1,4-C(2)-cyclam)Cl(2)]PF(6) is presented. The constraint imposed by the additional C(2) linkage distorts the bond angles significantly away from the ideal values of 90 and 180 degrees. The effect of the distortion is to enhance the aquation rate of trans-[Cr(1,4-C(2)-cyclam)Cl(2)](+) (k(obs) for trans-[Cr(1,4-C(2)-cyclam)(H(2)O)(2)](3+) formation = 6.5 x 10(-)(2) s(-)(1), 0.01M HNO(3), 25 degrees C) by over 5 orders of magnitude relative to trans-[Cr(cyclam)Cl(2)](+). The complexes trans-[Cr(1,4-C(2)-cyclam)Cl(2)](+) and trans-[Cr(1,4-C(2)-cyclam)(CN)(2)](+) are found to have extinction coefficients four to five times higher than their cyclam analogues, owed to the lack of centrosymmetry caused by the steric constraint. The trans-[Cr(1,4-C(2)-cyclam)(CN)(2)](+) complex is a very weak emitter in aqueous solution with a broad room-temperature emission centered at 735 nm (tau = 0.24 micros). Extended photolysis (350 nm, 15 h) of trans-[Cr(1,4-C(2)-cyclam)(CN)(2)](+) in aqueous solution results in CN(-) ligand loss. This is in stark contrast to its unconstrained cyclam analogue, which is photoinert and has a room-temperature emission lifetime of 335 micros.

Bridged Bicyclo Compounds, Heterocyclic↗
PubMed2005

Nucleotide excision repair functions in the removal of chromium-induced DNA damage in mammalian cells.

Some hexavalent chromium (Cr(VI))-containing compounds are human lung carcinogens. While ample information is available on the genetic lesions produced by Cr, surprisingly little is known regarding the cellular mechanisms involved in the removal of Cr-DNA adducts. Nucleotide excision repair (NER) is a highly versatile pathway that is responsive to a variety of DNA helix-distorting lesions. Binary Cr-DNA monoadducts do not produce a significant degree of helical distortion. However, these lesions are unstable due to the propensity of Cr(III) to form DNA adducts (DNA interstrand crosslinks, DNA-protein/amino acid ternary adducts) which may serve as substrates for NER. Therefore, the focus of this study was to determine the role of NER in the processing of Cr-DNA damage using normal (CHO-AA8) and NER-deficient [UV-5 (XP-D); UV-41 (ERCC4/XP-F)] hamster cells. We found that both UV-5 and UV-41 cells exhibited an increased sensitivity towards Cr(VI)-induced clonogenic lethality relative to AA8 cells and were completely deficient in the removal of Cr-DNA adducts. In contrast, repair-complemented UV-5 (expressing hamster XPD) and UV-41 (expressing human ERCC4) cells exhibited similar clonogenic survival and removed Cr-DNA adducts to a similar extent as AA8 cells. In order to extend these findings to the molecular level, we examined the ability of Cr(III)-damaged DNA to induce DNA repair synthesis in cell extracts. Repair synthesis was observed in reactions using extracts derived from AA8, or repair-complemented, but not NER-deficient cells. Cr(III)-induced repair resynthesis was sensitive to inhibition by the DNA polymerase delta/epsilon inhibitor, aphidicolin, but not 2',3'-dideoxythymidine triphosphate (ddTTP), a polymerase beta inhibitor. These results collectively suggest that NER functions in the protection of cells from Cr(VI) lethality and is essential for the removal of Cr(III)-DNA adducts. Consequently, NER may represent an important mechanism for preventing Cr(VI)-induced mutagenesis and neoplastic transformation.

Animals↗
PubMed2004

Soluble microbial products formation in anaerobic chemostats in the presence of toxic compounds.

Anaerobic chemostats fed on glucose (approximately 10 g chemical oxygen demand (COD)/L) were used to investigate the effects of toxicity on soluble microbial product (SMP) formation. Addition of the toxic compounds chloroform and chromium increased the net accumulation of SMP, despite reducing the percentage of SMP in the effluent due to the overwhelming production of volatile fatty acids (VFAs). In the reactor spiked with chloroform the normalized accumulation of SMP (SMP/So) increased from 2% to 8%, whereas in the reactor spiked with Cr (VI) the SMP/So ratio reached as high as 20% after the spike, and in both cases SMP net accumulation was proportional to the concentration of toxicant. After the chloroform and chromium spikes biomass seemed to produce more extra cellular polymeric substances (EPS) suggesting that this might have helped them to cope with the stress. Chromatography results indicate that some of the high MW compounds present in the SMP might have been due to EPS release into the bulk solution, and that other compounds, probably released as a result of cell lysis, were also present. Hydrolysis of EPS did not seem to contribute to SMP accumulation in the presence of toxic compounds, and DNA analysis suggested that cell lysis products was an important contribution to SMP accumulation, in the presence of chromium.

Bacteria, Anaerobic↗