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At least 613 records · Page 34Linked to original sources
PubMed1994

Acute bone marrow toxicity and pancytopenia following exposure to lead chromate, xylene, and ethylbenzene in a degloving injury.

A case of unique acute bone marrow toxicity and pancytopenia following subcutaneous exposure to lead chromate, xylene, and ethylbenzene in a previously healthy patient is reported. The patient sustained an extensive degloving injury to his lower extremity. The wound was contaminated with traffic paint containing lead chromate pigment along with a large volume of xylene and ethylbenzene solvent. Consequences of the patient's clinical course and management of degloving injuries are discussed.

Accidents, Traffic↗
PubMed1995

Decreases of CD4- and CD8-positive T lymphocytes in retired chromate workers.

To investigate the effects of chromates on the human immune system, we measured total T lymphocytes and their two major subpopulations (CD4+ and CD8+ T lymphocytes) in the peripheral blood of 19 retired male workers who had been exposed to chromate at a chemical plant. The results indicated that both CD4+ and CD8+ T lymphocytes were significantly decreased, resulting in decreases in total T lymphocytes and total lymphocytes.

Adult↗
PubMed1995

Chromate-induced chromium(V) formation in live mice and its control by cellular antioxidants: an L-band electron paramagnetic resonance study.

A recent note from our laboratory reported that L-band (1.2 GHz) electron paramagnetic resonance spectroscopy can be utilized in detecting the formation of Cr(V) intermediates from chromate-treated whole mice. Since Cr(V) is thought to be one of the key species in the mechanism of chromate's toxicity, we carried out additional measurements with improved sensitivity. The new spectra show partially resolved hyperfine structure from protons that suggests that the Cr(V) ion is ligated to NAD(P)H moieties via oxygens. Using laboratory-synthesized Cr(V) (K3CrO8) as a standard, the yield of Cr(V) formation was estimated to be 153 +/- 12 nmol after intravenous injection of 100 microliters of 100 mM sodium dichromate into mice. Pretreatment of the mice with ascorbic acid and glutathione significantly reduced the Cr(V) formation yield in a dose-related manner, while pretreatment with NADH had the opposite effect. Injection of ascorbic acid also had the effect of enhancing the rate of Cr(V) disappearance in vivo. By comparing these results with in vitro results utilizing L-band as well as X-band (9.6 GHz) measurements, we conclude that L-band spectroscopy can indeed be effectively utilized for following the metabolism of Cr(V) in live mice and that Cr(V) formation can be controlled by utilizing cellular antioxidants in vivo.

Animals↗
PubMed1985

Chelation in metal intoxication XVII: Antidotal efficacy of polyaminocarboxylic acids on acute chromate toxicity.

Some polyaminocarboxylic acids containing amino and carboxyl groups as metal binding sites in different structural arrangements were evaluated for their relative efficacy in protecting against acute chromate intoxication in mice. Nitrilotriacetic acid (NTA) and 1,2 cyclohexylenediamine tetraacetic acid (CDTA) were most effective in preventing mortality (50-70%) due to a lethal dose of potassium chromate at one-tenth of their respective LD50.

Amino Acids↗
PubMed1993

Bronchial carcinoma mortality in the German chromate-producing industry: the effects of process modification.

This study updates a 1982 report on mortality at two German chromate-producing factories. The main objective of the study was to establish whether the change-over to a production process using lime-free conversion of chromite ore, thus eliminating the formation of calcium chromate, had resulted in a distinct reduction in bronchial carcinoma mortality among workers exposed for the first time after the change-over (completed in 1958 in Leverkusen and 1964 in Uerdingen). A total of 1417 workers with at least 1 year of exposure were enrolled in the study. The observation period ended on 31 December 1988. The expected number of deaths was calculated using population statistics for North Rhine-Westphalia. The risk was determined in the form of a standardised mortality ratio (SMR), i.e. the ratio of observed deaths to expected deaths. In the group of 739 workers exposed before the process change-over was completed, 432 died during the observation period, 66 of them from bronchial carcinoma. This significant excess produced an SMR of 2.27 (95% confidence interval: 1.78-2.85). Where the cause of death was unknown, cases were allocated to a cause of death on the basis of the percentage occurrence of various causes of death in the specific subcohort. The cohort of 678 workers first exposed after the process modification had been completed had a slightly increased SMR for lung cancer of 1.26 (95% confidence interval: 0.58-2.38) based on nine cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Mortality study among workers producing chromate pigments in France.

In a follow-up study of 294 men who had worked for at least 6 months in a chromate-producing factory in France between 1958 and 1987, only 16 were lost to follow-up and the number of person-years in the study was 5207. Occupational data were provided by the administration of the plant. The causes of deaths were ascertained from hospital and general practitioners' records. The observed numbers of deaths were compared with the expected numbers based on local rates with adjustment for age, sex and calendar time (standardized mortality ratio, SMR). The overall mortality did not differ significantly from that expected (SMR = 1.20, 95% CI = 0.98-1.47), whereas mortality due to lung cancer was in significant excess (SMR = 3.60, 95% CI = 2.13-5.68). Significantly higher lung cancer SMRs were found for workers whose duration of employment was more than 10 years. A non-significant excess was observed for all forms of digestive tract cancer (SMR = 1.30, 95% CI = 0.60-2.47). There were two cases of brain cancer when 0.24 was expected (SMR = 8.44, 95% CI = 1.02-30.49). No previous report has mentioned an association of brain cancer with chromate pigments; however, because of the small numbers involved, a chance excess should be considered.

Adult↗
PubMed1992

Mutagenic activity of copper(II) chromate and dichromate complexes with polypyridines.

Copper(II) chromate and dichromate complexes with 2,2'-bipyridyl and 1,10-phenathroline were tested for their mutagenic activity in the standard Ames test. All of six tested complexes exhibited markedly lower mutagenic activity than the reference compounds--potassium dichromate and sodium chromate. The blockage of Cr(VI) reduction capability in the presence of the complex Cu2+ ion and the competition between copper and chromium ions in the interaction with cellular components are discussed in the light of the results of our previous chemical study.

2,2'-Dipyridyl↗
PubMed2005

Chromate and selenate hydrocalumite solid solutions and their applications in waste treatment.

Hydrocalumite, a calcium aluminate hydrate phase, consists of positively-charged structure units, and is therefore an ideal candidate for accommodating anionic contaminants. In this study, a series of batch experiments was carried out to examine the uptake of chromate and selenate by hydrocalumite. To determine the uptake capacity and long-term stability, hydrocalumite solid solutions between chromate/selenate and hydroxyl were synthesized over a reaction time of more than one year. At a ratio of water to initial solids added (CaAl2O4+CaO) of 75:1, the maximum uptake capacities were over 77 and 114 g/kg for Cr and Se, respectively. These values are very close to the theoretical uptake capacities of chromate and selenate hydrocalumite end-members (81 and 118 g/kg, respectively). The oxyanion removal efficiency from solution was above 95%. Due to the high uptake capacity and anion removal efficiency of hydrocalumites, their application in wastewater treatment is promising. Hydrocalumites are also important hydration products of cementitious materials and the long-term stability of these phases is of significance for application in solidification/stabilization technology.

Aluminum Compounds↗
PubMed2001

Bioremediation of toxic chromium from electroplating effluent by chromate-reducing Pseudomonas aeruginosa A2Chr in two bioreactors.

The chromate-reducing ability of Pseudomonas aeruginosa A2Chr was compared in batch culture, with cells entrapped in a dialysis sac, and with cells immobilized in an agarose-alginate film in conjunction with a rotating biological contactor. In all three systems, the maximum Cr(VI) reduction occurred at 10 mg Cr(VI)/l. Whereas at 50 mg Cr(VI)/l concentration, only 16% of the total Cr(VI) was reduced, five spikings with 10 mg chromate/l at 2-h intervals led to 96% reduction of the total input of 50 mg Cr(VI)/l. Thus maximum Cr(VI) reduction was achieved by avoiding Cr(VI) toxicity to the cells by respiking with lower Cr(VI) concentrations. At 10 mg Cr(VI)/l, the pattern of chromate reduction in dialysis-entrapped cells was almost similar to that of batch culture and 86% of the bacterially reduced chromium was retained inside the dialysis sac. In electroplating effluent containing 100 mg Cr(VI)/l, however, the amount of Cr(VI) reduced by the cells immobilized in agarose-alginate biofilm was twice and thrice the amount reduced by batch culture and cells entrapped in a dialysis sac, respectively.

Biodegradation, Environmental↗
PubMed2001

Chromate reduction and 16S rRNA identification of bacteria isolated from a Cr(VI)-contaminated site.

A gram-positive, hexavalent chromium [chromate: Cr(VI)]-tolerant bacterium, isolated from tannery waste from Pakistan, was identified as a Microbacterium sp. by 16S rRNA gene sequence homology. The strain (designated as MP30) reduced toxic Cr(VI) only under anaerobic conditions at the expense of acetate as the electron donor. The bacterium was able to grow aerobically in L-broth supplemented with 15 mM CrO4(2-) but then did not reduce Cr(VI). At a concentration of 2.4x10(9) cells/ml, 100 microM sodium chromate was reduced within 30 h; however, the maximum specific reduction rate was obtained at lower initial cell concentrations.

Base Sequence↗
PubMed1991

Evidence for the generation of hydroxyl radicals from a chromium(V) intermediate isolated from the reaction of chromate with glutathione.

The formation of hydroxyl radicals from a chromium(V) complex isolated from the reaction of glutathione with chromate has been demonstrated in spin trapping experiments using dimethylsulfoxide and 3,5-dibromo-4-nitrosobenzene sulfonate. Mechanisms for the formation of radicals in such systems are discussed. These results help to explain the ability of solutions containing chromate and glutathione to cause strand breaks in DNA.

Chromates↗
PubMed1989

Vitamin B2-enhancement of sodium chromate (VI)--Induced DNA single strand breaks: ESR study of the action of vitamin B2.

Incubation of Chinese hamster V-79 cells with Na2CrO4 plus vitamin B2 resulted in an increase of Na2CrO4-induced DNA single strand breaks. Electron spin resonance (ESR) studies showed that vitamin B2 enhanced the formation of both hydroxyl radical and tetraperoxochromate (V) during the reaction of Na2CrO4 with hydrogen peroxide. Furthermore, ESR studies demonstrated that a chromium (V) species with a g value of 1.977 was formed by the reaction of Na2CrO4 with vitamin B2. These results indicate that chromate reacts with vitamin B2 to form chromium (V) species and also suggest that the enhancement effect of vitamin B2 on chromate-induced DNA single strand breaks may result from an increase of chromium (V)-related hydroxyl radical formation.

Animals↗
PubMed1979

Sister chromatid exchanges induced in cultured mammalian cells by chromate.

Chromate compounds induced sister chromatoid exchanges (SCEs) and chromosome aberrations in cultured mammalian cells. Similar increases in SCE frequency were observed in human fibroblasts exposed to the compounds K2Cr2O7 and K2CrO4. Marked increases in SCE frequency in cells exposed to chromate for a 48-h period were detected at concentrations between 10(-7) and 10(-6) M. Chromosome aberrations (primarily chromatid breaks) were also produced in human cells exposed to K2CrO4 at concentrations between 8 . 10(-7) and 3 . 10(-6) M. K2CrO4, but not the trivalent compound CrCl3, induced SCEs in Chinese hamster ovary (CHO) cells at low concentrations.

Adult↗
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↗
PubMed1983

Chemical reduction of silver chromate: a procedure for electron microscopical analysis of Golgi-impregnated neurons.

A procedure is described by which the solid silver chromate precipitate present in Golgi-impregnated neurons is reduced by a photographic developer into metallic silver grains or particles. The remaining silver chromate is subsequently removed, and the fine structure and synaptic relationships of the impregnated neurons can be studied with the electron microscope. Three developers, Hydrochinone, Kodalith and D 19 were tested on cortical neurons in Vibratome sections of rapid Golgi-impregnated rat brains. Considerable differences were observed as regards penetration of the developer into the sections, uniformity of development, size and location of the silver particles produced during the development, and the quality of preservation of the ultrastructural details both in the impregnated neurons and the surrounding neuropil. Following the chemical reduction procedure the metallic silver deposit can be converted into metallic gold by a gold toning technique. Of the 3 tested developers, Kodalith and D 19 met the demands: good ultrastructural preservation, high contrast at both light microscopic (LM) and electron microscopic (EM) levels, reliable and easy to perform, minimum of test runs. Because of the high contrast provided by Kodalith and D 19, these substances are well suited for neuroanatomical tracing studies which make use of a transport or degeneration technique combined with Golgi-EM. In contrast to Kodalith, D 19 has little effect on the ultrastructure of the impregnated cells. Therefore, this developer can also be used for ultrastructural studies of Golgi-impregnated, light microscopically identified neurons.

Animals↗
PubMed1991

Protective effect of vitamin E against chromosomal aberrations and mutation induced by sodium chromate in Chinese hamster V79 cells.

The effect of vitamin E on chromosomal aberrations and mutation caused by Na2CrO4 was investigated in Chinese hamster V79 cells. Pretreatment with 25 microM alpha-tocopherol succinate (vitamin E) for 24 h prior to chromate exposure (2.5-5 microM) resulted in a decrease of metal-induced chromosomal aberrations. Na2CrO4 (2.5-7.5 microM) induced mutations at the HGPRT locus, but only within a very limited concentration range. This mutagenic response could also be suppressed by pretreatment with vitamin E. These results suggest that vitamin E can protect cells from the clastogenic and mutagenic action of chromate compounds, possibly through its ability to scavenge chromium(V) and/or free radicals.

Animals↗
PubMed1992

DNA damage induced by carcinogenic lead chromate particles in cultured mammalian cells.

Particulate lead chromate is a highly water-insoluble cytotoxic and carcinogenic agent, but its mechanism of action remains obscure. We investigated its effects on DNA damage in CHO cells after a 24-h exposure using alkaline or neutral filter elution and cytogenetic studies. Concentrations (0.08, 0.4 and 0.8 micrograms/cm2), which reduced the colony-forming efficiency of CHO cells to 94, 50 and 10%, respectively, produced dose-dependent DNA single-strand breaks and DNA-protein crosslinks, but no DNA double-strand breaks or DNA-DNA crosslinks were observed. The single-strand breaks were absent from cells given a 24-h recovery period after removal of the treatment medium, even though most of the particles remained adhered to cells and to the culture dish. In contrast, both the DNA-protein crosslinks and chromosomal aberrations persisted even after the 24-h recovery period. These results suggest that the mechanism of the particle-induced early DNA single-strand breaks may be different from DNA-protein crosslinks and the lesions leading to chromosomal aberrations, or alternatively, that the repair of single-strand breaks is more efficient than the repair of DNA-protein crosslinks in the unavoidable continuing presence of carcinogen. These results also suggest that the chromosome damage may be related to the persistent DNA-protein crosslinks, and further confirm the genotoxic activity of carcinogenic lead chromate particles.

Animals↗
PubMed1984

The reduction of chromium (VI) to chromium (III) by glutathione: an intracellular redox pathway in the metabolism of the carcinogen chromate.

The capacity of glutathione (GSH) to reduce Cr(VI) to Cr(III) in vitro was investigated. The reaction was determined spectrophotometrically by following the absorption of Cr(VI) at 370 nm. At stoichiometric conditions (molar ratio Cr(VI)/GSH of 1:3) the reduction was strongly dependent on the solution's pH. It was much slower at pH 7.4 than at pH values below 5. An excess of GSH (100- or 1000-fold) accelerated the reaction. In any case, 3 GSH molecules were required to reduce 1 molecule of chromate. Incubation of human red blood cells (RBC) with an excess of Na2CrO4 (10 mM) decreased the GSH content of the cells to 10% of the original amount. This depletion of GSH was similar to that obtained when RBC were incubated with 62 mM diethylmaleate (DEM), a well known GSH depleting agent. Sephadex G-100 chromatography of lysates from human RBC incubated with radioactive chromate (51Cr(VI] showed a strong affinity of 51Cr for hemoglobin: 97% of the applied dose was bound to hemoglobin whilst only minor amounts of 51Cr were found in the low-molecular fractions. However, incubations of prepared lysates (as opposed to intact cells) with 10 mM Na2 51CrO4 markedly raised the chromium content of low-molecular fractions (probably GSH-Cr-complexes), probably indicative of a role of GSH in the intra-cellular reduction of Cr(VI) to Cr(III), the latter being regarded as the ultimately toxic species of this metal.

Chromates↗