Hexavalent chromium, as sodium chromate in an aq soln, was reduced rapidly to trivalent chromium in the presence of glutathione (0.3-3.0 mM). Such glutathione-dependent redn of hexavalent chromium can take place in the cytosolic space of hexavalent chromium exposed cells, since glutathione is found in reactive concn in this compartment.
来源:Hazardous Substances Data Bank (HSDB)
代谢
谷胱甘肽（GSH）将六价铬（Cr(VI)）还原为三价铬（Cr(III)）的能力在体外进行了研究。通过在370纳米处跟踪六价铬的吸光度，以分光光度法确定了反应。在化学计量条件下（Cr(VI)/GSH的摩尔比为1:3），还原反应强烈依赖于溶液的pH值。在pH 7.4时，反应比pH值低于5时要慢得多。当GSH过量（100倍或1000倍）时，会加速反应。无论如何，需要3个GSH分子来还原1个铬酸分子。将人红细胞（RBC）与过量的Na2CrO4（10 mM）一起孵化，会使细胞中的GSH含量降低到原来的10%。这种GSH的耗尽与当红细胞与62 mM的DEM（一种已知的GSH耗尽剂）一起孵化时得到的耗尽相似。使用放射性铬酸（51Cr(VI)）孵化的人红细胞裂解液通过Sephadex G-100色谱法分析显示，51Cr对血红蛋白有很强的亲和力：97%的施用剂量结合到血红蛋白上，而低分子量部分中只发现了少量的51Cr。然而，将准备好的裂解液（而不是完整的细胞）与10 mM Na2(51)CrO4一起孵化显著提高了低分子量部分中的铬含量（可能是GSH-Cr复合物），这可能表明GSH在细胞内将Cr(VI)还原为Cr(III)的作用，后者被认为是这种金属的最终有毒物种。
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 (51)Cr(VI] showed a strong affinity of (51)Cr for hemoglobin: 97% of the applied dose was bound to hemoglobin whilst only minor amounts of (51)Cr were found in the low-molecular fractions. However, incubations of prepared lysates (as opposed to intact cells) with 10 mM Na2 (51)CrO4 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.
Comparative metabolic fate of labelled chromium chloride and sodium chromate and interaction of these compounds in the rat liver and blood were investigated after their oral and intravenous administration. Gastrointestinal absorption of both compounds was below 1% of the oral dose, but trivalent chromium showed higher radioactivity than the hexavalent form in rats (biological half-life: CrCl3 91.79 days, Na2CrO4 22.24 days). The higher residual activity of the trivalent chromium was also observed after intravenous administration. Both forms of chromium were excreted more in the urine via the kidney than in the intestinal tract after intravenous administration. When (51)CrCl3 and Na2(51)CrO4 were injected into rats, in the time-distribution patterns of( 51)Cr in the organs, a significant difference was shown between oxidation states of the two compounds, especially in subcellular fractions of the liver and blood constituents. This significant difference mainly observed in the rat blood came from the fact that trivalent chromium possessed a high binding activity for transferrin in plasma, while hexavalent chromium was permeable into red cells and bound with hemoglobin.
Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (A12, L16)
IDENTIFICATION AND USE: Sodium chromate forms yellow orthorhombic crystals. It is used in inks, dyeing, paint pigment, leather tanning, other chromates, and protection of iron against corrosion. (51)Chromium, as sodium chromate ((51)Cr), is used to label red blood cells so that red cell survival and red cell volume can be measured. HUMAN EXPOSURE AND TOXICITY: Eye contact can cause severe damage with possible loss of vision. A 51-year-old man committed suicide by ingesting a fatal dose of sodium chromate solution. He unexpectedly lost consciousness 6 hrs after the ingestion and died approximately 20.5 hrs later. The patient's death was assumed to have been caused by circulatory collapse due to internal bleeding and the direct toxicity of chromate compounds with hepatic malfunction and possibly disseminated intravascular coagulation. None of the results showed statistically significant differences that would suggest an excess risk for malignant neoplasms, particularly lung cancer, among workers engaged in the manufacture of chromate pigment in Japan. When tested in cultured human bronchial epithelial cells, it was found that 1, 2.5, 5 and 10 uM sodium chromate induced 66, 35, 0 and 0% relative survival, respectively. The amount of chromosome damage increased with concentration after 24 hr exposure to sodium chromate. Specifically, 1, 2.5 and 5 microM damaged 25, 34 and 41% of metaphase cells with the total amount of damage reaching 33, 59 and 70 aberrations per 100 metaphases, respectively. Ten micromolar sodium chromate induced profound cell cycle delay and no metaphases were found. In other experiment, cells exposed to 1 microM sodium chromate for 24, 48 and 72 hr induced 23, 13 and 17% damaged metaphases, respectively. ANIMAL STUDIES: Rats treated ip with sodium chromate(VI) at 2 mg/kg chromium 3 times per week for up to 60 days developed liver damage. In a study examining the effects of chromium(VI) on motor activity, no effects were noted in six rats provided with drinking water containing sodium chromate at 0.07 g/L chromium(VI). A significant decrease in motor activity was noted 7 days after six rats were provided with drinking water containing sodium chromate at 0.7 g/L chromium(VI) (p< 0.02), and 1 day after six rats were given a single intraperitoneal injection of sodium chromate at 2 mg/kg body weight chromium(VI) (p< 0.01). Sodium chromate gave positive results in Escherichia coli WP2 reverse mutation test. Sodium chromate gave positive (significant increases in chromatid breaks and fragments) results in cytogenetics testing in cultured Chinese hamster CHO cells at doses of 5 to 10x10-6 molar. Treatment of chick embryo hepatocytes with sodium chromate resulted in the rapid uptake of chromate and the induction of DNA lesions in a time and concn dependent manner. DNA interstrand cross links, strand breaks and DNA-protein cross links were observed after treatment of hepatocytes with chromate concn which did not affect cell viability. Treatment of Chinese hamster ovary cells with 150 and 300 uM sodium chromate (Na2CrO4) for 2 hr decreased colony-forming efficiency by 46 and 92%, respectively. These treatments induced dose-dependent internucleosomal fragmentation of cellular DNA beyond 24 hr after chromate treatment. ECOTOXICITY STUDIES: When tested in hawksbill sea turtle cells, concentrations of 0.25, 0.5, 1, 2.5, and 5uM sodium chromate induced 84, 69, 46, 25, and 3% relative survival, respectively. Sodium chromate induced 3, 9, 9, 14, 21, and 29% of metaphases with damage, and caused 3, 10, 10, 16, 26, and 39 damaged chromosomes in 100 metaphases at concentrations of 0, 0.25, 0.5, 1, 2.5, and 5uM sodium chromate, respectively. In medaka cells, concentrations of 1, 5 and 10 uM sodium chromate damaged 17, 32 and 43% of metaphases, respectively and these same concentrations 1, 2.5, 5 and 10 uM sodium chromate damaged 14, 24 and 49% of metaphases, respectively, in North Atlantic right whale lung cells and 11, 32 and 41% of metaphases, respectively, in North Atlantic right whale testes cells.
Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (A12, L16, A34, A35, A36)
WEIGHT OF EVIDENCE CHARACTERIZATION: Under the current guidelines (1986), Cr(VI) is classified as Group A - known human carcinogen by the inhalation route of exposure. Carcinogenicity by the oral route of exposure cannot be determined and is classified as Group D. Under the proposed guidelines (1996), Cr(VI) would be characterized as a known human carcinogen by the inhalation route of exposure on the following basis. Hexavalent chromium is known to be carcinogenic in humans by the inhalation route of exposure. Results of occupational epidemiological studies of chromium-exposed workers are consistent across investigators and study populations. Dose-response relationships have been established for chromium exposure and lung cancer. Chromium-exposed workers are exposed to both Cr(III) and Cr(VI) compounds. Because only Cr(VI) has been found to be carcinogenic in animal studies, however, it was concluded that only Cr(VI) should be classified as a human carcinogen. Animal data are consistent with the human carcinogenicity data on hexavalent chromium. Hexavalent chromium compounds are carcinogenic in animal bioassays, producing the following tumor types: intramuscular injection site tumors in rats and mice, intrapleural implant site tumors for various Cr(VI) compounds in rats, intrabronchial implantation site tumors for various Cr(VI) compounds in rats and subcutaneous injection site sarcomas in rats. In vitro data are suggestive of a potential mode of action for hexavalent chromium carcinogenesis. Hexavalent chromium carcinogenesis may result from the formation of mutagenic oxidatitive DNA lesions following intracellular reduction to the trivalent form. Cr(VI) readily passes through cell membranes and is rapidly reduced intracellularly to generate reactive Cr(V) and Cr(IV) intermediates and reactive oxygen species. A number of potentially mutagenic DNA lesions are formed during the reduction of Cr(VI). Hexavalent chromium is mutagenic in bacterial assays, yeasts and V79 cells, and Cr(VI) compounds decrease the fidelity of DNA synthesis in vitro and produce unscheduled DNA synthesis as a consequence of DNA damage. Chromate has been shown to transform both primary cells and cell lines. HUMAN CARCINOGENICITY DATA: Occupational exposure to chromium compounds has been studied in the chromate production, chromeplating and chrome pigment, ferrochromium production, gold mining, leather tanning and chrome alloy production industries. Workers in the chromate industry are exposed to both trivalent and hexavalent compounds of chromium. Epidemiological studies of chromate production plants in Japan, Great Britain, West Germany, and the United States have revealed a correlation between occupational exposure to chromium and lung cancer, but the specific form of chromium responsible for the induction of cancer was not identified ... Studies of chrome pigment workers have consistently demonstrated an association between occupational chromium exposure (primarily Cr(VI)) and lung cancer. Several studies of the chromeplating industry have demonstrated a positive relationship between cancer and exposure to chromium compounds. ANIMAL CARCINOGENICITY DATA: Animal data are consistent with the findings of human epidemiological studies of hexavalent chromium ... /Chromium (VI)/
Evaluation: There is sufficient evidence in humans for the carcinogenicity of chromium(VI) compounds. Chromium(VI) compounds cause cancer of the lung. Also positive associations have been observed between exposure to Chromium(IV) compounds and cancer of the nose and nasal sinuses. There is sufficient evidence in experimental animals for the carcinogenicity of chromium(VI) compounds. Chromium(VI) compounds are carcinogenic to humans (Group 1). /Chromium(VI) compounds/
(51)Chromium labelled sodium, zinc and lead chromates were studied. Sodium chromate and the less soluble zinc chromate were absorbed into the blood, resulting in increased urinary excretion of chromium. ... The less water soluble the chromate, the higher was its elimination via the feces. Absorbed chromium was retained in the spleen and bone marrow in all three cases, and also in the liver and kidneys in the case of sodium chromate. Chromium levels in blood and urine are not indicative of inhalation exposure to insoluble chromates.
Percutaneous absorption of labelled sodium chromate occurred in guinea pigs: a maximum of 4% of the dose applied on the skin disappeared within 5 hours, and labelled chromium was detected in a number of organs.
Following intratracheal administration of sodium chromate solution to rabbits, about 45% (as Cr) remained in the lungs 4 hours after instillation; 15% was excreted in urine. The highest concentration of chromium (IV) was reached in red cells after about 3 hours, and the corresponding plasma concentration at that time was about one-third of that in red cells.
Disclosed is an improvement on a process in which sodium chromate is reacted with sulfuric acid to produce sodium bichromate and sodium sulfate, and the sodium bichromate is reacted with sulfuric acid to produce chromic acid and sodium bisulfate. In the improvement, the sodium sulfate and sodium bisulfate are reacted with hydrogen chloride to produce sulfuric acid, which is recycled, and sodium chloride.
Re-calcination and extraction process for the detoxification and
申请人：Situ; Qi-Jiang
公开号：US05395601A1
公开（公告）日：1995-03-07
A re-calcination and extraction process for the detoxification and comprehensive utilization of chromic residues, comprising adding small amount of residue ore powder, sodium carbonate, or additionally, a certain amount of coke powder to the poisonous chromic residues, and calcining the mixture in a re-calcinating apparatus at 1000.degree.-1200.degree. C., for 30-60 minutes. The re-calcined grog is extracted with water, to obtain an extractive liquor containing sodium chromate. The extractive liquor can be used to produce chromium oxide, basic chromium sulfate or medium chrome yellow; while the extracted residues can be sintered at high temperatures with iron ore powder and coke to obtain a massive self-melting sintered iron, which can be further converted to a low-chromium cast iron. This process can thoroughly detoxify the chromic residues, effectively recover Cr2O3 and remove water-soluble Cr+6, whereby various important industrial materials are produced. The method brings very good economical and environmental benefits.
The invention relates to a process for the production of sodium dichromate and sodium dichromate solutions by oxidative roasting of chrome ores under alkaline conditions, leaching of the furnace clinker obtained with water or an aqueous chromate-containing solution, adjustment of the pH to from 7 to 9.5, removal of the insoluble constituents by filtration, a sodium monochromate solution being obtained, conversion of the monochromate ions of this solution into dichromate ions by acidification and crystallization of sodium dichromate by concentration of this solution, characterized in that the acidification is carried out with carbon dioxide under pressure with removal of sodium hydrogen carbonate, the remaining solution is then very largely freed from sodium monochromate by cooling to a temperature below 10.degree. C. and filtration, any monochromate ions still present in the remaining solution are converted into dichromate ions by addition of an acid and the sodium monochromate filtered off is added to the sodium monochromate solution before conversion with carbon dioxide into a sodium dichromate solution.
Method for removing chromium from chromium containing waste material
申请人：Chrome Technology Inc.
公开号：US05007960A1
公开（公告）日：1991-04-16
A method is provided for removing chromium from a chromium containing waste material wherein the waste material is dried by indirect heating, sized to a particle size of less than 0.105 mm, mixed with alkaline and oxidizing reactants, and reacted in a reaction vessel by indirect heating using approximately the stoichiometric oxygen requirement to form a reaction material containing water soluble chromates. The reaction material is cooled and resized, and then subjected to an aqueous solvent extraction to produce a solid phase containing substantially no chromium and an aqueous phase containing water soluble chromates. This aqueous phase is subjected to evaporation resulting in a concentrated chromate phase. The waste material has been rendered non-hazardous and the chromium has been recovered as useful chromates.
There is provided an insecticidal composition comprising, in admixture with an agriculturally acceptable carrier, an insecticidally effective amount of a tetrahydroquinazoline compound of the formula ##STR1## wherein R, R.sup.1, R.sup.2, R.sup.3, R.sup.5, R.sup.6, R.sup.7, R.sup.8, and R.sup.9 are as defined herein, and methods of using the same. Certain novel substituted-phenyl tetrahydroquinazoline compounds per se are also identified.
