Hexavalent chromium compounds are known carcinogens for the respiratory tract in humans. The mechanism of cell transformation by hexavalent chromium compounds is not fully understood although a role for intracellular reduction is sought. The aim of this study was to determine the distribution of Cr valence states in human cells after in vitro exposure to soluble or particulate chromium compounds. A synchrotron X-ray-based microprobe was used to investigate the cellular reduction of Cr(VI) and to image chromium oxidation states in cells. It was shown that soluble Cr(VI) compounds are fully reduced to Cr(III) in cells. Cr(III) is homogeneously distributed within the cell volume and therefore present within the nucleus. In the case of low solubility particulate chromate compounds, Cr(VI) can coexist in the cell environment, as particles in the perinuclear region, together with intracellular and intranuclear Cr(III). Chemical distribution maps also suggest that intracellular Cr(III) originates from extracellular dissolution and reduction of lead chromate rather than from intracellular engulfed particles. The possible stronger carcinogenicity of low solubility chromate vs soluble chromate compounds may derive from the combinative genotoxic effects of intranuclear Cr(III) and the persistent exposure to a strong oxidant, Cr(VI). /Soluble and particulate chromates/
Exposure to certain particulate hexavalent chromium [Cr(VI)] compounds, such as lead chromate (PbCrO4), has been associated with lung cancer and respiratory tract toxicity. Previous studies indicate that the solubility of Cr(VI)-compounds is an important factor in Cr(VI)-induced carcinogenesis. The present study investigates reactive oxygen species (ROS) generation by PbCrO4 particles and cellular responses using RAW 264.7 cells. A mixture containing PbCrO4 and RAW 264.7 cells generated hydroxyl radical ((.)OH), using cellularly generated H2O2 as a precursor, as measured by electron spin resonance (ESR) spin trapping in combination with H2O2 and (.)OH scavengers, catalase and sodium formate. The effect of ascorbic acid on (.)OH radicals was also measured using ESR. Confocal microscopy showed that particles could become either bound to the cell surface or engulfed over a 120 min time period. H2O2 generation and O2 consumption were also increased after treatment of the cells with PbCrO4. Both NF-kappaB and AP-1 were activated after exposure to PbCrO4 particles as measured by the NF-kappaB or AP-1 luciferase reporter plasmid assay. Our investigation thus demonstrated that the RAW 264.7 cells phagocytized the PbCrO4 particles leading to accumulation of the particles within vacuoles in the cytoplasm. These particles could induce chronic production of ROS and activation of NF-kappaB and AP-1. Such induction of transcription pathways may be involved in the inflammatory and carcinogenic responses induced by Cr(VI)-containing particles. /Lead chromate oxide/
Free radical reactions are believed to play an important role in the mechanism of Cr(VI)-induced carcinogenesis. Most studies concerning the role of free radical reactions have been limited to soluble Cr(VI). Various studies have shown that solubility is an important factor contributing to the carcinogenic potential of Cr(VI) compounds. Here, we report that reduction of insoluble PbCrO4 by glutathione reductase in the presence of NADPH as a cofactor generated hydroxyl radicals (.OH) and caused DNA damage. The .OH radicals were detected by electron spin resonance (ESR) using 5,5-dimethyl-N-oxide as a spin trap. Addition of catalase, a specific H2O2 scavenger, inhibited the .OH radical generation, indicating the involvement of H2O2 in the mechanism of Cr(VI)-induced .OH generation. Catalase reduced .OH radicals measured by electron spin resonance and reduced DNA strand breaks, indicating .OH radicals are involved in the damage measured. The H2O2 formation was measured by change in fluorescence of scopoletin in the presence of horseradish peroxidase. Molecular oxygen was used in the system as measured by oxygen consumption assay. Chelation of PbCrO4 impaired the generation of .OH radical. The results obtained from this study show that reduction of insoluble PbCrO4 by glutathione reductase/NADPH generates .OH radicals. The mechanism of .OH generation involves reduction of molecular oxygen to H2O2, which generates .OH radicals through a Fenton-like reaction. The .OH radicals generated by PbCrO4 caused DNA strand breakage.
Lead and chromium are absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. Chromium 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, L136)
IDENTIFICATION AND USE: Lead chromate is a yellow or orange-yellow powder. It is used as a pigment for paints and inks; in oil and water colors; printing fabrics; decorating china and porcelain; in chemical analysis of organic substances; and in traffic paints. HUMAN EXPOSURE AND TOXICITY: Lead chromate is toxic by ingestion and inhalation. Although no evidence has been found that lead-chromate causes lung cancer in lead chromate workers, it cannot be unequivocally stated that heavy exposures to lead chromate does not present a cancer hazard. One possible mechanism for lead chromate-induced carcinogenesis is through centrosome dysfunction, leading to the induction of aneuploidy. Lead in lead chromate could cause possible neurotoxicity. Increasing concentrations of lead chromate induced increasing amounts of cytotoxicity and clastogenicity in human skin cells. ANIMAL STUDIES: A single sc injection of 30 mg lead chromate(VI) oxide in water to 2 groups of 40 rats gave rise to 26/40 & 27/40 sarcomas, respectively, at site of injection within 117-150 weeks. No local sarcoma occurred in 60 vehicle-treated control rats. Lead chromate induced 14 fibrosarcomas & 17 rhabdomyosarcomas at the site of injection in 31/47 rats given monthly im injections of lead chromate. In addition, 3/24 lead chromate-treated rats had renal carcinomas. No such tumors appeared in a similar group of 22 controls injected with the vehicle. No lung tumors were found in rabbits and guinea pigs after intratracheal instillation. The potential mutagenicity of lead chromate was tested by following battery of microbial tests: the Escherichia coli pola+/pola- survival test; the Salmonella/microsome his+ reversion assay; the E coli trp+ reversion test plate assay; the E coli gal+ forward mutation test; & the Saccharomyces cerevisiae assay for mitotic recombination. Lead chromate was mutagenic in Salmonella & in Saccharomyces. Metabolic activation by rat liver homogenate (S9) was not required. Apparently, chromate ion is responsible for mutagenicity of lead chromate. An insoluble chromic compound, lead chromate (PbCrO4), was not cytotoxic nor mutagenic on V79 cells, probably because it is taken up by the cells very slowly. ECOTOXICITY STUDIES: Lead chromate was both cytotoxic and genotoxic to sea turtle cells. Concentrations of 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced 108, 79, 54, and 7% relative survival, respectively. Additionally, concentrations of 0, 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced damage in 4, 10, 15, 26, and 36% of cells and caused 4, 11, 17, 30, and 56 chromosome aberrations in 100 metaphases, respectively. Increasing concentrations of lead chromate induce increasing amounts of cytotoxicity and clastogenicity in sperm whale skin cells.
Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, its main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. 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, T4, A20, A22, L136)
Lead and lead compounds are reasonably anticipated to be human carcinogens based on limited evidence of carcinogenicity from studies in humans and sufficient evidence of carcinogenicity from studies in experimental animals. /Lead and Lead compounds/
(51)Cr-labelled sodium, zinc and lead chromates were studied. Sodium chromate and the less soluble zinc chromate were absorbed by 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.
Transmission electron microscopy (TEM) equipped with energy-dispersive x-ray analysis (EDX), electron spectroscopy for chemical analysis (ESCA), secondary ion mass spectrometry (SIMS), and laser microprobe for mass analysis (LAMMA) were used to follow the fate of chromium compounds deposited in the sheep tracheal lobe. Four chromium compounds were used: two chromium(VI) compounds (lead chromate and chromium trioxide) and two chromium(III) compounds (chronic oxide and chromium sulfate). Chromium trioxide is very soluble and the other three are slightly soluble. The compositions, concentrations, and sizes of particles were determined in the bronchoalveolar lavages (BAL) at d 2, 3, 5, and 30 after instillation and on the lung samples collected at d 31. The concentrations of particles in the BAL samples separated the chromium compounds in two groups where Cr2O3 and PbCrO4 (as Pb) were higher than Cr2(SO4)3, PbCrO4 (as Cr), and CrO3. The half-life for alveolar clearance of Cr2O3 and Cr2(SO4)3 has been calculated respectively at 11 and 80 d. Prismatic PbCrO4 particles break up in the lung and sustain a high concentration of isometric particles of lead chromate and another lead-containing compound in the BAL. The CrO3 instilled particles react with endogenous compounds or are transformed to insoluble hydroxyl complexes instead of diffusing very rapidly through the alveolar-capillary barrier. The alveolar clearance as measured in the BAL is not different from the control.
Thermal, structural and optical properties of Al2CoO4-Crocoite composite nanoparticles used as pigments
作者:M. Inês B. Bernardi、Vinícius D. Araújo、Alexandre Mesquita、Geraldo J. M. Frigo、Lauro J. Q. Maia
DOI:10.1007/s10973-009-0164-7
日期:2009.9
Al2CoO4–PbCrO4 and Al2CoO4–Pb2CrO5 crystalline powders in different proportions were obtained by the polymeric precursor method. Differential scanning calorimetry (DSC) and thermogravimetry (TG) techniques were used to accurately characterize the distinct thermal events occurring during synthesis. The TG and DSC results revealed a series of overlapping decomposition reactions due to different exothermal events, which were identified as H2O and NOx elimination and polymer pyrolysis. The X-ray diffraction patterns of the xAl2CoO4–(1 − x)PbCrO4 and xAl2CoO4–(1 − x)Pb2CrO5 mixed compounds, with x = 1, 0.75, 0.5, 0.25 and 0, were obtained in the crystalline form with their respective phases, and proved consistent with the nominal compositions. The synthesis of these two systems yielded nine different colors and shades.
采用聚合物前驱体法制备了不同比例的Al2CoO4-PbCrO4和 -Pb2CrO5结晶粉末。使用差示扫描量热法(DSC)和热重分析(TG)技术来准确表征合成过程中发生的不同热事件。 TG 和 DSC 结果揭示了由于不同的放热事件导致的一系列重叠分解反应,这些反应被确定为 H2O 和 NOx 消除和聚合物热解。 x –(1 − x)PbCrO4 和 x –(1 − x)Pb2CrO5 混合化合物的 X 射线衍射图,其中 x = 1、0.75、0.5、0.25 和 0,分别以晶型形式获得。相,并证明与标称成分一致。这两个系统的合成产生了九种不同的颜色和色调。
Electrochemical reactivity of lead chromate in carboxylic acids
作者:A. Bennouna、B. Durand、O. Vittori
DOI:10.1016/0013-4686(87)85064-8
日期:1987.9
The electrochemical behaviour of leadchromate samples is studied by means of a cpe with conducting binder. Voltammetric curves recorded with ethanoic or methanoic acids as electrolyte and binder exhibit mainly two electrochemical steps. The first one is an irreversible process resulting from the progressive dissolution of the powdered solid as the potential is made more cathodic and from the simultaneous
A New Approach to Synthesis of Layered Fluorites Containing Molecular Anions: Synthesis of Ln<sub>2</sub>O<sub>2</sub>CO<sub>3</sub>, K(LnO)CO<sub>3</sub>, and Ln<sub>2</sub>O<sub>2</sub>CrO<sub>4</sub> via Metathesis Reactions
作者:Dmitri O. Charkin、Roman O. Grischenko、Arman A. Sadybekov、Richard J. Goff、Philip Lightfoot
DOI:10.1021/ic701558m
日期:2008.4.1
layered, structure type. In addition, significantly easier and more efficient synthetic pathways were found to the known compounds [Ln2O2]K2(CO3)2 and [La2O2]CrO4. The structure of the latter compound has been determined from neutron powder diffraction data. Factors affecting reaction pathways and products are discussed, as well as prospects for applying the approach to more complex layered compounds
Method of encapsulating particles and the resultant product
申请人:The Harshaw Chemical Company
公开号:US03946134A1
公开(公告)日:1976-03-23
A protective coating consisting of an aluminum or magnesium phosphate complex is used to encapsulate a wide variety of organic and inorganic particles. The coating is particularly applicable to organic and inorganic pigments and serves to improve the light, heat and chemical stability of these pigments. The coating is formed in situ by complexing the phosphate with the metal, preferably in the presence of ions of fluoride or fluoborate and depositing the same onto the surface of the particles.
Single-crystalline PbCrO<sub>4</sub>Nanowires and Their Hydrothermal Transformation to Amorphous PbCr<sub>3</sub>O<sub>10</sub>Nanotubes
作者:Xian-Luo Hu、Ying-Jie Zhu
DOI:10.1246/cl.2004.880
日期:2004.7
Single-crystalline PbCrO4 nanowires have been successfully synthesized by a simple solution method at room-temperature. Amorphous PbCr3O10 nanotubes could be hydrothermally prepared from PbCrO4 nanowires in the presence of PVP. This simple method needs no any seed, catalyst, or template, and may also be extended to the fabrication of other 1-D chromates.