Chromium
Potassium Dichromate
Ochrobactrum
Chromium Isotopes
Tungsten
Shewanella
Lead
Drug Contamination
Flavin Mononucleotide
Biodegradation, Environmental
Perissodactyla
Alcaligenes
Oxidation-Reduction
Chemical Industry
Spiro Compounds
Drug Antagonism
Pseudomonas putida
Vanadium
Oxidoreductases
Arthrobacter
Chromosomal Instability
Metals, Heavy
Sulfur
Nickel
Glutathione Reductase
Guanosine
Molybdenum
Metals
Escherichia coli K12
Mutagenicity Tests
Riboflavin
Substance Abuse Detection
Ascorbic Acid
Singlet Oxygen
NAD
Mutagens
Bronchi
Metal Nanoparticles
Electron Spin Resonance Spectroscopy
Drug Resistance, Bacterial
DNA Damage
Spectrum Analysis, Raman
Gene Expression Regulation, Bacterial
Gold
Culture Media
Lung
Colorimetry
Cricetinae
Coloring Agents
Glutathione
Carcinogens
Electrophoresis, Capillary
Occupational Exposure
Aneuploidy
Environmental Monitoring
Regulatory Elements, Transcriptional
Bacillus cereus
Cricetulus
Operon
Radiometry
Plasmids
Centrosome
DNA
Solubility
Ultracentrifugation
Hydrogen-Ion Concentration
Escherichia coli
Molecular Sequence Data
Cell Survival
Zinc
Hydrogen Peroxide
Cloning, Molecular
Cell Transformation, Neoplastic
Copper
Biotransformation
Spectrometry, Mass, Electrospray Ionization
CHO Cells
Drug Resistance, Microbial
Dose-Response Relationship, Drug
Temperature
Sequence Analysis, DNA
Molecular Structure
Base Sequence
Fibroblasts
Chromatography, High Pressure Liquid
Amino Acid Sequence
Biological Transport
Pseudomonas aeruginosa
DNA-Binding Proteins
Oxidative Stress
Transcription, Genetic
Reproducibility of Results
Chromate efflux by means of the ChrA chromate resistance protein from Pseudomonas aeruginosa. (1/216)
Everted membrane vesicles of Pseudomonas aeruginosa PAO1 harboring plasmid pCRO616, expressing the ChrA chromate resistance protein, accumulated four times more (51)CrO(4)(2-) than vesicles from plasmidless cells, indicating that a chromate efflux system functions in the resistant strain. Chromate uptake showed saturation kinetics with an apparent K(m) of 0.12 mM chromate and a V(max) of 0. 5 nmol of chromate/min per mg of protein. Uptake of chromate by vesicles was dependent on NADH oxidation and was abolished by energy inhibitors and by the chromate analog sulfate. The mechanism of resistance to chromate determined by ChrA appears to be based on the active efflux of chromate driven by the membrane potential. (+info)Mortality among aircraft manufacturing workers. (2/216)
OBJECTIVES: To evaluate the risk of cancer and other diseases among workers engaged in aircraft manufacturing and potentially exposed to compounds containing chromate, trichloroethylene (TCE), perchloroethylene (PCE), and mixed solvents. METHODS: A retrospective cohort mortality study was conducted of workers employed for at least 1 year at a large aircraft manufacturing facility in California on or after 1 January 1960. The mortality experience of these workers was determined by examination of national, state, and company records to the end of 1996. Standardised mortality ratios (SMRs) were evaluated comparing the observed numbers of deaths among workers with those expected in the general population adjusting for age, sex, race, and calendar year. The SMRs for 40 cause of death categories were computed for the total cohort and for subgroups defined by sex, race, position in the factory, work duration, year of first employment, latency, and broad occupational groups. Factory job titles were classified as to likely use of chemicals, and internal Poisson regression analyses were used to compute mortality risk ratios for categories of years of exposure to chromate, TCE, PCE, and mixed solvents, with unexposed factory workers serving as referents. RESULTS: The study cohort comprised 77,965 workers who accrued nearly 1.9 million person-years of follow up (mean 24.2 years). Mortality follow up, estimated as 99% complete, showed that 20,236 workers had died by 31 December 1996, with cause of death obtained for 98%. Workers experienced low overall mortality (all causes of death SMR 0.83) and low cancer mortality (SMR 0.90). No significant increases in risk were found for any of the 40 specific cause of death categories, whereas for several causes the numbers of deaths were significantly below expectation. Analyses by occupational group and specific job titles showed no remarkable mortality patterns. Factory workers estimated to have been routinely exposed to chromate were not at increased risk of total cancer (SMR 0.93) or of lung cancer (SMR 1.02). Workers routinely exposed to TCE, PCE, or a mixture of solvents also were not at increased risk of total cancer (SMRs 0.86, 1.07, and 0.89, respectively), and the numbers of deaths for specific cancer sites were close to expected values. Slight to moderately increased rates of non-Hodgkin's lymphoma were found among workers exposed to TCE or PCE, but none was significant. A significant increase in testicular cancer was found among those with exposure to mixed solvents, but the excess was based on only six deaths and could not be linked to any particular solvent or job activity. Internal cohort analyses showed no significant trends of increased risk for any cancer with increasing years of exposure to chromate or solvents. CONCLUSIONS: The results from this large scale cohort study of workers followed up for over 3 decades provide no clear evidence that occupational exposures at the aircraft manufacturing factory resulted in increases in the risk of death from cancer or other diseases. Our findings support previous studies of aircraft workers in which cancer risks were generally at or below expected levels. (+info)Purification to homogeneity and characterization of a novel Pseudomonas putida chromate reductase. (3/216)
Cr(VI) (chromate) is a widespread environmental contaminant. Bacterial chromate reductases can convert soluble and toxic chromate to the insoluble and less toxic Cr(III). Bioremediation can therefore be effective in removing chromate from the environment, especially if the bacterial propensity for such removal is enhanced by genetic and biochemical engineering. To clone the chromate reductase-encoding gene, we purified to homogeneity (>600-fold purification) and characterized a novel soluble chromate reductase from Pseudomonas putida, using ammonium sulfate precipitation (55 to 70%), anion-exchange chromatography (DEAE Sepharose CL-6B), chromatofocusing (Polybuffer exchanger 94), and gel filtration (Superose 12 HR 10/30). The enzyme activity was dependent on NADH or NADPH; the temperature and pH optima for chromate reduction were 80 degrees C and 5, respectively; and the K(m) was 374 microM, with a V(max) of 1.72 micromol/min/mg of protein. Sulfate inhibited the enzyme activity noncompetitively. The reductase activity remained virtually unaltered after 30 min of exposure to 50 degrees C; even exposure to higher temperatures did not immediately inactivate the enzyme. X-ray absorption near-edge-structure spectra showed quantitative conversion of chromate to Cr(III) during the enzyme reaction. (+info)Apoptosis and P53 induction in human lung fibroblasts exposed to chromium (VI): effect of ascorbate and tocopherol. (4/216)
Some forms of hexavalent chromium [Cr(VI)] are known to cause damage to respiratory tract tissue, and are thought to be human lung carcinogens. Because Cr(VI) is mutagenic and carcinogenic at doses that evoke cell toxicity, the objective of these experiments was to examine the effect of Cr(VI) on the growth, survival, and mode of cell death in normal human lung fibroblasts (HLF cells). DNA adduct formation was monitored as a marker for bioavailability of genotoxic chromium. We also examined the modulation of these endpoints by vitamins C and E. Long-term Cr(VI) exposures were employed, which decreased clonogenic cell survival by 25% to 95% in a dose-dependent manner. The predominant cellular response to Cr(VI) was growth arrest. We found that Cr(VI) caused up to 20% of HLF cells to undergo apoptosis, and documented apoptotic morphology and the phagocytosis of apoptotic bodies by neighboring cells. P53 levels increased 4- to 6-fold in chromium-treated cells. In contrast with previous studies using CHO cells, the present study using HLFs found that pretreatment with either vitamin C or E did not exhibit a significant effect on Cr-induced apoptosis or clonogenic survival. In addition, pretreatment with vitamin C did not affect the p53 induction observed after chromium treatment. Neither vitamin had any effect on Cr-DNA adduct formation. These data indicate that although pretreatment with vitamin C or E alters the spectrum of cellular and/or genetic lesions induced by chromium(VI), neither vitamin altered the initiation or progression of apoptosis in diploid human lung cells. (+info)Organization-dependent effects of toxic bivalent ions microtubule assembly and glycolysis. (5/216)
The effects of bivalent ions on tubulin dynamics and the upper phase of glycolysis were investigated at different organization levels in vitro. Cu2+, Cd2+, Hg2+ and CrO4(2-) inhibit the tubulin polymerization at an IC50 of 14-24 microM with high cooperativity and also induce microtubule disassembly. The apparent binding constants of the ions to tubulin, estimated by fluorescence quenching, vary between 6 and 28 microM. BIAcore measurements for tubulin-tubulin interaction suggest that the presence of Cu2+ affects neither koff nor kon, but the amount of the bound tubulin. While the inhibitory effect of Cu2+ on tubulin polymerization is partially abolished by cross-linking of microtubules with substoichiometric amounts of phosphofructokinase or decoration of tubules with cytosolic proteins, in the presence of kinase but not with cytosolic proteins the tubules are resistant to CrO4(2-). No inhibitory effect of Cu2+ or CrO4(2-) on microtubule assembly was detected in the MAP-containing cytosolic fraction. Electron microscopy revealed that tubules assembled in the presence of Cu2+ or CrO4(2-) ions contain aggregates of thread-like oligomers that are less conspicuous in the presence of cytosolic proteins. Cu2+, Cd2+, and Hg2+ inhibit the glycolytic flux in the cytosolic fraction characterized at equilibrium by an IC50 of 10-14 microM with high cooperativity. Tubulin diminishes the inhibitory effect of the cations. These data indicate that the responses elicited by the bivalent ions are highly dependent on the supramolecular organization of the systems. (+info)Activation of JNK, p38 and ERK mitogen-activated protein kinases by chromium(VI) is mediated through oxidative stress but does not affect cytotoxicity. (6/216)
In this study we have explored the involvement of oxidative stress in Cr(VI)-induced JNK, p38 and ERK signaling pathways and their effects on Cr(VI) cytotoxicity in human non-small cell lung carcinoma CL3 cells. Exposure to K(2)Cr(2)O(7) markedly activated JNK and p38 and moderately activated ERK in a dose- (10-80 microM) and time-dependent (1-12 h) manner. The activated p38 decreased markedly and rapidly and the activated JNK decreased gradually when Cr(VI) was removed from the medium. Post-incubation of Cr(VI)-treated cells with H(2)O(2) increased the activities of JNK and p38, but not ERK. Co-administering Cr(VI) with 3-amino-1,2, 4-triazole (3AT), a catalase inhibitor, enhanced p38 activation, but did not influence JNK and ERK activation by Cr(VI). Conversely, co-administering Cr(VI) with mannitol, a hydroxyl radical scavenger and a Cr(V) chelator, reduced p38 activation and increased JNK and ERK activation by Cr(VI). These results indicate that p38 activation by Cr(VI) is positively correlated with oxidative stress, while JNK activity can be enhanced by either a quencher (mannitol) or activator (H(2)O(2)) of redox reactions in Cr(VI)-exposed CL3 cells. However, both 3AT and mannitol reduced the cytotoxicity of Cr(VI), but H(2)O(2) did not. The JNK activated by Cr(VI) was decreased (approximately 50%) by expression of a kinase-defective form of MKK7 (MKK7A) but not that of MKK4 (MKK4KR), suggesting that activation of JNK by Cr(VI) is mediated through MKK7. SB202190, a specific inhibitor of p38, markedly decreased JNK but did not change ERK activation by Cr(VI). PD98059, a specific inhibitor of ERK kinases MKK1/2, blocked ERK and p38 but did not alter JNK activation by Cr(VI). Neither the specific kinase inhibitors nor expression of MKK7A altered Cr(VI)-induced cytotoxicity. Together, these results suggest that activation of the JNK, p38 and ERK pathways by Cr(VI) is mediated through diverse redox mechanisms, yet their activation does not correlate with Cr(VI) cytotoxicity. (+info)Cyclosporin A inhibits chromium(VI)-induced apoptosis and mitochondrial cytochrome c release and restores clonogenic survival in CHO cells. (7/216)
A variety of key events in the molecular apoptotic pathway involve the mitochondria. Cyclosporin A (csA) affects the mitochondria by inhibiting the mitochondrial permeability transition (MPT), thereby preventing disruption of the transmembrane potential. The role of the MPT in apoptosis is not fully understood, but inhibition of the MPT may prevent the release of mitochondrial caspase activators, such as cytochrome c (cyt c), into the cytosol. Certain hexavalent chromium [Cr(VI)] compounds are known occupational respiratory tract toxins and carcinogens. We have previously shown that these compounds induce apoptosis as a predominant mode of cell death and that this effect can be observed in cell culture using soluble Cr(VI). We show here that Cr(VI)-induced apoptosis in Chinese hamster ovary (CHO) cells involves disruption of mitochondrial stability. Using a cyt c-specific monoclonal antibody, we observed a dose-dependent release of mitochondrial cyt c in cytosolic extracts of CHO cells exposed to apoptogenic doses of sodium chromate. Co-treatment of these cells with csA inhibited the release of cyt c and abrogated Cr(VI)-induced apoptosis as determined by a reduction in internucleosomal DNA fragmentation. Co-treatment with csA also markedly increased clonogenic survival of Cr(VI)-treated CHO cells. In contrast, the general caspase inhibitor Z-VAD-FMK markedly inhibited most of the morphological and biochemical parameters of apoptosis but did not prevent cyt c release and did not increase clonogenic survival. These results suggest that the MPT plays an important role in the regulation of mitochondrial cyt c release and that this may be a critical point in the apoptotic pathway in which cells are irreversibly committed to death. (+info)Chromate reduction by a pseudomonad isolated from a site contaminated with chromated copper arsenate. (8/216)
A pseudomonad (CRB5) isolated from a decommissioned wood preservation site reduced toxic chromate [Cr(VI)] to an insoluble Cr(III) precipitate under aerobic and anaerobic conditions. CRB5 tolerated up to 520 mg of Cr(VI) liter(-1) and reduced chromate in the presence of copper and arsenate. Under anaerobic conditions it also reduced Co(III) and U(VI), partially internalizing each metal. Metal precipitates were also found on the surface of the outer membrane and (sometimes) on a capsule. The results showed that chromate reduction by CRB5 was mediated by a soluble enzyme that was largely contained in the cytoplasm but also found outside of the cells. The crude reductase activity in the soluble fraction showed a K(m) of 23 mg liter(-1) (437 microM) and a V(max) of 0.98 mg of Cr h(-1) mg of protein(-1) (317 nmol min(-1) mg of protein(-1)). Minor membrane-associated Cr(VI) reduction under anaerobiosis may account for anaerobic reduction of chromate under nongrowth conditions with an organic electron donor present. Chromate reduction under both aerobic and anaerobic conditions may be a detoxification strategy for the bacterium which could be exploited to bioremediate chromate-contaminated or other toxic heavy metal-contaminated environments. (+info)Causes of Chromosomal Instability:
1. Genetic mutations: Mutations in genes that regulate the cell cycle or chromosome segregation can lead to CIN.
2. Environmental factors: Exposure to certain environmental agents such as radiation and certain chemicals can increase the risk of developing CIN.
3. Errors during DNA replication: Mistakes during DNA replication can also lead to CIN.
Types of Chromosomal Instability:
1. Aneuploidy: Cells with an abnormal number of chromosomes, either more or fewer than the normal diploid number (46 in humans).
2. Structural changes: Deletions, duplications, inversions, translocations, and other structural changes can occur in the chromosomes.
3. Unstable chromosome structures: Chromosomes with abnormal shapes or structures, such as telomere shortening, centromere instability, or chromosome breaks, can also lead to CIN.
Effects of Chromosomal Instability:
1. Cancer: CIN can increase the risk of developing cancer by disrupting normal cellular processes and leading to genetic mutations.
2. Aging: CIN can contribute to aging by shortening telomeres, which are the protective caps at the ends of chromosomes that help maintain their stability.
3. Neurodegenerative diseases: CIN has been implicated in the development of certain neurodegenerative diseases such as Alzheimer's and Parkinson's.
4. Infertility: CIN can lead to infertility by disrupting normal meiotic recombination and chromosome segregation during gametogenesis.
Detection and Diagnosis of Chromosomal Instability:
1. Karyotyping: This is a technique used to visualize the entire set of chromosomes in a cell. It can help identify structural abnormalities such as deletions, duplications, or translocations.
2. Fluorescence in situ hybridization (FISH): This technique uses fluorescent probes to detect specific DNA sequences or proteins on chromosomes. It can help identify changes in chromosome structure or number.
3. Array comparative genomic hybridization (aCGH): This technique compares the genetic material of a sample to a reference genome to identify copy number changes.
4. Next-generation sequencing (NGS): This technique can identify point mutations and other genetic changes in DNA.
Treatment and Management of Chromosomal Instability:
1. Cancer treatment: Depending on the type and stage of cancer, treatments such as chemotherapy, radiation therapy, or surgery may be used to eliminate cancer cells with CIN.
2. Prenatal testing: Pregnant women with a family history of CIN can undergo prenatal testing to detect chromosomal abnormalities in their fetuses.
3. Genetic counseling: Individuals with a family history of CIN can consult with a genetic counselor to discuss risk factors and potential testing options.
4. Lifestyle modifications: Making healthy lifestyle choices such as maintaining a balanced diet, exercising regularly, and not smoking can help reduce the risk of developing cancer and other diseases associated with CIN.
In conclusion, chromosomal instability is a common feature of many human diseases, including cancer, and can be caused by a variety of factors. The diagnosis and management of CIN require a multidisciplinary approach that includes cytogenetic analysis, molecular diagnostics, and clinical evaluation. Understanding the causes and consequences of CIN is crucial for developing effective therapies and improving patient outcomes.
1. Asbestosis: a lung disease caused by inhaling asbestos fibers.
2. Carpal tunnel syndrome: a nerve disorder caused by repetitive motion and pressure on the wrist.
3. Mesothelioma: a type of cancer caused by exposure to asbestos.
4. Pneumoconiosis: a lung disease caused by inhaling dust from mining or other heavy industries.
5. Repetitive strain injuries: injuries caused by repetitive motions, such as typing or using vibrating tools.
6. Skin conditions: such as skin irritation and dermatitis caused by exposure to chemicals or other substances in the workplace.
7. Hearing loss: caused by loud noises in the workplace.
8. Back injuries: caused by lifting, bending, or twisting.
9. Respiratory problems: such as asthma and other breathing difficulties caused by exposure to chemicals or dust in the workplace.
10. Cancer: caused by exposure to carcinogens such as radiation, certain chemicals, or heavy metals in the workplace.
Occupational diseases can be difficult to diagnose and treat, as they often develop gradually over time and may not be immediately attributed to the work environment. In some cases, these diseases may not appear until years after exposure has ended. It is important for workers to be aware of the potential health risks associated with their job and take steps to protect themselves, such as wearing protective gear, following safety protocols, and seeking regular medical check-ups. Employers also have a responsibility to provide a safe work environment and follow strict regulations to prevent the spread of occupational diseases.
There are several types of aneuploidy, including:
1. Trisomy: This is the presence of an extra copy of a chromosome. For example, Down syndrome is caused by an extra copy of chromosome 21 (trisomy 21).
2. Monosomy: This is the absence of a chromosome.
3. Mosaicism: This is the presence of both normal and abnormal cells in the body.
4. Uniparental disomy: This is the presence of two copies of a chromosome from one parent, rather than one copy each from both parents.
Aneuploidy can occur due to various factors such as errors during cell division, exposure to certain chemicals or radiation, or inheritance of an abnormal number of chromosomes from one's parents. The risk of aneuploidy increases with age, especially for women over the age of 35, as their eggs are more prone to errors during meiosis (the process by which egg cells are produced).
Aneuploidy can be diagnosed through various methods such as karyotyping (examining chromosomes under a microscope), fluorescence in situ hybridization (FISH) or quantitative PCR. Treatment for aneuploidy depends on the underlying cause and the specific health problems it has caused. In some cases, treatment may involve managing symptoms, while in others, it may involve correcting the genetic abnormality itself.
In summary, aneuploidy is a condition where there is an abnormal number of chromosomes present in a cell, which can lead to various developmental and health problems. It can occur due to various factors and can be diagnosed through different methods. Treatment depends on the underlying cause and the specific health problems it has caused.
There are several types of lung neoplasms, including:
1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.
Lung diseases can also be classified based on their cause, such as:
1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.
Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
Chromate
Calcium chromate
Potassium chromate
Caesium chromate
Cadmium chromate
Sodium chromate
Zinc chromate
Chromate ester
Strontium chromate
Ammonium chromate
Barium chromate
Magnesium chromate
Silver chromate
Lead(II) chromate
Hagdale Chromate Railway
Europium(III) chromate
Nickel(II) chromate
Iron(III) chromate
Chromate and dichromate
Chromate conversion coating
Di-tert-butyl chromate
Chromic acid
List of inorganic compounds
Molybdenum
Diphenylcarbazide
Stool guaiac test
Pyrotechnic composition
Karin Aurivillius
Delay composition
Cadmium
CDC - NIOSH Pocket Guide to Chemical Hazards -
Chromic acid and chromates
Calcium chromate 10827-V
Sodium Chromate Cr 51 - PubMed
EPIGENETIC STRESS AND CHROMATE CARCINOGENESIS
Lithium chromate (Li2CrO4) (ICSD 1972)
View source for Bismuth chromate - CAMEO
Effects of nickel, chromate, and arsenite on histone 3 lysine methylation - PubMed
Has European Union legislation to reduce exposure to chromate in cement been effective in reducing the incidence of allergic...
82-35-308-55 | DZUS® Lion Quarter-Turn Receptacle, Medium Size, Press-in, Steel Zinc Plate, Bright chromate | Southco
US Zinc Chromate Yellow ACUS23, ACUS23 Enamel Satin | WEM Colourcoats | 14ml
Optimization of Chromate Reduction by Whole Cells of |i|Arthrobacter|/i| sp. SUK 1205 Isolated from Metalliferous Chromite Mine...
HS Code pour Chromates d'ammonium
Chromate SLG
Potassium Chromate Manufacturer, Supplier, Exporter
Red Oxide Zinc Chromate Primer
Chromate post 63'' no feet - StateRestaurant
Double chromate cup holder with 4 plastic cups
HBM4EU chromates study: determinants of exposure to hexavalent chromium in plating, welding and other occupational settings<...
Subjects: Chromates -- poisoning - Digital Collections - National Library of Medicine Search Results
HBM4EU chromates study - Overall results and recommendations for the biomonitoring of occupational exposure to hexavalent...
ZINC CHROMATE HYDROXIDE Manufacturer, ZINC CHROMATE HYDROXIDE, Supplier, Exporter
PR-1773 Low Adhesion Non-Chromate Corrosion Access Door Sealant
Registration Dossier - ECHA
Calcium chromate (13765-19-0) | Chemical Effects in Biological Systems
Interactive effects of chromate and arsenate on their uptake and spe
TT-P-600 Primer Coating, Zinc Chromate (In Pressurized Dispensers) 1 - Chemsol
PPG Aerospace PR-1775 B-2 Gray PWA36760 Spec Non-Chromate Corrosion In
"Chromate Dissociation from Primer Paint in Simulated Lung Fluid" by Tiffany J. R. Morgan
Strontium chromate5
- OSHA has proposed a new strontium chromate exposure standard that would potentially cause Air Force paint facilities to be in violation of the proposed standard if adopted. (afit.edu)
- A number of agencies have classified strontium chromate as a human carcinogen by the inhalation route, on the basis of occupational and animal studies. (cdc.gov)
- The carcinogenicity of strontium chromate is attributed to the hexavalent chromium ion and not to strontium. (cdc.gov)
- The International Agency for Research on Cancer (IARC) has assigned strontium chromate, along with other chromates, to Group 1, as a human carcinogen (IARC 1990, 2002a). (cdc.gov)
- The only stable strontium compound that may cause cancer is strontium chromate, but this is due to chromium not strontium. (cdc.gov)
Chromium4
- Members of the genus Arthrobacter capable of surviving in various chromium contaminated industrial areas such as tannery, chromite mining area and Department of Energy (DOE) waste sites have been explored for their chromate reducing potential by several authors [4,7-10]. (scirp.org)
- HBM4EU chromates study - Overall results and recommendations for the biomonitoring of occupational exposure to hexavalent chromium. (bvsalud.org)
- In the first step, the Advanced Oxidation Process (AOP) - a combination of hydrogen peroxide and ozone or ultraviolet (UV) radiation - is used to breakdown biological/organic species in biological fluids and to oxidize Iow-valent chromium to chromate. (nih.gov)
- If chromium exists at different oxidation states, this novel method, converting chromium to chromate, gives the total chromium content in biological fluids. (nih.gov)
Pigments3
- Composition = Bi2O3-2CrO3 ==Resources and Citations== * H. Kuhn, M.Curran, "Chrome Yellow and Other Chromate Pigments", ''Artists Pigments'', Volume 1, R. Feller (ed. (mfa.org)
- Zinc chromate and red oxide are two pigments that are commonly used in metal primers. (entrepreneurindia.co)
- Environmental organisations have welcomed a ruling by the Tribunal of the EU that overturns the authorisation granted to Dominion Colour Corporation (DCC) to supply red and yellow lead chromate pigments to European markets. (ipen.org)
Zinc2
- Zinc chromate provides more corrosion resistance than red oxide, although red oxide is excellent for exposure to sunlight and exterior exposure. (entrepreneurindia.co)
- Concerned about corrosion, zinc chromate will give better corrosion resistance. (entrepreneurindia.co)
Exposure2
- Has European Union legislation to reduce exposure to chromate in cement been effective in reducing the incidence of allergic contact dermatitis attributed to chromate in the UK? (bmj.com)
- Conclusion The timing of this significant decline in the UK incidence of chromate attributed ACD, and the greater decline in workers potentially exposed to cement strongly suggests that the EU Directive2003/53/EC was successful in reducing exposure to chromate in cement in the UK. (bmj.com)
CrVI1
- Arsenate (AsV) and chromate (CrVI) inhibit each other's uptake and translocation in As-hyperaccumulator Pteris vittata . (researcher-app.com)
Potassium1
- Potassium chromate (K 2 CrO 4 ) is a yellow chemical indicator used for identifying concentrations of chloride ions in a salt solution with silver nitrate (AgNO 3 ). (powderpackchem.com)
Paints3
- This proposed reduction make the continued use of chromate containing primer paints very difficult. (afit.edu)
- There is currently no acceptable replacements for chromate containing primer paints on AF aircraft. (afit.edu)
- IPEN and its partner organisations are continuing the fight against the use of lead chromates in paints. (ipen.org)
Lithium1
- Lithium chromate and trichloroethylene. (cdc.gov)
Exposures1
- Exposures to 13 micrograms/cubic meter (microg/m3) of chromates and 160ppm of toluene (108883) exceeded recommended limits in the spray painting area of the aluminum fishing boat facility. (cdc.gov)
Corrosion2
- PR-1773 Class B is a low adhesion, non-chromate, corrosion inhibitive sealant. (bergdahl.com)
- Lamaka, S.: Chromate-Free Corrosion Protection Strategies for Magnesium Alloys-A Review: PART I-Pre-Treatment and Conversion Coating. (hereon.de)
Reduction3
- Freshly grown whole cells of this bacterium were evaluated for chromate reduction under batch culture using Vogel Bonner (V. B.) broth as the base. (scirp.org)
- Reduction of chromate increased with increase in cell density which attained maximum at 10 10 cells/ml, however, reverse was the phenomenon when the concentration of Cr(VI) increased gradually. (scirp.org)
- Glycerol, glycine and glucose promoted chromate reduction efficiency of the cells when used as electron donors. (scirp.org)
Compound1
- NIH: [https://pubchem.ncbi.nlm.nih.gov/compound/Bismuth-chromate Information sheet] ==Physical and Chemical Properties== * Soluble in acids and alkalis. (mfa.org)
Primer2
- This study suggests that paint particles with chromate bound in primer paint may be unavailable for bodily absorption if inhaled and a reduced standard for painting applications may be unnecessary. (afit.edu)
- Results of the dissociation of chromate in primer paint particles implies the chromate dissociation may be hindered. (afit.edu)
Study1
- An overview of Genetic Toxicology Mammalian Cell Mutagenicity study conclusions related to Calcium chromate (13765-19-0). (nih.gov)
Results1
- Results There was a significant decline in the incidence of both ACD attributed to chromate (incidence rate ratio 0.48, 95% CI 0.36 to 0.64) and ACD not-attributed chromate (0.76, 95% CI 0.69 to 0.85) between the time period preceding the EU legislation (2002-2004) and the postlegislation period (2005-2009). (bmj.com)
Total1
- The fraction of chromate dissolved was them compared to the total chromate originally collected. (afit.edu)
Metal1
- Glass holder made of metal wire, chromate, it included four plastic glass. (kitchenwarefromitaly.com)
Form1
- The Bureau procedure consists of reacting chromite with molten naoh under oxidizing conditions to form sodium chromate (na2cro4). (cdc.gov)
Method1
- Method Changes in the incidence of work-related ACD cases returned to The Health and Occupation Reporting network by dermatologists were analysed taking in to account attribution to chromate and occupation. (bmj.com)
Workers1
- High-risk notification of chromate and bichromate production workers. (cdc.gov)
Analysis1
- This membrane containing a di-ammonium dicationic ligand preconcentrates chromate for its electrochemical analysis. (nih.gov)
Code1
- En cliquant sur le bouton "Trouver le code SH associé" ci-dessus, vous pouvez trouver le code HS universel à 6 chiffres (valable pour presque tous les pays du monde) et les codes déclarables pour l'UE, le Royaume-Uni, les États-Unis, le Japon, la Chine, l'Inde et la Turquie (par ex. (findhs.codes)
Chromium3
- The only stable strontium compound that may cause cancer is strontium chromate, but this is due to chromium not strontium. (cdc.gov)
- In the first step, the Advanced Oxidation Process (AOP) - a combination of hydrogen peroxide and ozone or ultraviolet (UV) radiation - is used to breakdown biological/organic species in biological fluids and to oxidize Iow-valent chromium to chromate. (nih.gov)
- If chromium exists at different oxidation states, this novel method, converting chromium to chromate, gives the total chromium content in biological fluids. (nih.gov)
Sodium8
- Information in this record refers to the use of sodium chromate Cr 51 as a diagnostic agent. (nih.gov)
- No information is available on the use of sodium chromate Cr 51 during breastfeeding. (nih.gov)
- The manufacturer recommends withholding breastfeeding after a diagnostic dose of sodium chromate Cr 51, but does not provide a specific duration. (nih.gov)
- An overview of Genetic Toxicology Micronucleus Mice study conclusions related to Sodium chromate (7775-11-3). (nih.gov)
- The Bureau procedure consists of reacting chromite with molten naoh under oxidizing conditions to form sodium chromate (na2cro4). (cdc.gov)
- Sodium chromate crystals were produced that contained less than 0.01 pct naoh. (cdc.gov)
- La haute teneur en sel du pain blanc pourrait être un facteur qui contribue à la forte consommation de sodium au Maroc, surtout quand nous savons que le pain est un aliment de base dans le pays. (who.int)
- Toutes les politiques et initiatives visant à réduire la consommation de sodium devraient cibler le pain comme outil stratégique pour réduire l'apport en sel. (who.int)
Toluene1
- Exposures to 13 micrograms/cubic meter (microg/m3) of chromates and 160ppm of toluene (108883) exceeded recommended limits in the spray painting area of the aluminum fishing boat facility. (cdc.gov)