Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chromium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1983

Purification and chromium-excretory function of low-molecular-weight, chromium-binding substances from dog liver.

From liver of dogs injected iv with potassium dichromate (38 mg/kg body wt), a low-molecular-weight chromium-binding substance (LMCr) was purified into two subfractions, LMCr I and LMCr II, which differ in physical and chemical properties. LMCr I was identified to be an anionic, organic chromium compound with a molecular weight of 1500. It contained glutamic acid, glycine, and cysteine as the predominant amino acids and firmly bound chromium in a ratio of one chromium(III) to one molecule of LMCr I. LMCr II was isolated in crystalline form and demonstrated to be a water-soluble, inorganic chromium(III) complex consisting of Na2HPO4 . 7H2O and Na2HPO4 . 2H2O. Although its crystallization reduced the chromium content, it had a maximum chromium-binding capacity as much as one chromium per one phosphorus in water. The mixture of LMCr I and LMCr II as approximated to be the natural composition showed a lower acute toxicity as measured by lethality in mice and had higher rates of urinary excretion and renal clearance in rabbits, accompanied by lower rates of renal tubular reabsorption and retention in kidney and liver than potassium dichromate(VI) and chromium(III) chloride. Pretreatment with chromium-free LMCr II remarkably reduced the mortality rates of mice acutely poisoned with chromium chloride. These results indicate that LMCr plays an important role in the detoxification and excretion of chromium in mammals.

Amino Acids↗
PubMed2005

A newly synthetic chromium complex--chromium(phenylalanine)3 improves insulin responsiveness and reduces whole body glucose tolerance.

Low-molecular-weight organic chromium complexes such as chromium picolinate are often used as dietary supplements to improve insulin sensitivity and to correct dyslipidemia. However, toxicity associated with such chromium compounds has compromised their therapeutic value. The aim of this study was to evaluate the impact of a newly synthesized complex of chromium with phenylalanine, Cr(pa)3 on insulin-signaling and glucose tolerance. Cr(pa)3 was synthesized by chelating chromium(III) with D-phenylalanine ligand in aqueous solution. In mouse 3T3-adipocytes, Cr(pa)3 augmented insulin-stimulated glucose-uptake as assessed by a radioactive-glucose uptake assay. At the molecular level, Cr(pa)3 enhanced insulin-stimulated phosphorylation of Akt in a time- and concentration-dependent manner without altering the phosphorylation of insulin receptor. Oral treatment with Cr(pa)3 (150 microg/kg/d, for six weeks) in ob/ob+/+ obese mice significantly alleviated glucose tolerance compared with untreated obese mice. Unlike chromium picolinate, Cr(pa)3 does not cleave DNA under physiological reducing conditions. Collectively, these data suggest that Cr(pa)3 may represent a novel, less-toxic chromium supplement with potential therapeutic value to improve insulin sensitivity and glycemic control in type II diabetes.

Adipocytes↗
PubMed2006

Synthesis and characterization of the octahydrotriborate complexes Cp*V(B3H8)2 and Cp*Cr(B3H8)2 and the unusual cobaltaborane cluster Cp*2Co2(B6H14).

The new compounds CpV(B(3)H(8))(2), CpCr(B(3)H(8))(2), and Cp(2)Co(2)(B(6)H(14)) have been synthesized by treating the pentamethylcyclopentadienyl complexes [CpVCl(2)](3), [CpCrCl(2)](2), and [CpCoCl](2) with NaB(3)H(8). X-ray crystallography shows that CpV(B(3)H(8))(2) and CpCr(B(3)H(8))(2) have the same ligand sets but different molecular structures: the vanadium compound contains two bidentate B(3)H(8) ligands (i.e., bound to the metal center via two vicinal hydrogen atoms), whereas the chromium compound has one bidentate B(3)H(8) ligand and one B(3)H(8) ligand bound in an unprecedented fashion via two geminal hydrogen atoms. The "gem-bound" B(3)H(8) group itself has an atypical structure consisting of a BH(2)-BH(2)-BH(3) triangle with one additional hydrogen atom bridging the unique BH(2)-BH(2) edge. The B-B distances are nearly identical within experimental error at 1.790(5), 1.792(5), and 1.786(6) Angstrom. The relationship between the electronic and molecular structures of the V and Cr compounds is briefly discussed. The structure of Cp(2)Co(2)(B(6)H(14)) can be viewed in two different ways: as a dicobalt complex in which two CpCo units are each bound to four adjacent boron atoms of an S-shaped B(6)H(14) ligand, or as an eight-vertex hypho cluster compound. In the former case, the B(6)H(14) ligand is best regarded as a dianionic bi-borallyl group H(3)B(mu-H)BH(mu-H)BHBH(mu-H)BH(mu-H)BH(3) in which one hydrogen at each end of the chain is involved in an agostic interaction. From a cluster point of view, the structure of Cp(2)Co(2)(B(6)H(14)) can be generated by removing three adjacent high-connectivity vertices from the eleven-vertex closo polyhedron. The Co-B distances vary from 2.008(5) to 2.183(4) Angstrom, and the B-B distances within in the S-shaped chain range from 1.734(8) to 1.889(6) Angstrom. Finally, a new synthesis of the known molybdenum compound Cp(2)Mo(2)(B(5)H(9)) is described; its structure as established by X-ray crystallography closely resembles that of the previously described (C(5)H(4)Me) analogue.

Journal Article↗
PubMed2001

Cancer mortality in relation to environmental chromium exposure.

From the 1950s to the 1980s, hexavalent chromium compounds were used as additives at certain water-cooling towers at three southern California gas compressor facilities. Claims of potential residential chromium exposure prompted the examination of age-adjusted mortality rates during 1989 to 1998 for lung cancer, all cancer, and all deaths for neighborhoods near versus distant from the plants. Differences in the rates between areas tended to be small and not statistically significant. The only significant difference was a lower, rather than higher, rate of total cancer among women in the potentially exposed areas. Study limitations preclude a definitive assessment of risk, but similar to previous investigations of cancer in relation to environmental chromium exposure in other locations, this study found no evidence of a cancer hazard among residents living near these California gas compressor facilities.

California↗
PubMed1998

Chromium picolinate toxicity.

OBJECTIVE: To describe a case of toxicity secondary to chronic ingestion of 6-12 times the recommended daily allowance of over-the-counter (OTC) chromium picolinate. CASE SUMMARY: A 33-year-old white woman presented with weight loss, anemia, thrombocytopenia, hemolysis, liver dysfunction (aminotransferase enzymes 15-20 times normal, total bilirubin 3 times normal), and renal failure (serum creatinine 5.3 mg/dL; blood urea nitrogen 152 mg/dL). She had ingested chromium picolinate 1200-2400 microg/d for the previous 4-5 months to enhance weight loss. The patient had chromium plasma concentrations 2-3 times normal. Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome were ruled out by clinical findings, peripheral blood smears, and a bone marrow biopsy. The patient was managed with supportive measures and received blood product transfusions and hemodialysis. Hemolysis stabilized and liver function improved over 6 days. Liver function returned to normal prior to discharge. Renal function began to return on day 12 and her serum creatinine on discharge was 1.3 mg/dL. One year later, all laboratory values were within normal limits. DISCUSSION: Trivalent chromium is an essential trace element that is considered safe when ingested in normal quantities. Trivalent chromium compounds are used by patients to enhance weight loss, increase lean body mass, and/or improve glycemic control. Information regarding the toxicity of chromium picolinate is limited. CONCLUSIONS: Chromium supplements may cause serious renal impairment when ingested in excess. Medication histories should include attention to the use of OTC nutritional supplements often regarded as harmless by the public and lay media.

Acute Kidney Injury↗
PubMed2001

[The effect of tannery waste products on viability of selected bacteria from activated sludge].

In this study we have investigated the influence of sludge on the activity of bacteria strains: Acinetobacter baumannii, Aeromonas hydrophila and Pseudomonas cepacia. To our studies we have taken waste materials used in the chromium compound leather tanning process as well as materials from leather fat and waste materials, in general. It was confirmed that 1:20 dilution of chromium tanning leather waste, retanage and leather fat allowed the survivability of bacteria in all three strains. Through our research we were able to establish that general sewage with a decreased level of chromium practically did not effect the survivability of bacteria in a sewage environment. Both types of waste, city sewage as well as leather waste, were shown not to facilitate bacterial growth. If chromium waste flow into city sewage without treatment, bacteria can only survive at a dilution level of 1:20, which will not affect the survivability of bacteria used in biological waste treatment.

Acinetobacter↗
PubMed2002

Hazardous air pollutants and asthma.

Asthma has a high prevalence in the United States, and persons with asthma may be at added risk from the adverse effects of hazardous air pollutants (HAPs). Complex mixtures (fine particulate matter and tobacco smoke) have been associated with respiratory symptoms and hospital admissions for asthma. The toxic ingredients of these mixtures are HAPs, but whether ambient HAP exposures can induce asthma remains unclear. Certain HAPs are occupational asthmagens, whereas others may act as adjuncts during sensitization. HAPs may exacerbate asthma because, once sensitized, individuals can respond to remarkably low concentrations, and irritants lower the bronchoconstrictive threshold to respiratory antigens. Adverse responses after ambient exposures to complex mixtures often occur at concentrations below those producing effects in controlled human exposures to a single compound. In addition, certain HAPs that have been associated with asthma in occupational settings may interact with criteria pollutants in ambient air to exacerbate asthma. Based on these observations and past experience with 188 HAPs, a list of 19 compounds that could have the highest impact on the induction or exacerbation of asthma was developed. Nine additional compounds were identified that might exacerbate asthma based on their irritancy, respirability, or ability to react with biological macromolecules. Although the ambient levels of these 28 compounds are largely unknown, estimated exposures from emissions inventories and limited air monitoring suggest that aldehydes (especially acrolein and formaldehyde) and metals (especially nickel and chromium compounds) may have possible health risk indices sufficient for additional attention. Recommendations for research are presented regarding exposure monitoring and evaluation of biologic mechanisms controlling how these substances induce and exacerbate asthma.

Air Pollutants↗
PubMed1998

Arrest of replication by mammalian DNA polymerases alpha and beta caused by chromium-DNA lesions.

We have previously shown that trivalent chromium, and hexavalent chromium in the presence of one of its primary in vivo reductants, ascorbate, can bind to DNA and form interstrand crosslinks capable of obstructing replication. This effect was demonstrated in vitro by using Sequenase Version 2.0 T7 DNA polymerase; its parent enzyme, the unmodified T7 DNA polymerase; and Escherichia coli polymerase I large (Klenow) fragment; and it was demonstrated ex vivo by using Taq polymerase and DNA from chromium-treated human lung cells as template. This study was performed to determine whether DNA-bound chromium affects mammalian DNA polymerases in the same manner. Two mammalian enzymes, DNA polymerase alpha and DNA polymerase beta, were used. DNA polymerase alpha is a processive enzyme believed to be the primary lagging-stand synthetase, whereas DNA polymerase beta is a non-processive enzyme believed to function in DNA repair by filling single stranded gaps one base at a time. DNA polymerase arrest assays were performed with each of these enzymes to replicate DNA with toxicologically relevant levels of chromium adducts produced by either trivalent chromium or hexavalent chromium and ascorbate. Both enzymes responded to chromium-DNA damage by arresting replication, and the arrests increased in a dose-dependent manner. Furthermore, the guanine-specific pattern of arrests produced when an exonuclease-free preparation of DNA polymerase beta was used corresponded exactly to the arrest patterns produced in vitro by the exonuclease-free enzyme Sequenase and ex vivo by Taq polymerase. These results suggest that replication arrest may be a common response of polymerases to DNA-chromium lesions and provide a plausible mechanism for the inhibition of DNA synthesis and S-phase cell-cycle delay that occurs in mammalian cells treated with genotoxic chromium compounds.

Ascorbic Acid↗
PubMed1985

Cancer risk of arc welders exposed to fumes containing chromium and nickel.

A retrospective follow-up study among chromium- and nickel-exposed welders, which took into consideration welding procedures, duration of exposure, and smoking habits, yielded an increased cancer risk in a comparison with an internal reference group of turners, milling cutters, and drillers, as well as in a comparison with the general population of the Federal Republic of Germany. Due to the cohort size (1 224 welders, 1 694 turners) and the fact that the observation period is still too short, confirmed statements as to the target cancer sites cannot yet be made. However, it emerges that welding with coated electrodes shows a higher cancer risk as compared to the other welding processes observed. This finding may be explained by the fact that the share of hexavalent chromium compounds in the welding fumes is greater with coated electrodes than with other processes so that a follow-up study observing the health risks of chromium and nickel fumes separately would be warranted. For the confirmation of a more favorable outcome with gas-shielded welding, a larger investigation group or a longer observation period would be required.

Adolescent↗
PubMed1992

Induction of ribonucleoside diphosphate reductase gene transcription by chemicals in Escherichia coli.

A fusion between the promoter of the nrdA gene of Escherichia coli and the lacZ gene has been constructed, and the induction of nrdA gene expression by 20 organic and 20 inorganic chemicals has been studied. The inducing compounds of the SOS genes, such as bleomycin, captan, ciprofloxacin, enoxacin, hydroxyurea, N-methyl-N'-nitro-N-nitrosoguanidine, mitomycin C, nalidixic acid, ofloxacin and hexavalent chromium compounds also trigger the expression of the nrdA gene. Other chemicals such as aluminium, manganese and zinc salts, reported as negative in the SOS Chromotest, are also inducers of the nrdA gene. These results suggest that ribonucleoside diphosphate reductase transcription is increased by chemicals able to either block DNA synthesis or to alter the enzymes participating in the DNA replication. Induction of nrdA gene is an effect to be further considered in the study of alterations produced by physical or chemical treatments which act upon DNA metabolism.

Escherichia coli↗
PubMed1986

Kinetics of the metal components of intratracheally instilled stainless steel welding fume suspensions in rats.

The kinetics of iron, chromium, nickel, and cobalt from manual metal arc and metal inert gas stainless steel welding fumes were studied. Neutron activated welding fumes, in aqueous suspensions, were instilled intratracheally into rats. The follow up continued for up to 106 days. From both fumes, approximately 10% of the injection bolus was immediately lost into the gastrointestinal tract, to be recovered in the faeces within three days. Thereafter, a pronounced difference was seen in the kinetics of the two types of fumes. After the first day, chromium, nickel, and iron were lost from the lungs with half times of about 53, 49, and 73 days after exposure to MMA/SS fumes, whereas practically no loss could be seen in the metal components of the metal inert gas welding fumes within two months. The disposition of chromium from MMA/SS fumes closely resembled that of intratracheally instilled water soluble chromates. On the other hand, the disappearance of trivalent chromium from MIS/SS fumes was considerably slower than that of the practically water insoluble chromates, or even of trivalent chromium salts. Thus the physical characteristics of the fume appreciably affect the kinetics of the clearance of chromium compounds from the lungs.

Animals↗
PubMed2003

Oxidative stress, hogg1 expression and NF-kappaB activity in cells exposed to low level chromium.

Chromium compounds are carcinogenic to the human lung, although the detailed biochemical mechanism is still unclear. To understand the carcinogenic mechanism in cells exposed to low level hexavalent chromium, we measured the generation of reactive oxygen species (ROS) and 8-hydroxydeoxyguanosine (8-OH-dG), the transcription of hogg1, which encodes an 8-OH-dG repair protein, and NF-kappaB activation levels in the A549 human lung epithelial cell line after exposure to Cr (VI) at concentrations of 12.5 to 800 microM. In A549 cells, ROS levels and DNA binding by NF-kappaB increased in proportion to the concentration of Cr (VI). These increases were diminished by pretreatment with catalase, superoxide dismutase, or D-mannitol, but the levels of 8-OH-dG and expression of hogg1 did not change significantly with Cr (VI) exposure. These results suggest that the induction of ROS and the activation of NF-kappaB are important in the carcinogenic mechanism of Cr (VI), but it is unlikely that Cr (VI) concentrations below 800 microM increase 8-OH-dG levels or the expression of hogg1.

Blotting, Northern↗
PubMed1975

Legislation on prevention of occupational dermatoses.

Legislation is one way to eliminate sensitizers and irritants. Purity requirements, declaration and labelling, industrial health codes and pre-employment occupational aptitude examinations are useful in combating occupational and contact dermatitis by drugs and products of daily use. Chromium compounds, turpentine, balsam of Peru, benzocaine and other can be eliminated by administration and legislation.

Balsams↗
PubMed1989

Inorganic chemistry of chromium and its speciation in Whetlerite.

Chromium compounds are among the impregnants that enhance the ability of carbon air filters to absorb and destroy toxic agents such as CK and AC. The possibility of inhaling chromium-containing carbon dust from such filters has caused concern because, in addition to being an essential nutrient, chromium has been identified as a chemical carcinogen in humans. The essentiality or carcinogenicity of chromium depends upon its chemical speciation. Solubility and oxidation state are particularly important factors in assessing the potential hazards associated with the possible inhalation of chromium-containing dusts from these impregnated carbons or Whetlerites. The chemical speciation of the chromium in Whetlerite was found to be: from 0.6 to 1.3% insoluble trivalent chromium; from 1.0 to 1.3% insoluble hexavalent chromium; and from 0.7 to 0.9% soluble hexavalent chromium. The impregnation process, and the resulting speciation of chromium in Whetlerite, is consistent with the inorganic chemistry of chromium.

Air Pollutants, Occupational↗
PubMed1977

Comparative toxicity of trivalent and hexavalent chromium to rabbits. II. Morphological changes in some organs.

Toxicity of trivalent and hexavalent chromium compounds was investigated in experimental rabbits to ascertain health hazards among industrial workers of miners occupationally exposed to such chemicals. Brain, kidney and myocardium showed a tendency to accumulate chromium irrespective of its valency state; the morphological changes were more marked in animals exposed to hexavalent chromium. However, no definite co-relation could be observed between the concentration of the metal and the degree of histological changes in these organs.

Animals↗
PubMed1994

Metal mutagenesis in transgenic Chinese hamster cell lines.

Metals are toxic agents for which genotoxic effects are often difficult to demonstrate. To study metal mutagenesis, we have used two stable hprt/gpt+ transgenic cell lines that were derived from Chinese hamster V79 cells. Both the G12 and G10 cell lines are known to be very sensitive to clastogens such as X-rays and bleomycin, with the mutagenic response of the integrated xanthine guanine phosphoribosyl transferase (gpt) gene in G10 usually exceeding that of the same gene in the transgenic G12 cells. In studies with carcinogenic insoluble nickel compounds, a high level of mutagenesis was found at the gpt locus of G12 cells but not at the endogenous hypoxanthine phosphoribosyl transferase (hprt) locus of V79 cells. We have since demonstrated the similar recovery of a high frequency of viable G12 mutants with other insoluble nickel salts including nickel oxides (black and green). The relative mutant yield for the insoluble nickel compounds (G12 > G10) is the opposite of that obtained with nonmetal clastogens (G10 > G12). In the G12 cells, nickel mutagenesis may be related to the integration of the gpt sequence into a heterochromatic region of the genome. For some of the insoluble nickel compounds, significant inhibition of both cytotoxicity and mutant yield resulted when the G12 cells were pretreated with vitamin E. In comparison with the nickel studies, the mutagenic responses to chromium compounds in these cell lines were not as dramatic. Mutagenesis of the gpt target could not be demonstrated with other metals such as mercury or vanadium.

Animals↗