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PubMed1982

Mutagenicity of a series of hexacoordinate cobalt(III) compounds.

15 cobalt(III) compounds have been tested for DNA-damaging capabilities using an E. coli differential repair assay and for mutagenicity in strains of Salmonella typhimurium. 4 of these compounds were active in both systems. Although the general ligand requirements for genetic activity of cobalt(III) appear to closely parallel those of chromium(III) and rhodium(III), the genetic activity of cobalt compounds seems particularly dependent upon the structure of the ligands coordinated about the metal ion. By a simple methyl substitution on the organic ligands, a compound completely devoid of activity, e.g. trans-[Co(pyr)4Cl2]Cl, could be made slightly mutagenic in Salmonella typhimurium strains e.g. trans-[Co(3-pic)4Cl2]Cl. Substitution at the 4-position rather than the 3-position on the same pyridine ring, e.g. trans-[Co(4-pic)4Cl2]Cl, results in a 50-fold enhancement of activity in both repair and mutagenesis systems. The difference in genetic activity is attributed to the influence of the ligands on the relative lability of the metal complex.

Cobalt↗
PubMed2005

Absence of toxic effects in F344/N rats and B6C3F1 mice following subchronic administration of chromium picolinate monohydrate.

Chromium picolinate monohydrate (CPM) is a synthetic compound heavily marketed to consumers in the United States for use as a dietary supplement for muscle building and weight loss. The National Toxicology Program (NTP) tested the toxicity of this compound based on the potential for widespread consumer exposure and lack of information about its toxicity. Groups of 10 male and 10 female F344/N rats and B6C3F(1) mice were exposed to 0, 80, 240, 2000, 10,000, or 50,000 ppm CPM in feed for 13 weeks. CPM administration produced no effect on body weight gain or survival of rats or mice. Organ weights and organ/body weight ratios in exposed animals were generally unaffected by CPM. No compound-related changes in hematology and clinical chemistry parameters were observed. There were no histopathological lesions attributed to CPM in rats or mice.

Administration, Oral↗
PubMed2001

Two atropisomers of tricarbonyl[eta6-6-chloro-3-(3-chloro-2-methylphenyl)-2,4,8-trimethyl-1,2,3,4-tetrahydro-2,4-dibora-1,3-diazanaphthlene]-chromium(0).

The structures of two atropisomers of the title compound, [Cr(C16H18B2Cl2N2)(CO)3], are reported. For both compounds, the Cr(CO)3 moiety is bound to the C6 aromatic ring of the molecule; the existence of atropisomers resulting from the non-equivalence of both faces of the C6 aromatic ring is a consequence of the 3-chloro-2-methylphenyl ring being nearly perpendicular to the mean plane of the 2,4-dibora-1,3-diazanaphthalene ring. The orientation of the Cr(CO)3 tripod relative to the C6 aromatic ring is such that it is nearly eclipsed in one isomer (2.4 degrees rotation from being eclipsed with C--N, C--Cl and C--H) and slightly twisted (16.2 degrees ) from an eclipsed conformation in the other.

Journal Article↗
PubMed1993

Biomonitoring exposure to metal compounds with carcinogenic properties.

Several metals such as arsenic, beryllium, chromium and nickel are carcinogenic to man when they occur in certain well-defined physicochemical forms. The carcinogenic potential of these metals is linked to their mutagenic properties. The determination of the metal or possibly of its metabolites in biological media and the cytogenetic examination of somatic cells are two methods that can currently be used to monitor exposure of populations at risk. Due to the use of inappropriate methodology, the value of the positive cytogenetic results published so far appears questionable. By contrast, the concentrations of metals in blood, urine, or other biological materials can be determined with accurate and precise methods. Although it does not permit a direct assessment of the carcinogenic risk, this approach is currently the most suitable for monitoring exposed populations.

Arsenic↗
PubMed1995

Physiological and toxicological changes in the skin resulting from the action and interaction of metal ions.

The human environment contains more than 50 metal or metalloid elements. At least 15 are recognized as trace elements, with zinc, calcium, copper, magnesium, and iron having specific roles in skin morphogenesis and function. The present review focuses on the presumed role of metal ions in the skin, their competition for carrier proteins, and membrane receptors. Evidence presented shows that the balance of trace metal ions is critical for normal skin and repair mechanisms following injury. Xenobiotic ions can impair this balance, leading to pathological change. The skin acts as an organ of elimination of excess trace metals and xenobiotic ions from the body, but mechanisms of voidance vary for different metals. Metal ions are an important cause of allergies, and evidence is presented to show that the majority of metals or metal compounds can induce allergic changes. Except for chromium and nickel, which are among the most common human allergens, animal models have provided little information. At least cadmium, thorium, lead, chromium, nickel, beryllium, and arsenic and proven or putative carcinogens in animals or humans on the basis of cytological or epidemiological evidence. However, only arsenic exhibits a clear predilection for the skin. Other metals such as gold can induce subcutaneous sarcoma following injection, but the relevance of this observation in terms of human occupational risk is discounted.

Animals↗
PubMed2000

Linear trichromium complexes with the anion of 2,6-di(phenylimino)piperidine.

The anion of 2,6-di(phenylimino)piperidine (DPhIP) has been found to support linear chains of three metal atoms. Three new compounds, [Cr3(DPhIP)4Cl]Cl.(1).5CH2Cl2.0.5H2O (1.1.5CH2Cl2.0.5H2O), [Cr3(DPhIP)4(CH3CN)]- (PF6)2.H2O.4CH3CN (2.H2O.4CH3CN), and [Cr3(DPhIP)4(F)(CH3CN)](BF4)2.5CH3CN (3.5CH3CN), have been synthesized and characterized by X-ray crystallography. Compound 1 has a linear chain of three chromium atoms arranged in an unsymmetrical fashion, with two of them forming a quadruply bonded unit (Cr-Cr distance 1.932(2) A) and the third being a non-metal-metal-bound 5-coordinate unit (Cr...Cr distance 2.659(2) A). The fifth coordination site is occupied by a chloride ion, and another chloride ion is located in the interstices of the crystal. The trimetal unit in compound 2 is structurally similar to that in compound 1 except that the axial ligand in 2 is a CH3CN molecule. Compound 3 is an oxidation product prepared by reaction of 1 with AgBF4. Here, a square pyramidal CrIII unit, FCrN4, and a Cr-Cr quadruply bonded (Cr-Cr distance 1.968(2) A) unit, with an axially coordinated acetonitrile molecule, form the trichromium chain. The CrIII...CrII separation of 2.594(2) A in 3 is too long to be considered a bonding interaction.

Journal Article↗
PubMed2003

Electron spin resonance study of chromium(V) formation and decomposition by basalt-inhabiting bacteria.

Bacterial reduction of Cr(VI) to Cr(III) compounds may produce reactive intermediates Cr(V) and Cr(IV), which can affect the mobility and toxicity of chromium in environments. To address this important subject, we conducted an electron spin resonance (ESR) study to understand the kinetics of the formation and decomposition of Cr(V) during Cr(VI) reduction by different gram-positive Cr(VI)-tolerant bacteria, which were isolated from polluted basalts from the United States of America and the Republic of Georgia. Results from our batch experiments show that during Cr(VI) reduction, the macromolecules at the cell wall of these bacteria could act as an electron donor to Cr(VI) to form a stable square-pyramidal Cr(V) complexes, which were reduced further probably via a one-electron transfer pathway to form Cr(IV) and Cr(III) compounds. The Cr(V) peak at the ESR spectrum possessed superhyperfine splitting characteristic of the Cr(V) complexes with diol-containing molecules. It appears that the kinetics of Cr(V) formation and decomposition depended on the bacterial growth phase and on the species. Both formation and decomposition of Cr(V) occurred more quickly when Cr(VI) was added at the exponential phase. In comparison with other gram-positive bacteria from the republic of Georgia, the formation and decomposition of Cr(V) in Arthrobacter species from the Unites States was significantly slower.

Arthrobacter↗
PubMedDate not supplied

Reduction of chromium(VI) and its relationship to carcinogenesis.

Although Cr(VI)-containing compounds are well-documented carcinogens, their mechanism of action is still not well understood. Recent studies have suggested that reduction of Cr(VI) to its lower oxidation states and related free-radical reactions play an important role in carcinogenesis. This article summarizes recent studies on (1) the reduction of Cr(VI) by ascorbate, diol- and thiol-containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals; (2) free-radical production with emphasis on hydroxy radical generation via Fenton or Haber-Weiss type reactions; and (3) free-radical-induced cellular damage, such as DNA strand breaks, hydroxylation of 2'-deoxyguanosine, and activation of nuclear transcription factor kappa B.

Animals↗
PubMed1985

Chromium bond detection in isolated erythrocytes: a new principle of biological monitoring of exposure to hexavalent chromium.

Internal stress to chromium is only relevant in occupational medicine if it is due to the handling of hexavalent chromium. Cr(VI) ions, after uptake by inhalation or percutaneously are carried in the blood plasma and penetrate--depending on the concentration--into the erythrocytes. Due to the intracellular reduction to Cr(III) and the concurrent intracellular protein binding, the erythrocytes represent an easily accessible target organ for quantitative chromium determination after occupational exposure to Cr(VI) compounds. The results of an earlier experimental study indicate that human plasma too is capable of spontaneous reduction of Cr(VI) ions of up to 2 ppm to Cr(III). This plasma reduction capacity (PRC) can be increased and accelerated considerably by adding ascorbic acid (AA). These findings were supported in this investigation by proving a decreased binding of Cr(VI) inside the erythrocytes under the effect of AA. This leads to the assumption that only those Cr(VI) concentrations can penetrate the membrane of the erythrocytes and enter the cell which either come into contact with the membrane during the reduction process or exceed this limit concentration of 2 ppm. Only in these two instances can corresponding chromium findings be analyzed in isolated and washed erythrocytes. These results are compared with those obtained by conventional methods, such as Cr determination in the blood and/or urine. Our findings indicate that a single determination of chromium concentration in the erythrocytes will permit the monitoring of critical cases of Cr(VI) exposure. This is a new type of biological monitoring in the sense of a condensed longitudinal study, in order to find out whether threshold concentrations have been respected over a given period.

Air Pollutants, Occupational↗
PubMed1998

Histochemical staining of chromium with 2-(8-quinolylazo)-4,5-di-p-tolylimidazole.

A new highly sensitive staining agent for chromium (Cr) has been introduced. This staining agent, 2-(8-quinolylazo)-4,5-di-p-tolylimidazole (QTI), was found to be more than ten times as sensitive for Cr than the conventional staining agent, Chromazurol S, and QTI also stained cadmium, copper, lead and zinc. Differentiation between the staining of Cr and other metals was achieved by immersing the tissue sections in dilute alkylamine solutions before they were stained with QTI. Thus, it was possible to selectively stain for Cr by blocking other metals.

Animals↗
PubMed2001

Genotoxic ability of cadmium, chromium and nickel salts studied by kinetochore staining in the cytokinesis-blocked micronucleus assay.

The aneugenic and clastogenic ability of cadmium chloride(II), cadmium sulfate(II), nickel chloride(II), nickel sulfate(II), chromium chloride(III) and potassium dichromate(IV) have been evaluated through kinetochore-stained micronucleus test. Traditional genotoxicity assays evaluate DNA damage, gene mutations and chromosome breakage. However, these tests are not adequate to detect aneugenic agents that do not act directly on DNA. Staining kinetochores in the cytokinesis-blocked micronucleus assay is a useful way to discriminate between clastogens and aneuploidogens and may allow a rapid identification of aneuploidy-inducing environmental compounds. Human diploid fibroblasts (MRC-5) were employed. All compounds increased micronuclei frequency in a statistically significant way. However, increases in kinetochore-positive micronuclei frequencies were higher than in kinetochore-negative ones. The present work demonstrates the genotoxic ability of the cadmium and chromium salts studied. Aneugenic as well as clastogenic ability could be observed with this assay. Nickel salts, as it was expected because of their known weak mutagenicity, showed lower genotoxic effects than the other metal salts studied. As the test employed only allows the detection of malsegregation, it is proposed that this mechanism is at least one of those by which the tested metal salts induced aneuploidy. On the other hand, visualization of kinetochores in all experiments suggests that the compounds studied did not act by damaging these structures.

Adult↗
PubMed1997

Subtoxic intracellular trivalent chromium is not mutagenic: implications for safety of chromium supplementation.

For reasons that are outlined, toxicologists have long suspected that intranuclear trivalent chromium mediates much if not all of the well-documented genotoxicity of hexavalent chromium. However, more recent evidence suggests that this genotoxicity is in fact attributable to free radical damage catalyzed by hexavalent chromium under reducing aerobic conditions. Subtoxic intranuclear concentrations of trivalent chromium, while they can be clastogenic in vitro, do not appear to induce point mutations and thus are unlikely to mediate the carcinogenicity of hexavalent compounds. Furthermore, there is considerable doubt that sublethal doses of trivalent chromium can produce tissue levels high enough to induce clastogenic damage in vivo. These considerations elucidate the virtual non-toxicity of orally-administered trivalent chromium in any dose, and strongly suggest that dietary supplementation with trivalent chromium in reasonable amounts is unlikely to carry any genotoxic risk. However, further animal studies are advisable to rule out the possibility of clastogenicity when grossly 'megadose' amounts are ingested.

Animals↗