Aneugenic effects of some metal compounds assessed by chromosome counting in MRC-5 human cells

Güerci, Alba Mabel; Seoane, Analía Isabel; Dulout, Fernando Noel

doi:10.1016/s1383-5718(00)00057-7

Cited by 30 publications

(18 citation statements)

References 37 publications

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“…Increased frequencies of hypoploid cells induced by cadmium chloride, cadmium sulfate, potassium dichromate, and cacodilic acid were reported in MRC-5-treated cells analyzed by this technique [Güerci et al, 2000].…”

Section: Introductionmentioning

confidence: 84%

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Malsegregation as a possible mechanism of aneuploidy induction by metal salts in MRC‐5 human cells

Seoane¹,

Güerci²,

Dulout³

2002

Environ and Mol Mutagen

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Many aneugenic compounds are known to affect one or more components of the mitotic apparatus leading to an erroneous migration of chromosomes. Malsegregation occurs when a chromosome (or a chromatid) fails to migrate and remains at the metaphase plate. Nondisjunction implies the lack of dissociation between sister chromatids and the migration of both together to the same pole. The aim of the present study was to provide evidence that the aneugenic effect of some metal salts is the consequence of malsegregation at anaphase and that it is not caused by nondisjunction mechanisms. The frequencies of lagging chromosomes at anaphase-telophase of mitosis, hypoploid metaphases, and kinetochore-positive micronuclei induced by cadmium chloride, potassium dichromate, and cacodilic acid (dimethylarsinic acid) in MRC-5 human cells were compared. The data indicate that all the tested compounds are able to induce aneuploidy in MRC-5 human cells. Positive, statistically significant correlations were found when kinetochore-positive micronuclei, hypoploidy, and lagging chromosome frequencies were compared. The results suggest that malsegregation is the main mechanism involved in the induction of aneuploidy by metal salts in MRC-5 cells.

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Section: Introductionmentioning

confidence: 84%

“…Part of the data used for these comparisons was previously published in Güerci et al [2000] (chromosome counting data) and Seoane and Dulout [2001] (micronuclei analysis). Our analysis provides evidence that malsegregation at anaphase rather than nondisjunction is the main cause of the aneuploidy induced by metal salts.…”

Section: Introductionmentioning

confidence: 99%

Malsegregation as a possible mechanism of aneuploidy induction by metal salts in MRC‐5 human cells

Seoane¹,

Güerci²,

Dulout³

2002

Environ and Mol Mutagen

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“…MRC-5 cells were used in the cytokinesis-blocked micronucleus assay. Experimental procedures, compound dilutions and doses assayed have been described in previous papers (Dulout and Furnus, 1988;Furnus et al, 1990;Seoane and Dulout, 1994;Seoane and Dulout, 1999;Seoane, 1999;Güerci et al, 2000) RESULTS Irradiation increased the frequency of aneuploid cells with a corresponding decrease of diploid cells, except for the dose of 100 rad (Figure 1). Pulse treatments with different doses of DES also increased the frequency of aneuploid cells in relation with the dose employed but not with the duration of the treatment.…”

Section: Introductionmentioning

confidence: 85%

“…Chromosome counting reliability and usefulness was demostrated by Dulout and Natarajan (1987). The aneugenic ability of the synthetic estrogen diethylstilbestrol (DES), acetaldehyde, propionaldehyde, chloral hydrate, cadmium chloride, cadmium sulfate, potassium dichromate and cacodilic acid has been evaluated by employing this assay (Dulout and Natarajan, 1987;Dulout and Furnus, 1988;Furnus et al, 1990, Güerci et al, 2000. Anaphase-telophase analysis was employed to test the aneugenic ability of propionaldehyde, cadmium chloride, cadmium sulfate, potassium dichromate, chromium chloride (III), nickel chloride and nickel sulfate (Seoane and Dulout, 1994;Seoane, 1999).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms involved in the induction of aneuploidy: the significance of chromosome loss

2000

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The induction of aneuploidy by physical and chemical agents using different test systems was evaluated. The effect of X-rays, caffeine, acetaldehyde, ethanol, diethylstilbestrol, propionaldehyde, and chloral hydrate was studied by chromosome counting in Chinese hamster embryonic diploid cells. Aneugenic ability of cadmium chloride, cadmium sulfate, potassium dichromate, chromium chloride, nickel chloride, and nickel sulfate was assessed by means of anaphase-telophase analysis in Chinese hamster ovary cells. Chromosome counting in human fibroblasts (MRC-5 cell line) was employed to evaluate the effect of cacodilic acid, cadmium chloride, cadmium sulfate, and potassium dichromate. Finally, the induction of kinetochore-positive and kinetochore negative micronuclei by cadmium chloride, cadmium sulfate, potassium dichromate, chromium chloride, and nickel chloride was studied using CREST antibodies. When the effect of different agents was determined by chromosome counting, an increase of hypoploid but not of hyperploid cells was observed. Anaphase-telophase analysis showed that metal salts increased the frequency of lagging chromosomes. This finding has been confirmed by the increment of kinetochore-positive micronuclei using CREST antibodies. Therefore, chromosome loss could be considered as the main cause of induced aneuploidy.
A indução de aneuploidia por agentes físicos e químicos usando diferentes sistemas de teste foi avaliada. O efeito de raios-X, cafeína, acetaldeído, etanol, dietilestilbestrol, propionaldeído e hidrato de cloral foi estudado por contagem cromossômica em células diplóides embriônicas de hamster chinês. A habilidade aneugênica de cloreto de cádmio, sulfato de cádmio, dicromato de potássio, cloreto de crômio, cloreto de níquel e sulfato de níquel foi avaliada por meio de análise de anáfase-telófase em células de ovário de hamster chinês. A contagem cromossômica em fibroblastos humanos (linhagem celular MRC-5) foi empregada para avaliar o efeito de ácido cacodílico, cloreto de cádmio, sulfato de cádmio e dicromato de potássio. Finalmente, a indução de micronúcleos positivos e negativos para cinetocoro por cloreto de cádmio, sulfato de cádmio, dicromato de potássio, cloreto de crômio e cloreto de níquel foi estudada usando anticorpos CREST. Quando o efeito de agentes diferentes foi determinado por contagem cromossômica, observou-se um aumento de células hipoplóides mas não de hiperplóides. A análise anáfase-telófase mostrou que sais metálicos aumentaram a freqüência de cromossomos "lagging". Este achado foi confirmado pelo aumento de micronúcleos positivos para cinetocoro usando anticorpos CREST. Portanto, a perda cromossômica poderia ser considerada a principal causa de aneuploidia induzida

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“…This also explains the mitotic arrest in human lymphocytes (Kligerman et al 2003(Kligerman et al , 2005, V79 cells (Eguchi et al 1997) or A431 cells (Naranmandura et al 2007 a) caused by methylarsonic acid, dimethylarsinous acid, dimethylarsinic acid, dimethylthioarsinic acid and trimethylarsine oxide. Hypoploidy or hyperploidy in MRC-5 cells were induced at 12.5 µM dimethylarsinic acid and above (Güerci et al 2000). Dimethylarsinic acid and trimethylarsine oxide, but not methylarsonic acid, caused tetraploids in V79 cells (Eguchi et al 1997).…”

Section: In Vitromentioning

confidence: 93%

Methylarsenic compounds [MAK Value Documentation, 2014]

Hartwig

2018

The MAK‐Collection for Occupational Health and Safety

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The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has evaluated methylarsenic compounds considering all toxicological endpoints. Available publications and unpublished study reports are described in detail. Methylarsenic compounds are the carcinogenic metabolites of arsenic and its inorganic compounds, which are proven human carcinogens. Methylated arsenic compounds are able to interfere with all important cellular processes. In mice and rats, dimethylarsinic acid was clearly carcinogenic. Trimethylarsine oxide caused liver adenomas in F344 rats and with methylarsenic acid, preneoplastic liver effects were found. If all aspects are considered, methylarsenic compounds are classified in Carcinogen Category 1. Methylarsenic compounds are genotoxic in vitro and in vivo. As they are bioavailable and can reach the germ cells, they are classified in Category 3 A for Germ Cell Mutagens. Methylarsenic compounds are genotoxic carcinogens, for which no safe systemic exposure can be estimated. It must be assumed that even small amounts absorbed percutaneously increase the carcinogenic risk. Therefore, methylarsenic compounds are designated with an “H” (for substances that can be absorbed through the skin in toxicologically relevant amounts). Dimethylarsinic acid induced developmental toxicity in rats. Apart from a well‐documented case report, there are no clear findings available to conclude a skin‐sensitizing potential in humans.

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Aneugenic effects of some metal compounds assessed by chromosome counting in MRC-5 human cells

Cited by 30 publications

References 37 publications

Malsegregation as a possible mechanism of aneuploidy induction by metal salts in MRC‐5 human cells

Malsegregation as a possible mechanism of aneuploidy induction by metal salts in MRC‐5 human cells

Mechanisms involved in the induction of aneuploidy: the significance of chromosome loss

Methylarsenic compounds [MAK Value Documentation, 2014]

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