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

Seoane, Analía Isabel; Dulout, Fernando Noel

doi:10.1016/s1383-5718(00)00145-5

Cited by 105 publications

(46 citation statements)

References 52 publications

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“…Swierenga and Basrur (1968) and Anderson (1985) reported the spindle-inhibiting effect of Ni compounds and suggested that aneuploidy might be induced. Seoane and Dulout (2001) studied the aneugenic and clastogenic ability of a serie of metals including Ni chloride (II) and Ni sulfate (II) by using the kinetochore-stained micronucleus test in human diploid fibroblasts (MRC-5). Ni salts induced a weak but significant increase in micronuclei frequency.…”

Section: Chromosomal Alterationsmentioning

confidence: 99%

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Publication¹

2015

EFS2

119

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EFSA received a request from the Hellenic Food Authority (EFET) for a scientific opinion on the risk to human health from the presence of nickel (Ni) in food, particularly in vegetables. The EFSA Panel on Contaminants in the Food Chain (CONTAM Panel) decided to extend the risk assessment also to drinking water. The reproductive and developmental toxicity in experimental animals was selected as the critical effect for the assessment of chronic effects of Ni. A tolerable daily intake of 2.8 µg Ni/kg body weight (b.w.) per day was derived from a lower 95 % confidence limit for a benchmark dose at 10 % extra risk (BMDL 10 ) of 0.28 mg/kg b.w. for post-implantation fetal loss in rats. The current dietary exposure to Ni raises concern when considering the mean and 95th percentile chronic exposure levels for all different age groups. The systemic contact dermatitis (SCD) elicited in Ni-sensitive humans after oral exposure to Ni was selected as the critical effect suitable for the assessment of acute effects of Ni. A lowest BMDL 10 of 1.1 µg Ni/kg b.w. was derived for the incidence of SCD following oral exposure to Ni of human volunteers. The CONTAM Panel applied a margin of exposure (MOE) approach and considered an MOE of 10 to be indicative of a low health concern. The MOEs calculated considering the estimated mean and the 95th percentile acute exposure levels were considerably below 10 for all age groups. Overall, the CONTAM Panel concluded that, at the current levels of acute dietary exposure to Ni, there is a concern that Ni-sensitized individuals may develop eczematous flare-up skin reactions. The CONTAM Panel noted the need for mechanistic studies to assess the human relevance of the effects on reproduction and development observed in experimental animals and for additional studies on human absorption of nickel from food, for example in combination with duplicate diet studies. Following a call for data on Ni levels in food and drinking water (water intended for human consumption and mineral waters), a total of 18 885 food samples and 25 700 drinking water samples were available in the final dataset to estimate dietary exposure to nickel. No speciation data were provided. Samples were collected between 2003 and 2012 in 15 different European countries, with almost 80 % of the total collected in one Member State. The most reported analytical methods were inductively coupled plasma-mass spectrometry (ICP-MS) and atomic absorption spectrometry (AAS), that represented 54 % and 42 % of the methods reported, respectively. The highest sensitivity was reported for the analysis of drinking water with a limit of quantification (LOQ) of 0.001 µg/L (for both ICP-MS and AAS). In food, ICP-MS showed the lowest LOQ for the analysis of 'Alcoholic beverages' (0.002 µg/kg) while the lowest LOQ reported with AAS was 1 µg/kg for samples of 'Fish and seafood' and 'Sugar and confectionery'. In the final dataset, left-censored data represented 66 % of the analytical results, with 35 % in food samples and 89 % in drinking water sa...

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Section: Chromosomal Alterationsmentioning

confidence: 99%

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Publication¹

2015

EFS2

119

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“…In the short term Cr(VI) causes both aneugenic and clastogenic damage (Sugden and Stearns, 2000;Seone and Dulout, 2001). It causes double and single DNA strand breaks, Cr-DNA base/ phosphate adducts, base oxidation, abasic sites, proteinCr-DNA crosslinks, and DNA-Cr-DNA interstrand crosslinks (see O'Brien et al, 2003;Ha et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…It causes double and single DNA strand breaks, Cr-DNA base/ phosphate adducts, base oxidation, abasic sites, proteinCr-DNA crosslinks, and DNA-Cr-DNA interstrand crosslinks (see O'Brien et al, 2003;Ha et al, 2004). It can induce aneuploidy (Seone and Dulout, 2001). V(V) has a different toxicity.…”

Section: Introductionmentioning

confidence: 99%

Effects of hTERT on metal ion-induced genomic instability

et al. 2006

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There is currently a great interest in delayed chromosomal and other damaging effects of low-dose exposure to a variety of pollutants which appear collectively to act through induction of stress-response pathways related to oxidative stress and ageing. These have been studied mostly in the radiation field but evidence is accumulating that the mechanisms can also be triggered by chemicals, especially heavy metals. Humans are exposed to metals, including chromium (Cr) (VI) and vanadium (V) (V), from the environment, industry and surgical implants. Thus, the impact of low-dose stress responses may be larger than expected from individual toxicity projections. In this study, a short (24 h) exposure of human fibroblasts to low doses of Cr (VI) and V (V) caused both acute chromosome damage and genomic instability in the progeny of exposed cells for at least 30 days after exposure. Acutely, Cr (VI) caused chromatid breaks without aneuploidy while V (V) caused aneuploidy without chromatid breaks. The longerterm genomic instability was similar but depended on hTERT positivity. In telomerase-negative hTERTÀ cells, Cr (VI) and V (V) caused a long lasting and transmissible induction of dicentric chromosomes, nucleoplasmic bridges, micronuclei and aneuploidy. There was also a long term and transmissible reduction of clonogenic survival, with an increased b-galactosidase staining and apoptosis. This instability was not present in telomerasepositive hTERT þ cells. In contrast, in hTERT þ cells the metals caused a persistent induction of tetraploidy, which was not noted in hTERTÀ cells. The growth and survival of both metal-exposed hTERT þ and hTERTÀ cells differed if they were cultured at subconfluent levels or plated out as colonies. Genomic instability is considered to be a driving force towards cancer. This study suggests that the type of genomic instability in human cells may depend critically on whether they are telomerase-positive or -negative and that their sensitivities to metals could depend on whether they are clustered or diffuse.

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“…However, Cr + ³ compounds such as chromium chloride (CrCl 3 ) can be genotoxic in vitro leading to induction of micronuclei (MN) in human fibroblasts, according to study by Seoane and Dulout (2001). In a similar study with tannery workers exposed to Cr + ³, Meibian et al (2008) demonstrated that this metal can cause DNA damage to human lymphocytes.…”

Section: Mutagenicmentioning

confidence: 99%

Evaluation of mutagenic effects of pure hydroxyapatite doped with chromium (III) through the SMART Test in Drosophila melanogaster Meigen, 1830 (Diptera: Drosophilidae)

Pantaleão¹,

Santos²,

Anjos³

et al. 2017

Braz. J. Biol. Sci.

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Abstract. Hydroxyapatite (HAP) is a bioceramic used in the medical and dental areas as a bone replacement factor due to its chemical similarity to the mineral phase of bones and teeth. Its use in implants stimulate the growth of bone tissue, showing no toxicity or rejection of the host tissue. Its nanostructured form has been shown to be a viable alternative for photoprotection when doped with metal ions, such as trivalent chromium (Cr + ³). Due to the reach of this form among the population, this work evaluated the mutagenic potential of pure nanostructured hydroxyapatite (HAP) and doped with trivalent chromium (Cr + ³) (HCrIII) by means of the Somatic Mutation and Recombination Test (SMART Test) on Drosophila melanogaster Meigen, 1830 (Diptera: Drosophilidae) wings. Larvae resulting from standard crosses (ST) and high metabolic bioactivation (HB), treated with PAH and with HCrIII at concentrations 16.66 mg/mL, 8.33 mg/mL, and 4.16 mg/mL. As positive and negative controls, urethane and dodecyl sulfate sodium (SDS) were used, respectively. The frequencies of the different categories of mutant spots observed in offspring of HAP (HAP) and HCrIII treated crosses were not significantly different from those observed in the negative control. These data show that pure and chromium-doped (Cr + ³) nanoestructured hydroxyapatite do not exhibit mutagenicity. Keywords

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

Cited by 105 publications

References 52 publications

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Effects of hTERT on metal ion-induced genomic instability

Evaluation of mutagenic effects of pure hydroxyapatite doped with chromium (III) through the SMART Test in Drosophila melanogaster Meigen, 1830 (Diptera: Drosophilidae)

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