Chromosomal changes: induction, detection methods and applicability in human biomonitoring

Mateuca, Raluca; Lombaert, Noömi; Aka, Peter; Decordier, Ilse; Kirsch‐Volders, Micheline

doi:10.1016/j.biochi.2006.07.004

Cited by 298 publications

(209 citation statements)

References 105 publications

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“…Uncorrected merotelic attachments lead to the exclusion of lagging chromosomes from the main nucleus during mitotic exit (21). In such an event, a centromere-positive micronucleus is generated.…”

Section: Resultsmentioning

confidence: 99%

“…When lagging chromosomes persist until mitotic exit, they form micronuclei in the subsequent interphase (20). Aside from spindle defects, faulty repair can generate micronuclei through the loss of centromere sequences (21). To compare micronucleus formation under different conditions, primary MEFs from Dido, Ku80, and ATM mutants were labeled with an antibody to the DSB marker γH2A.X (22), and the frequency of micronuclei was determined (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Centromere-localized breaks indicate the generation of DNA damage by the mitotic spindle

Guerrero

Gamero

Trachana

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Most carcinomas present some form of chromosome instability in combination with spindle defects. Numerical instability is likely caused by spindle aberrations, but the origin of breaks and translocations remains elusive. To determine whether one mechanism can bring about both types of instability, we studied the relationship between DNA damage and spindle defects. Although lacking apparent repair defects, primary Dido mutant cells formed micronuclei containing damaged DNA. The presence of centromeres showed that micronuclei were caused by spindle defects, and cell cycle markers showed that DNA damage was generated during mitosis. Although the micronuclei themselves persisted, the DNA damage within was repaired during S and G2 phases. DNA breaks in Dido mutant cells regularly colocalized with centromeres, which were occasionally distorted. Comparable defects were found in APC mutant cell lines, an independent system for spindle defects. On the basis of these results, we propose a model for break formation in which spindle defects lead to centromere shearing.centrosome | chromosome instability | double-strand break | H2A.X

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Centromere-localized breaks indicate the generation of DNA damage by the mitotic spindle

Guerrero

Gamero

Trachana

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Robertsonian translocations cause structure forms as meta-and submeta-centric chromosomes through centric exchanges of two acrocentrics due to the single strand's breaks in the minor SAT DNA located in the centromeric regions of mice chromosomes. Thus, the rate of exchanges between non-homologous chromosomes in the mouse is particularly high [121].…”

Section: Crb Crb Crb Crbmentioning

confidence: 99%

“…chemicals) [120]. SSB resulting from Pb influence were reported by [101,121]. Chromatide breaks observed in metaphase would result from incomplete or failed repair [106].…”

Section: Crb Crb Crb Crbmentioning

confidence: 99%

Zeolites versus Lead Toxicity

R¹

2015

J Bioequiv Availab

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“…The present study suggests that the mutagenic effect of Ca 3 SiO 5 is clastogenic or aneugenic because these defects are detected by the micronucleus test, but not by the comet assay 29 .…”

Section: Discussionmentioning

confidence: 95%

Evaluation of the genotoxicity and mutagenicity of Ca3SiO5-based cement

et al. 2016

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Ca 3 SiO 5 is new cement based on the composition of Portland that has been developed to have superior physicochemical and biological properties. In a clinical evaluation, the cement did not appear to have cytotoxic properties and allowed for the proliferation of pulp cells and gingival fibroblasts. However, no previous studies have evaluated the genotoxicity or the mutagenicity of Ca 3 SiO 5 in vivo. Therefore, the goal of this study is to evaluate the genotoxic and mutagenic potential of Ca 3 SiO 5 -based cement in vivo. Twenty-four male Wistar rats were divided into 3 groups (n = 8). Group A rats received subcutaneous implantation of Ca 3 SiO 5 in the dorsum. Group B rats received a single dose of cyclophosphamide (positive control). Group C rats received subcutaneous implantation of empty tubes in the dorsum (negative control). After 24 hours, all animals were euthanized and the bone marrow of the femurs was collected for use in the comet assay and the micronucleus test. The comet assay revealed that the Ca 3 SiO 5 group had a tail intensity of 23.57 ± 7.70%, the cyclophosphamide group had a tail intensity of 27.43 ± 7.40%, and the negative control group had a tail intensity of 24.75 ± 5.55%. The average number of micronuclei was 6.25 (standard deviation, SD = 3.53) in the Ca 3 SiO 5 group, 9.75 (SD = 2.49) in the cyclophosphamide group, and 0.75 (SD = 1.03) in the negative control group. There was an increase in the micronuclei frequency in the Ca 3 SiO 5 group compared to that of the negative control group (p < 0.05). Our data showed that exposure to the Ca 3 SiO 5 -based cement resulted in an increase in the frequency of micronuclei, but no genotoxicity was detected according to the comet assay.

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Chromosomal changes: induction, detection methods and applicability in human biomonitoring

Cited by 298 publications

References 105 publications

Centromere-localized breaks indicate the generation of DNA damage by the mitotic spindle

Centromere-localized breaks indicate the generation of DNA damage by the mitotic spindle

Zeolites versus Lead Toxicity

Evaluation of the genotoxicity and mutagenicity of Ca3SiO5-based cement

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