Studying the genotoxicity of vincristine on human lymphocytes using comet assay, micronucleus assay and TCR gene mutation test in vitro

Jiang, Wei; Lu, Yezheng; Chen, Zhijian; Chen, Shijie; Zhang, Meibian; Jin, Lei; Jianlin, Lou; He, Jiliang

doi:10.1016/j.tox.2008.07.057

Cited by 21 publications

(11 citation statements)

References 25 publications

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“…Correlating the medicines’ and the markers’ frequency, we cannot rule out an influence of the pharmacological treatment to which subjects were exposed at the clinic on the increase in bud frequency. This finding could be expected, as this marker is associated with gene amplification triggered by cellular toxicity [ 27 , 28 ]. However, some other studies show the influence of the crack withdrawal in abnormal levels of biochemical factors [ 5 , 6 ], which may explain this increase in bud frequency.…”

Section: Resultsmentioning

confidence: 90%

Genomic Instability in Human Lymphocytes from Male Users of Crack Cocaine

Freitas

Palazzo

Andrade

et al. 2014

IJERPH

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Recent research suggests that crack cocaine use alters systemic biochemical markers, like oxidative damage and inflammation markers, but very few studies have assessed the potential effects of crack cocaine at the cellular level. We assessed genome instability by means of the comet assay and the cytokinesis-block micronucleus technique in crack cocaine users at the time of admission to a rehabilitation clinic and at two times after the beginning of withdrawal. Thirty one active users of crack cocaine and forty control subjects were evaluated. Comparison between controls and crack cocaine users at the first analysis showed significant differences in the rates of DNA damage (p = 0.037). The frequency of micronuclei (MN) (p < 0.001) and nuclear buds (NBUDs) (p < 0.001) was increased, but not the frequency of nucleoplasmic bridges (NPBs) (p = 0.089). DNA damage decreased only after the end of treatment (p < 0.001). Micronuclei frequency did not decrease after treatment, and nuclear buds increased substantially. The results of this study reveal the genotoxic and mutagenic effects of crack cocaine use in human lymphocytes and pave the way for further research on cellular responses and the possible consequences of DNA damage, such as induction of irreversible neurological disease and cancer.

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Section: Resultsmentioning

confidence: 90%

Genomic Instability in Human Lymphocytes from Male Users of Crack Cocaine

Freitas

Palazzo

Andrade

et al. 2014

IJERPH

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“…Previous studies have shown that Vinca alkaloids have the potential to induce genotoxic effects in different biological systems. The VCR and VBL have been shown to increase the frequency of micronuclei in experimental animals and in cultured human lymphocytes [ 10 - 13 ]. In addition, they have also been shown to cause chromosomal mutations in vivo and in cultured cancer cells [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Assessment of genotoxicity of vincristine, vinblastine and vinorelbine in human cultured lymphocytes: a comparative study

Mhaidat

Al-Zoubi

Khabour

et al. 2016

Balkan Journal of Medical Genetics

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Vincristine (VCR), vinblastine (VBL) and vinorelbine (VRL) are anticancer agents from the Vinca alkaloid family that have the potential to induce genotoxic effect. The aim of the present study was to compare the genotoxic effect of VCR, VBL and VRL. Levels of 8-hydroxy-2-deoxy guanosine (8-OHdG) and sister chromatid exchanges (SCEs) were measured in cultured human blood lymphocytes treated with VCR, VBL and VRL at concentrations of 0.01 and 0.1 μg/mL. Results showed that VCR, VBL and VRL significantly increased the 8-OHdG levels (p <0.05), whereas it did not cause a significant increase in the frequencies of SCEs in human blood lymphocytes as compared to controls. On the other hand, all three agents significantly increased cells mitotic index (p <0.05). At both tested concentrations, the magnitude of the increase in 8-OHdG was VBL>VCR>VRL. In conclusion, VCR, VBL and VRL induce DNA damage as indicated by the increase in the 8-OHdG biomarker but with different magnitude.

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“…The better specificity of the p53 genotoxicity assay is illustrated by the results obtained with microtubule poisons (Table 1), that act as anti-mitotic drugs via spindle assembly checkpoint activation [23]. Indeed, we detected no genotoxicity induced by these drugs whereas these molecules had been classified genotoxic in the Comet and micronuclei formation assays [24]. This discrepancy might be explained by the fact that these drugs cause a mitotic arrest in normal cells, which may produce misleading results in assays based on analysis of nuclear structure.…”

Section: Figmentioning

confidence: 60%