Genotoxic activity of potassium permanganate in acidic solutions

Méo, Michel De; Laget, M.; Castegnaro, M.; Duménil, Gérard

doi:10.1016/0165-1218(91)90038-n

Cited by 91 publications

(38 citation statements)

References 15 publications

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“…Our results were comparable, indicating that healthy persons use the same repair mechanism, no matter if they are professionally exposed to ionising radiation or not. High standard deviation, also seen in the results of other author (DeMeo et al, 1991;Maluf et al, 2001;Maluf, 2004;Tice, 1995), implicated on the influence of interindividual differences. Since the comet assay measures primary DNA damage after the exposure, those results can be a marker of different gene activity.…”

Section: Discussionsupporting

confidence: 69%

The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation

Milić¹,

Rozgaj²,

Kašuba³

et al. 2011

Selected Topics in DNA Repair

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Section: Discussionsupporting

confidence: 69%

The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation

Milić¹,

Rozgaj²,

Kašuba³

et al. 2011

Selected Topics in DNA Repair

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“…The alkaline Comet assay was performed as described previously [Singh et al, 1988;De Meo et al, 1991]. Briefly, 20 ll of blood were mixed with 1 ml of RPMI supplemented with 10% fetal calf serum (FCS) and 2 mM L-glutamate.…”

Section: Alkaline Comet Assaymentioning

confidence: 99%

Assessment of occupational exposure to welding fumes by inductively coupled plasma‐mass spectroscopy and by the alkaline Comet assay

Botta¹,

Iarmarcovai²,

Chaspoul³

et al. 2006

Environ and Mol Mutagen

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Welding fumes are classified as possibly carcinogenic to humans (Group 2B) by the International Agency for Research on Cancer. In the current study, blood and urine concentrations of aluminum (Al), cadmium (Cd), cobalt (Co), chromium (Cr), manganese (Mn), nickel (Ni), lead (Pb), and zinc (Zn) were monitored by inductively coupled plasma-mass spectrometry (ICP-MS) in 30 welders and in 22 controls. In addition, DNA damage was examined in the lymphocytes of these subjects by the alkaline Comet assay. Two biological samples were taken from the welders at the beginning (BW) and at the end (EW) of a work week. In controls, collection of samples was limited to BW. Blood concentrations of Cd, Co, Cr, Ni, and Pb were higher in the welders than in the control group while higher concentrations of Al, Cd, Co, Cr, Ni, and Pb were detected in welder urines.There was no significant difference in the metal concentrations for the BW and EW welder samples. Increased levels of DNA damage were found in lymphocytes from welders as compared to the controls, and 20/30 welders had higher levels of DNA lesions in the EW than in the BW samples. Age had a significant effect on DNA damage in the control group. Spearman's rank correlation analysis indicated that there were positive correlations between blood concentrations of Al, Co, Ni, and Pb and the levels of DNA damage. A negative correlation was found between DNA damage and Mn in blood, while there was a positive correlation between urinary Mn concentration and DNA damage. These data indicate that occupational exposure to welding fumes increases DNA damage in lymphocytes. Environ. Mol. Mutagen. 47:284-295, 2006. V V C 2006 Wiley-Liss, Inc.

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“…Cells for comet analysis were exposed to the indicated drug concentrations at 37°C in the dark and analyzed immediately according to previously published procedures (21,23,42). Image analysis was performed by using Komet 5.5 software (Kinetic Imaging, Nottingham, U.K.).…”

Section: Methodsmentioning

confidence: 99%

Replication and homologous recombination repair regulate DNA double-strand break formation by the antitumor alkylator ecteinascidin 743

Soares

Escargueil

Poindessous

et al. 2007

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

144

111

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Adducts induced by the antitumor alkylator ecteinascidin 743 (ET-743, Yondelis, trabectedin) represent a unique challenge to the DNA repair machinery because no pathway examined to date is able to remove the ET adducts, whereas cells deficient in nucleotide excision repair show increased resistance. We here describe the processing of the initial ET adducts into cytotoxic lesions and characterize the influence of cellular repair pathways on this process. Our findings show that exposure of proliferating mammalian cells to pharmacologically relevant concentrations of ET-743 is accompanied by rapid formation of DNA double-strand breaks (DSBs), as shown by the neutral comet assay and induction of focalized phosphorylated H2AX. The ET adducts are stable and can be converted into DSBs hours after the drug has been removed. Loss of homologous recombination repair has no influence on the initial levels of DSBs but is associated with the persistence of unrepaired DSBs after ET-743 is removed, resulting in extensive chromosomal abnormalities and pronounced sensitivity to the drug. In comparison, loss of nonhomologous end-joining had only modest effect on the sensitivity. The identification of DSB formation as a key step in the processing of ET-743 lesions represents a novel mechanism of action for the drug that is in agreement with its unusual potency. Because loss of repair proteins is common in human tumors, expression levels of selected repair factors may be useful in identifying patients particularly likely to benefit, or not, from treatment with ET-743.cancer therapy ͉ natural products ͉ lesion processing ͉ DNA repair ͉ response prediction

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Genotoxic activity of potassium permanganate in acidic solutions

Cited by 91 publications

References 15 publications

The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation

The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation

Assessment of occupational exposure to welding fumes by inductively coupled plasma‐mass spectroscopy and by the alkaline Comet assay

Replication and homologous recombination repair regulate DNA double-strand break formation by the antitumor alkylator ecteinascidin 743

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