Principles and practice of DNA filter elution

Kohn, Kurt W.

doi:10.1016/0163-7258(91)90022-e

Cited by 148 publications

(97 citation statements)

References 76 publications

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“…ONOO Ϫ can also cause OHdG lesions through the formation of ⅐OH-like intermediates (Coddington et al, 1998). OHdG-DNA and ssDNA lesions in injured MNs could be related, because OH-DNA adducts can lead to abasic sites that are converted to DNA single-strand breaks (Kohn, 1991). The formation of ssDNA in preapoptotic MNs is consistent with a p53-dependent, Fas-regulated cell death mechanism.…”

Section: Onoosupporting

confidence: 49%

Adult Motor Neuron Apoptosis Is Mediated by Nitric Oxide and Fas Death Receptor Linked by DNA Damage and p53 Activation

Martin¹,

Chen²,

Liu³

2005

J. Neurosci.

137

163

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Section: Onoosupporting

confidence: 49%

Adult Motor Neuron Apoptosis Is Mediated by Nitric Oxide and Fas Death Receptor Linked by DNA Damage and p53 Activation

Martin¹,

Chen²,

Liu³

2005

J. Neurosci.

137

163

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“…Analysis of drug-induced DNA strand breaks was performed using the filter alkaline elution technique (Kohn, 1991) as already described (Montaudon et al, 1997). The cells were labelled with [methyl-3 H]thymidine (0.1 mCi ml -1 medium, Amersham Pharmacia Biotech), then treated with different drug concentrations for 2 h at 37˚C.…”

Section: Evaluation Of Dna Damage In C6 Cellsmentioning

confidence: 99%

Effects of the combination of camptothecin and doxorubicin or etoposide on rat glioma cells and camptothecin-resistant variants

et al. 2001

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Summary From the rat C6 glioma cell line in culture, we selected camptothecin-resistant variants by growth in the presence of increasing amounts of this drug (C6 CPT10 , C6 CPT50 and C6 CPT100 , growing respectively with 10, 50 and 100 ng ml -1 camptothecin). The degree of resistance to camptothecin ranged between 15-fold (C6 CPT10 ) and 30-fold (C6 CPT50 and C6 CPT100 ). The C6 CPT10 cell line presented a collateral sensitivity to etoposide (3.6-fold), while the C6 CPT50 and C6 CPT100 cell lines were cross-resistant to etoposide (1.8-fold) The resistant lines were characterised by a two-fold reduced content and catalytic activity of topoisomerase I, and C6 CPT50 and C6 CPT100 presented a significant increase in topoisomerase IIα content and catalytic activity and a marked overexpression of P-glycoprotein. We explored the cytotoxicity of combinations of a topoisomerase I inhibitor (camptothecin) and a topoisomerase II inhibitor (doxorubicin or etoposide) at several molar ratios, allowing the evaluation of their synergistic or antagonistic effects on cell survival using the median effect principle. The simultaneous combination of camptothecin and doxorubicin or etoposide was additive or antagonistic in C6 cells, slightly synergistic in the C6 CPT10 line and never more than additive in the C6 CPT50 and C6 CPT100 cell lines. The sequential combination of doxorubicin and camptothecin gave additivity in the order camptothecin → doxorubicin and antagonism in the order doxorubicin → camptothecin. Clinical protocols combining a topoisomerase I and a topoisomerase II inhibitor should be considered with caution because antagonistic effects have been observed with combinations of camptothecin and doxorubicin.

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“…micronuclei, mutations, structural chromosomal aberrations) that result from DNA damage, have been used to identify substances with genotoxic activity. This includes the most frequently used methods either the detection of DNA repair synthesis (unscheduled DNA synthesis or UDS) in individual cells, or the detection of DNA single strand breaks and alkaline labile sites in pooled cell populations using the alkaline elution assay (Kohn, 1991). A more practical and useful approach for assessing DNA damage is the single cell gel electrophoresis (SCGE) or the Comet assay (Singh et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the cytotoxic and genotoxic effects of goniothalamin in leukemic cell lines

Rajab

Hamid

Hassan

et al. 2005

Environ. Mutagen Res.

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The cytotoxic and genotoxic effects of goniothalamin, a plant styryllactone, were evaluated using the 3-(4,5 -dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and the Alkaline Comet assay respectively in human leukemic cell lines. Following 72 h of treatment, the IC 50 values of goniothalamin in human HL-60 promyelocytic leukemia cells and CEM-SS T-lymphoblastic cells were 4.5 µg/mL and 2.4 µg/mL respectively. The genotoxicity of goniothalamin in both HL-60 and CEM-SS cells was detected as early as 2 h following treatment at IC 10 and IC 25 concentrations. However, pretreatment with the antioxidant N-acetyl-cysteine (NAC) at 1 mM for 30 minutes did not abrogate genotoxicity of this compound. This result suggests that primary induction of DNA damage by goniothalamin may not involve oxidative damage. In conclusion, our results demonstrate genotoxic damage induced by goniothalamin in leukemic cells. Further studies are needed to ascertain the mode of action of goniothalamin in inducing DNA damage.

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Principles and practice of DNA filter elution

Cited by 148 publications

References 76 publications

Adult Motor Neuron Apoptosis Is Mediated by Nitric Oxide and Fas Death Receptor Linked by DNA Damage and p53 Activation

Adult Motor Neuron Apoptosis Is Mediated by Nitric Oxide and Fas Death Receptor Linked by DNA Damage and p53 Activation

Effects of the combination of camptothecin and doxorubicin or etoposide on rat glioma cells and camptothecin-resistant variants

Evaluation of the cytotoxic and genotoxic effects of goniothalamin in leukemic cell lines

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