Single Strand DNA Breaks in Human Lymphocytes Exposed to para-Phenylenediamine and its Derivatives

Chye, Soi M.; Hseu, You Cheng; Liang, Shih Hsiung; Chen, Chin Hui; Chen, Ssu Ching

doi:10.1007/s00128-007-9316-2

Cited by 25 publications

(17 citation statements)

References 17 publications

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“…Also, a significant correlation between visual scoring results and percentage tail DNA was found in measuring the genotoxicity of North Sea marine sediment [34], and in analyzing DNA damage in canine and feline leukocytes [35]. In our previous paper, the comet assay with visual scoring was also applied to detect the genotoxicity of petroleum [18], benzidine and its derivatives [17], and p-phenylenediamine and its derivatives [36]. Nevertheless, it would be advisable for investigator unfamiliar with the comet assay to set up individual calibration curves correlating visual and computer image analysis score so that intra-and interinvestigator variation between comet measurements reduced to a minimum [35].…”

Section: Discussionmentioning

confidence: 96%

Comparative investigations of genotoxic activity of five nitriles in the comet assay and the Ames test

Hseu

Chen

et al. 2009

Journal of Hazardous Materials

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Section: Discussionmentioning

confidence: 96%

Comparative investigations of genotoxic activity of five nitriles in the comet assay and the Ames test

Hseu

Chen

et al. 2009

Journal of Hazardous Materials

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“…ss-DNA breaks can result from a variety of factors including UV light [6], X-rays [7], ionizing radiation[8], toxins [9], chemicals[10], or by reactive oxygen species (oxidative stress) resulting as by-products of normal metabolic processes [11]. DNA breaks are increased in different human cell cultures when exposed to cigarette smoke [12-15].…”

Section: Discussionmentioning

confidence: 99%

Half a pack of cigarettes a day more than doubles DNA breaks in circulating leukocytes

Mozaffarieh¹,

Konieczka²,

Hauenstein³

et al. 2010

Tobacco Induced Diseases

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BackgroundThe mechanisms by which smoking induces damage is not known for all diseases. One mechanism believed to play a role is oxidative stress. Oxidative stress leads to cellular damage including DNA damage, particularly DNA breaks. We conducted this study to test the hypothesis that smokers have increased DNA breaks in their circulating leukocytes.MethodsA comparative quantification of single-stranded DNA breaks was performed by comet assay analysis in the circulating leukocytes of ten healthy smokers (average smoking rate: half a pack a day, range: 9-12 cigarettes a day) and ten age and sex matched healthy non-smokers. DNA breaks lead to smaller pieces of DNA, which migrate out of the nucleus forming a tail during gel-electrophoresis. Damage of an individual cell was quantified by the parameters tail moment and olive moment.ResultsSmoking had a clear effect on both study parameters (tail and olive moment). Smokers had more than double the amount of ss-DNA breaks in their circulating leukocytes than non-smokers [tail moment: 0·75 AU [smokers] compared to 0·2 AU [non-smokers]; olive moment: 0·85 AU [smokers] compared to 0·3 AU [non-smokers]; both p < 0·001].ConclusionSmoking half a pack a day interferes with DNA integrity. One potential explanation for the enhanced DNA breaks in smokers is oxidative stress.

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“…Les études in vitro ont montré que la p-PD, comme plusieurs autres amines aromatiques de la famille des anilines peut réagir avec l'ADN et provoquer des cassures [12]. L'effet génotoxique de la p-PD a été montré dans plusieurs études [13][14][15].…”

Section: Introductionunclassified

“…et Chye et coll. ont éga-lement mis en évidence les propriétés génotoxiques de la p-phénylènediamine et de ses dérivés acétylés [12,16]. Picardo et coll.…”

Section: Introductionunclassified

“…D'autres études ont révélé que la p-PD serait mutagène du fait qu'elle était capable de provoquer des mutations dans le TP53 et par conséquent une augmentation de l'expression et de l'accumulation de la protéine p53 mutée [18]. Il en résulte un dérèglement dans le contrôle du cycle cellulaire aboutissant à une tumeur [11,12]. En effet la p-PD a été associée à plusieurs cancers notamment des leucémies [19][20][21][22][23].…”

Section: Introductionunclassified

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Induction d’apoptose par la p-Phénylènediamine dans un myélome murin

et al. 2011

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Résumé -Objectif : Les mécanismes de toxicité et de génotoxicité induits par la Para-phénylèneDiamine (p-PD), un composant de la teinture pour cheveux suspecté d'être carcinogène, sur des cellules tumorales murines, type P3X63Ag8.653 ont été étudiés. Méthodes : L'effet de la p-PD sur la viabilité et celui sur la prolifération cellulaire ont été évalués par la méthode d'exclusion du bleu de trypan. Son effet sur l'ADN des cellules P3X63Ag8.653 a été analysé après une extraction d'ADN et une électrophorèse sur gel d'agarose puis confirmé par la technique TUNEL en cytométrie en flux. Résultats : Un blocage de la prolifération avec diminution de la viabilité cellulaire ont été observés. La fragmentation de l'ADN dose-dépendante témoignant de l'effet apoptotique a été détectée sur gel d'agarose et confirmée par cytométrie en flux (technique TUNEL). Conclusion : Les résultats obtenus montrent que la p-PD induit in vitro un blocage de la prolifération cellulaire et une apoptose dose-dépendante des cellules tumorales murines.Mots clés : Para-phénylèneDiamine (p-PD), apoptose, cellules tumorales murines, toxicité, teinture capillaire Abstract -Aims: The mechanism of toxicity and genotoxicity of p-Phenylenediamine (p-PD), a component of human permanent hair dye and suspected to be a carcinogen, on the growth of murine tumor cells (P3X63Ag8.653) was investigated. Methods: The effect of p-PD on cell viability and proliferation was evaluated by the trypan blue exclusion method. The effect on the P3X63Ag8.653 cell DNA was analyzed by gel electrophoresis and confirmed by flow cytometry analysis (TUNEL technique). Results: A dose-dependent DNA fragmentation analyzed by gel electrophoresis shows a strong correlation with the flow cytometry analysis (TUNEL technique), suggesting that the effect of p-PD on overall viability and proliferation is mediated by DNA damage and an increase in apoptosis. Conclusion: The results suggest that the effect of p-PD on overall viability and proliferation of murine tumor cells is mediated by DNA damage and an increase in apoptosis in a dose-dependent manner.

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Single Strand DNA Breaks in Human Lymphocytes Exposed to para-Phenylenediamine and its Derivatives

Cited by 25 publications

References 17 publications

Comparative investigations of genotoxic activity of five nitriles in the comet assay and the Ames test

Comparative investigations of genotoxic activity of five nitriles in the comet assay and the Ames test

Half a pack of cigarettes a day more than doubles DNA breaks in circulating leukocytes

Induction d’apoptose par la p-Phénylènediamine dans un myélome murin

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