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Cytotoxicity of cigarette smoke condensate is not due to DNA double strand breaks: Comparative studies using radiosensitive mutant and wild-type CHO cells
https://repo.qst.go.jp/records/44931
https://repo.qst.go.jp/records/449313322e5be-e3ba-4083-8f83-ff5687ba7fb5
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2007-08-02 | |||||
タイトル | ||||||
タイトル | Cytotoxicity of cigarette smoke condensate is not due to DNA double strand breaks: Comparative studies using radiosensitive mutant and wild-type CHO cells | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Kato, Takamitsu
× Kato, Takamitsu× Nagasawa, Hatsumi× Warner, Christy× Okayasu, Ryuichi× S., Bedford Joel× 加藤 宝光× 岡安 隆一 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Abstract Purpose: To determine whether cigarette smoke condensate (CSC) without metabolic activation induces direct DNA double strand breaks (DSB) in the G1 phase of various radiosensitive mutants of CHO cells and whether these breaks display collateral hypersensitivity to CSC with respect to cell killing. Materials & methods: We treated the G1- phase cultures of wild-type and DNA repair deficient mutants of CHO cells with various concentrations of CSC and examined the cell survival by colony formation assay and the induction of DNA double strand breaks by constant field gel electrophoresis as well as r-H2AX assay. Results: Gel analysis and r-H2AX focus assay showed significantly fewer, but still detectable levels of DSB per cell after CSC treatment compared to ionizing radiation (IR) exposures, even when equitoxic radiation exposures were delivered at a low dose rate over the same 8 hour exposure used for CSC treatments. None of the three non homologous end joining (NHEJ) deficient mutants were remarkably hypersensitive to CSC compared to wild-type cells. In contrast, UV-1 cells that are hypersensitive to several base damage and cross-linking agents showed a higher sensitivity to CSC compared to the other CHO cell lines. Conclusions: DNA DSB produced directly by CSC are not principally responsible for its cytotoxicity. Further, the present study does not rule out the possibility that some of these lesions may secondarily result in DSB, such as may occur during impeded DNA replication and whose repair may require systems other than NHEJ. |
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書誌情報 |
International Journal of Radiation Biology 巻 83, p. 583-591, 発行日 2007-09 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0955-3002 |