دورية أكاديمية
أعرض في EDS

X-ray-induced bystander responses reduce spontaneous mutations in V79 cells.

التفاصيل البيبلوغرافية
العنوان: X-ray-induced bystander responses reduce spontaneous mutations in V79 cells.
المؤلفون: Maeda M; Proton Medical Research Group, Research and Development Department, The Wakasa Wan Energy Research Center, 64-52-1 Nagatani, Tsuruga-shi, Fukui 914-0192, Japan., Kobayashi K, Matsumoto H, Usami N, Tomita M
المصدر: Journal of radiation research [J Radiat Res] 2013 Nov 01; Vol. 54 (6), pp. 1043-9. Date of Electronic Publication: 2013 May 09.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 0376611 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1349-9157 (Electronic) Linking ISSN: 04493060 NLM ISO Abbreviation: J Radiat Res Subsets: MEDLINE
أسماء مطبوعة: Publication: July 2012- : Oxford : Oxford University Press
Original Publication: Tokyo : Japan Radiation Research Society
مواضيع طبية MeSH: Bystander Effect/*physiology , Bystander Effect/*radiation effects , Chromosome Aberrations/*radiation effects , Fibroblasts/*physiology , Mutation/*genetics , Nitric Oxide/*metabolism, Animals ; Apoptosis/genetics ; Apoptosis/radiation effects ; Cell Line ; Cricetinae ; Cricetulus ; Fibroblasts/radiation effects ; Mutation/radiation effects ; Radiation Dosage
مستخلص: The potential for carcinogenic risks is increased by radiation-induced bystander responses; these responses are the biological effects in unirradiated cells that receive signals from the neighboring irradiated cells. Bystander responses have attracted attention in modern radiobiology because they are characterized by non-linear responses to low-dose radiation. We used a synchrotron X-ray microbeam irradiation system developed at the Photon Factory, High Energy Accelerator Research Organization, KEK, and showed that nitric oxide (NO)-mediated bystander cell death increased biphasically in a dose-dependent manner. Here, we irradiated five cell nuclei using 10 × 10 µm(2) 5.35 keV X-ray beams and then measured the mutation frequency at the hypoxanthine-guanosine phosphoribosyl transferase (HPRT) locus in bystander cells. The mutation frequency with the null radiation dose was 2.6 × 10(-)(5) (background level), and the frequency decreased to 5.3 × 10(-)(6) with a dose of approximately 1 Gy (absorbed dose in the nucleus of irradiated cells). At high doses, the mutation frequency returned to the background level. A similar biphasic dose-response effect was observed for bystander cell death. Furthermore, we found that incubation with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), a specific scavenger of NO, suppressed not only the biphasic increase in bystander cell death but also the biphasic reduction in mutation frequency of bystander cells. These results indicate that the increase in bystander cell death involves mechanisms that suppress mutagenesis. This study has thus shown that radiation-induced bystander responses could affect processes that protect the cell against naturally occurring alterations such as mutations.
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فهرسة مساهمة: Keywords: cell death; microbeam irradiation; mutation; nitric oxide; radiation-induced bystander responses
المشرفين على المادة: 31C4KY9ESH (Nitric Oxide)
تواريخ الأحداث: Date Created: 20130511 Date Completed: 20140515 Latest Revision: 20211021
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3823787
DOI: 10.1093/jrr/rrt068
PMID: 23660275
قاعدة البيانات: MEDLINE
الوصف
تدمد:1349-9157
DOI:10.1093/jrr/rrt068