期刊
BRITISH JOURNAL OF CANCER
卷 108, 期 1, 页码 91-98出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/bjc.2012.498
关键词
radiation; bystander effect; COX-2; transforming growth factor-beta; lung
类别
资金
- National Institutes of Health [CA 49062, ES 12888]
- NIH Resource Centre [RR 11623]
- NIH Environmental Center [ES 09089]
- Grants-in-Aid for Scientific Research [22241016] Funding Source: KAKEN
Background: Although radiation-induced bystander effects have been confirmed using a variety of endpoints, the mechanism(s) underlying these effects are not well understood, especially for in vivo study. Methods: A 1-cm(2) area (1cm x 1 cm) in the lower abdominal region of gpt delta transgenic mice was irradiated with 5Gy of 300 keV X-rays, and changes in out-of-field lung and liver were observed. Results: Compared with sham-treated controls, the Spi(-) mutation frequency increased 2.4-fold in non-targeted lung tissues at 24 h after partial body irradiation (PBIR). Consistent with dramatic Cyclooxygenase 2 (COX-2) induction in the non-targeted bronchial epithelial cells, increasing levels of prostaglandin, together with 8-hydroxydeoxyguanosine, in the out-of-field lung tissues were observed after PBIR. In addition, DNA double-strand breaks and apoptosis were induced in bystander lung tissues after PBIR. Conclusion: The PBIR induces DNA damage and mutagenesis in non-targeted lung tissues, especially in bronchial epithelial cells, and COX-2 has an essential role in bystander mutagenesis.
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