A mechanism for the reduced DNA damage in mice irradiated in fetuses and newborns

2015 Fiscal Year Final Research Report

• Project/Area Number: 26550032
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Risk sciences of radiation and chemicals
• Research Institution: Osaka Prefecture University
• Principal Investigator: KODAMA Seiji 大阪府立大学, 理学(系)研究科(研究院), 教授 (00195744)
• Research Collaborator: SAKAGUCHI Kenta 大阪府立大学, 理学系研究科生物科学専攻, 博士後期課程3年 ; KASHIWAGI Hiroki 大阪府立大学, 理学系研究科生物科学専攻, 博士後期課程3年 ; SHIRASAKA Yosuke 大阪府立大学, 理学系研究科生物科学専攻, 博士前期課程2年
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 放射線損傷 / 胎内被ばく / DNA2本鎖切断 / 染色体転座 / 神経幹/前駆細胞

Outline of Final Research Achievements

Fetal irradiation of humans and mice do not induce persistent chromosome translocations in lymphocytes similar to the level after adult irradiation. In the present study, we scored DNA double strand breaks and chromosome translocations in neural stem/progenitor cells of mice at 6 weeks of age and their mothers after they were exposed to 2 Gy of whole-body X-irradiation when the gestation period was 14.5 days. The results indicated that X-ray-induced DNA double strand breaks were not persistent in neural stem/progenitor cells of both offspring and their mothers, resulting in no difference between them. In contrast, the frequency of X-ray-induced chromosome translocations in offspring was significantly lower (p=0.0247, Chi-square with Yates’ correction) than that of mothers in neural stem/progenitor cells in addition to lymphocytes.

Free Research Field

放射線生物学