Environmental radiation on large Japanese field mice in Fukushima reduced colony forming potential in hematopoietic progenitor cells without inducing genomic instability

To study the environmental radiation effects of wild animals after the Fukushima Dai-ichi nuclear power plant accident, we assessed effects on hematopoietic progenitor cells (HPCs) in large Japanese field mice (Apodemus speciosus). A. speciosus were collected from three contaminated sites and control area. The air dose-rates at the control and contaminated areas were 0.96 ± 0.05 μGy/d (Hirosaki), 14.4 ± 2.4 μGy/d (Tanashio), 208.8 ± 31.2 μGy/d (Ide), 470.4 ± 93.6 μGy/d (Omaru), respectively. We investigated possible DNA damage and pro-inflammatory markers in the bone marrow (BM) cells. The colony-forming potential of BM cells was estimated by the number of HPC colony-forming cells. Radiation-induced genomic instability (RIGI) in HPCs was also analyzed by quantifying delayed DNA damage in CFU-GM clones. Although no significant differences in DNA damage and inflammation markers in BM cells from control and contaminated areas, the number of HPC colonies exhibited an inverse correlation with air dose-rate. With regard to RIGI, no significant differences in DNA damage of CFU-GM clones between the mice from the control and the three contaminated areas. Our study suggests that low dose-rate radiation of more than 200 Gy/d reduced HPCs, possibly eliminating genomically unstable HPCs.

为研究福岛第一核电站事故后野生动物所受的环境辐射效应，本研究评估了辐射对日本大林姬鼠（Apodemus speciosus）造血祖细胞（hematopoietic progenitor cells，HPCs）的影响。研究团队从三处污染区域与一处对照区域捕获了日本大林姬鼠。对照区域及各污染区域的空气剂量率分别为：弘前（Hirosaki）0.96±0.05 μGy/d、田名塩（Tanashio）14.4±2.4 μGy/d、井出（Ide）208.8±31.2 μGy/d、大丸（Omaru）470.4±93.6 μGy/d。我们对骨髓（bone marrow，BM）细胞中的潜在DNA损伤与促炎性标志物展开了检测；通过计数造血祖细胞集落形成细胞的数量，评估骨髓细胞的集落形成能力；此外还通过量化CFU-GM集落中的延迟性DNA损伤，分析了造血祖细胞的辐射诱导基因组不稳定性（radiation-induced genomic instability，RIGI）。尽管对照区域与污染区域小鼠的骨髓细胞中，DNA损伤与炎症标志物均未呈现显著差异，但造血祖细胞集落数量与空气剂量率呈负相关关系。关于辐射诱导基因组不稳定性，对照区域与三处污染区域小鼠的CFU-GM集落的DNA损伤水平未出现显著差异。本研究表明，剂量率高于200 μGy/d的低剂量率辐射会减少造血祖细胞数量，其潜在机制可能为清除基因组不稳定的造血祖细胞。