- 著者
-
鈴木 啓司
児玉 靖司
渡邉 正己
- 出版者
- 日本環境変異原学会
- 雑誌
- 環境変異原研究 (ISSN:09100865)
- 巻号頁・発行日
- vol.27, no.2, pp.111-115, 2005-07-31
Ionizing radiation induces genomic instability, which is transmitted through many generations after irradiation in the progeny of surviving cells. We have hypothesized that radiation-induced large deletion causes potentially unstable chromosome regions, which are involved in delayed induction of radiation-induced genomic instability. Using phosphorylation-specific antibodies against ATM and histone H2AX, whose phosphorylation is induced by DNA double strand breaks, we detected delayed induction of phosphorylated ATM and H2AX foci in the progeny of X-ray-surviving cells, which indicated delayed induction of DNA double strand breaks. Furthermore, we found delayed chromosomal instability in X chromosomes in clones which contain large deletion involving the HPRT loci. It is suggested that large deletion involving ~Mb region causes unstable chromatin structure, and it results in delayed rearrangement of chromosomes involved. These findings provide the possibility that manifestation of radiation-induced genomic instability results from delayed DNA breaks, i.e., the breaks lead to delayed chromosome rearrangements, delayed cell death etc., many generations after irradiation.