Abstract
For estimating a human health risk from low-dose ionizing radiation (IR), an adaptive response, acquiring a cellular radioresistance to the challenging IR by a pre-exposure to low-dose IR, is a concern. Cellular responses after low-dose exposure, a bystander effect and a genetic instability, are also suggested to be related to the adaptive response. It is important to explore the adaptive response in human cultured cells from not only health risk estimation but also DNA repair studies. We succeeded to detect the adaptive response in human lymphoblastoid cells, providing a reduction in the frequency of mutations induced after IR exposure. For better understanding of those genetic results, we need to elucidate the underlying mechanisms. Since the reduced mutation-frequency can be considered as a result of enhanced DNA- repair efficiency, we first examined the possible enhancement in repair efficiency of DNA double strand breaks (DSBs). The DSBs caused by challenging IR are required to be distinguished from those caused by priming low-dose IR. Therefore, instead of the challenging IR, the cells are infected with a restriction-enzyme I-SceI expression vector for introducing a DSB at a specific site of chromosome. In other words, we could obtain information about DSB repair efficiency under the same condition as genetic measurements. An availability of the I-SceI approach will be discussed here.
