Abstract
Low-dose rate (DR) irradiation to mammalian cells elicits a unique cellular response even if the lethal impact could be negligible. In particular, the double strand break (DSB)-inducible endpoints, including somatic mutation, genetic recombination and chromosomal translocation, have been characterized by responsive curves that their frequency shows a limited decline or an increase (inverse effect) as DR is diminished. To search factors specific for such responses, the behavior of human DSB-interactive proteins as candidates was assessed by an in vitro assay system. We found that that continuous low-DR irradiation of γ-ray to lymphoblastoid cells introduces several changes into the aggregative profile of nucleoproteins on DNAs with ends, in contrast with the unchangeable pattern of DNA-dependent protein kinase components. Notably, this alteration appears to maintain over several decades of cell division without detectable changes of major proteins. A critical range of low-DR radiation may provide a state compatible with proliferation, in which the structure and the activity of aggregative proteins might be modified in an epigenetic manner.
