Abstract
We have been investigating the cellular adaptive response of hprt mutation in normal human fibroblasts induced by the pre-treatment of low dose (rate) radiations, such as 137Cs gamma rays or 241Am-Be neutrons. Cells were pre-treated with the priming dose (1mGy/8h) of either 137Cs gamma ray or 241Am-Be neutron, following irradiation with the challenging dose (1.5Gy) of 200 kV X rays. For mutation induction at hprt locus detected as 6-thioguanine resistant clones, X-ray-induced mutation frequency in cells pre-treated with 1mGy of 137Cs gamma rays was reduced to around 70% in control cells irradiated with X-ray challenging dose alone. In cells pre-treated with 1 mGy of neutrons derived from 241Am-Be source, it was reduced to around 15%, comparing to the control cells. However, reduced X-ray-induced mutation frequency in cells pre-treated with low-dose neutrons was returned to the control level, when using a specific inhibitor of gap-junction mediated cell-cell communication (40 µM lindane). Furthermore, cells pre-treated with low-fluence proton microbeams accelerated with the Single Particle Irradiation system to Cell (SPICE) were suppressed X-ray-induced mutation induction, assuming that recoiled protons might be responsible to the interaction between fast neutrons and tissue (cells). These results suggest that a possible mechanism of neutron- induced adaptive response is a bystander effect via gap-junction mediated cell-cell communication. As reported at the last year's meeting, X-ray induced mutation frequency was enhanced around 4.0 times higher in carbon-ion pre-treated cells and 1.9 times higher in helium-ion pre-treated cells than that in control cells. There is evidence that radiation-induced adaptive responses depend on radiation quality of giving priming doses.
