Human melanoma cells that are resistant to gamma rays were irradiated with 14 MeV neutrons given at low doses ranging from 5 cGy to 1.12 Gy at a very low dose rate of 0.8 mGy min(-1) or a moderate dose rate of 40 mGy min(-1). The biological effects of neutrons were studied by two different methods: a cell survival assay after a 14-day incubation and an analysis of chromosomal aberrations in metaphases collected 20 h after irradiation. Unusual features of the survival curve at very low dose rate were a marked increase in cell killing at 5 cGy followed by a plateau for survival from 10 to 32.5 cGy. The levels of induced chromosomal aberrations showed a similar increase for both dose rates at 7.5 cGy and the existence of a plateau at the very low dose rate from 15 to 30 cGy. The existence of a plateau suggests that a repair process after low-dose neutrons might be induced after a threshold dose of 5-7.5 cGy which compensates for induced damage from doses as high as 32.5 cGy. These findings may be of interest for understanding the relative biological effectiveness of neutrons and the effects of environmental low-dose irradiation.

We recently reported that the exposure of cancer cells to 14 MeV neutrons at a very low dose rate (0.8 mGy min(-1)) produced a marked increase in cell killing at 5 cGy, followed by a plateau in survival and chromosomal damage. Simulation of the energy deposition events in irradiated cells may help to explain these unusual cell responses. We describe here a Monte Carlo simulation code, Energy Deposition in Cells Irradiated by Neutrons (EDCIN). The procedure considered the experimental setup and a hemispheric cell model. The simulation data fitted the dosimetric measurements performed using tissue-equivalent ionization chambers, Geiger-Müller counters, fission chambers, and silicon diodes. The simulation showed that 80% of the energy deposited in a single cell came from the interactions of neutrons outside the cell and only 20% came from neutron interactions inside the cell. Thus the "external" interactions that result in the production of recoil protons and secondary electrons may induce most of the biological damage, which may be repaired efficiently at low dose rate. The repair process may be triggered from a threshold level of damage, which would explain an initial increase cell death due to unrepaired sublethal damage, and then may compensate for induced damage, resulting in the plateaus.