A Comparison of In Vivo Cellular Responses to Cs-137 Gamma Rays And 320-kV X Rays.

Research reported here relates to comparing the relative effectiveness of 320-kV X rays compared to Cs-137 gamma rays for two in vivo endpoints in C.B-17 mice after whole-body exposure: (1) cytotoxicity to bone marrow cells and splenocytes evaluated at 24-hours post exposure and (2) bone marrow and spleen reconstitution deficits (repopulation shortfalls) evaluated at 6 weeks post exposure. We show that cytotoxicity dose-response relationships for bone marrow cells and splenocytes are complex, involving negative curvature (decreasing slope as dose increases), presumably implicating a mixed cell population comprised of large numbers of hypersensitive, modestly radiosensitive, and resistant cells. The radiosensitive cells appear to respond with 50% being killed by a dose < 0.5 Gy. The X-ray relative biological effectiveness (RBE), relative to gamma rays, for destroying bone marrow cells in vivo is > 1, while for destroying splenocytes it is < 1. In contrast, dose-response relationships for reconstitution deficits in the bone marrow and spleen of C.B-17 mice at 6 weeks after radiation exposure were of the threshold type with gamma rays being more effective in causing reconstitution deficit.

Biological microdosimetry based on radiation cytotoxicity data.

Researchers in the field of radiation microdosimetry have attempted to explain the relative biological effectiveness (RBE) of different ionising photon radiation sources on the basis of the singly stochastic, microdose metric lineal energy y, which only addresses physical stochasticity related to energy (ε) deposition via single events in the critical targets (cell nuclei assumed here). Biological stochasticity related to variable nuclei geometries and cell orientations (relative to the incoming radiation) is usually not addressed. Here a doubly stochastic microdose metric, the single-event hit size q (=ε/T), is introduced which allows the track length T to be stochastic. The new metric is used in a plausible model of metabolic-activity-based in vitro cytotoxicity of low-dose ionising photon radiation. The cytotoxicity model has parameters E{q} (average single-event hit size with q assumed to be exponentially distributed) and E{α}, which is the average value of the cellular response parameter α. E{α} is referred to as the biological signature and it is independent of q. Only E{q} is needed for determination of RBE. The model is used to obtain biological-microdosimetry-based q spectra for 320-kV X-rays and (137)Cs gamma rays and the related RBE for cytotoxicity. The spectra are similar to published lineal energy y spectra for 200-kV X-rays and (60)Co gamma rays for 1-µm biological targets.

Small γ-Ray Doses Prevent Rather than Increase Lung Tumors in Mice.

We show evidence for low doses of γ rays preventing spontaneous hyperplastic foci and adenomas in the lungs of mice, presumably via activating natural anticancer defenses. The evidence partly relates to a new study we conducted whereby a small number of female A/J mice received 6 biweekly dose fractions (100 mGy per fraction) of γ rays to the total body which prevented the occurrence of spontaneous hyperplastic foci in the lung. We also analyzed data from a much earlier Oak Ridge National Laboratory study involving more than 10,000 female RFMf/Un mice whereby single γ-ray doses from 100 to 1,000 mGy prevented spontaneous lung adenomas. We point out the possibility that the decrease in lung cancer mortality observed in The National Lung Screening Trial Research Team study involving lung tumor screening using low-dose computed tomography (CT) may relate at least in part to low-dose X-rays activating the body's natural anticancer defenses (i.e., radiation hormesis). This possibility was apparently not recognized by the indicated research team.