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Potential adaptations to ionizing radiation at the tissue level: hyperplasia and hyperradiosensitivity

Kolloquium der Abteilung 6

The aim of the presentation is to show two examples how changes in the tissue architecture can modulate the biological effects of ionizing radiation, and shortly discuss their implications on the system of radiation protection.

The first example is the induction of progenitor cell hyperplasia in the bronchial epithelium which decreases the cellular burden upon radon exposure. Considering the spatial heterogeneity of dose distribution in the airways, induction of hyperplasia may provide an explanation for inverse exposure rate effect observed in epidemiology of lung cancer among uranium miners, and supports the conclusion of many different studies that heterogeneous exposures do not result in higher risk than homogeneous exposures.

The second example is low dose hyperradiosensitivity (and induced radioresistance), which can be observed in the dose dependence of survival of different cell lines.  Several properties of the living systems have been explained by the principle of minimum mutation load. Applying this principle for cell survival upon radiation exposure results in surviving curves qualitatively similar to experimental data on hyperradiosensitivity, which shows that hypersensitivity may decrease the number of mutations induced by radiation.

Both phenomena highlight that risks related to radiation exposure depend not only on cellular effects, but also on tissue responses.