Abstract

Purpose: For adaptive response (AR) behavior, to model and analyze the dose rate dependence of AR. To examine and to model the influence of time interval between primer and challenge dose on the magnitude of radioprotection.Method and materials: Microdosimetry is used to examine effects of rate of critical volume specific energy depositions on activation of AR and induction of deleterious damage. The dose rate dependent adaptive response data, Shadley and Wiencke and Shadley et al. on AR fading, are analyzed.Results: We obtain good agreement with observed AR behavior. The 4 – 6 hour activation time for AR is from time necessary for the accumulation of enzymatic resources from the increased radioprotective capability for the recognition and repair of deleterious DNA damage and perhaps resources for reduction of RSO. The Shadley and Wiencke data, for the low 1.0 cGy primer dose, is as a result of a minimum rate of specific energy depositions (hits) for adaptive response to become operative and become fully activated. Increased deleterious damage with increased dose rate for a high 50 cGy primer dose is from a reduction in dose rate sparing as the rate approaches acute exposure.Conclusions: The microdosimetric model substantiates the prior observations in Part I that only several radiation-induced charged particle cell nucleus traversals are sufficient to activate adaptive response. Further however we find here that a minimum dose rate threshold is necessary. The model shows promise to provide insight into adaptive response time and dose rate behavior.

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