To date, the radiation-adaptive response has been reported as a low-dose-related phenomenon and has been associated with radiation hormesis. Well-known cancers are caused by non-radiation active reactants, in addition to radiation. A model of suppression for radiation-specific cancers was previously reported, but the model did not target radiation-nonspecific cancers. In this paper, we describe kinetic models of radiation-induced suppressors for general radiation non-specific cancers, estimating the dose M that induces the maximum hormesis effect while satisfying the condition that the risk is approximately proportional to a dose above NOAEL (No Observed Adverse Effect Level). The radiation hormesis effect is maximal when the rate constant for generation of a risk-reducing factor is the same as the rate constant for its decomposition. When the two rate constants are different, the dose M at which the radiation hormesis effect is maximized depends on both rate constants, but the dose M increases as the two rate constants approach each other, reaching a maximum dose. The theory proposed in this paper can only explain existing experiments with extremely short error bar lengths. This theory may lead to the discovery of unknown risk-reducing factor at low doses and the development of risk-reducing methods in the future.
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