Saturable repair models of radiation action in mammalian cells.

Abstract

Most quantitative models of radiation action in mammalian cells make the implicit assumption that all relevant repair processes proceed in a dose-independent manner. Thus it is implicitly assumed that the repair processes (1) follow totally unsaturated kinetics, (2) are not themselves inactivated by the radiation, and (3) are not enhanced by the presence of radiation damage. Contradiction of any of these three assumptions could have important theoretical and practical implications. The possible relevance of (1) and (2) in mammalian cells is discussed by considering a selection of saturable repair (and related) models. Repair inactivation is improbable, but repair saturation provides a ready explanation of common radiobiological phenomena without the need for the existence of "sublethal" damage. Furthermore, such models can "explain" additional phenomena which appear as contradictions to some sublethal damage models. Recent experiments by Wheeler and Wierowski have demonstrated the existence of dose-dependent repair of DNA damage in mammalian cells.