哺乳动物细胞辐射作用的饱和修复模型。

Radiation research. Supplement Pub Date : 1985-01-01
D T Goodhead
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引用次数: 0

摘要

大多数哺乳动物细胞中辐射作用的定量模型都隐含地假设所有相关的修复过程都以剂量无关的方式进行。因此,可以隐含地假设修复过程(1)遵循完全不饱和动力学,(2)本身不会因辐射而失活,(3)不会因辐射损伤的存在而增强。这三个假设中的任何一个的矛盾都可能具有重要的理论和实践意义。(1)和(2)在哺乳动物细胞中的可能相关性通过考虑选择饱和修复(及相关)模型来讨论。修复失活是不可能的,但修复饱和为常见的放射生物学现象提供了一个现成的解释,而不需要存在“亚致死”损伤。此外,这些模型可以“解释”与某些亚致死损伤模型相矛盾的其他现象。Wheeler和Wierowski最近的实验证明,哺乳动物细胞中存在剂量依赖性的DNA损伤修复。
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Saturable repair models of radiation action in mammalian cells.

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.

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