Alper T
Br J Cancer Suppl. 1984;6:137-43.
Repair models account for shoulders to survival curves by the postulate of a mode of repair which is depleted ("saturated") as dose increases, and which should therefore be distinguished, conceptually and linguistically, from what is commonly known as "repair of potentially lethal damage". Acceptance of repair models entails new interpretations of some radiobiological phenomena. "Recovery" of cells between dose fractions would be attributable to reconstitution or resynthesis of the putative agent of repair, so elucidation of the mechanism of such "recovery" requires a different approach from any that have been used in attempts to discover the nature of "sub-lethal lesions" or the mechanism of their repair--attempts that have not been attended by success. Even mammalian cells can yield exponential survival curves; but this fact has been ignored in some proposals for mechanisms of radiation-induced cell killing, and in "theories of RBE" based on multi-sublethal lesion models for shouldered survival curves. According to repair models, however, cells in general are basically single-hit detectors. Comparisons between the responses of repair-proficient cells and their deficient mutants to change in radiation quality support the hypothesis that increases in RBE are attributable to reduced capacity for some mode(s) of repair as LET increases; but there is evidence that some capacity remains, even at very high values of LET.
修复模型通过一种修复模式的假设来解释肩部存活曲线，这种修复模式会随着剂量增加而耗尽（“饱和”），因此在概念和语言上应与通常所说的“潜在致死性损伤的修复”区分开来。接受修复模型需要对一些放射生物学现象进行新的解释。剂量分割之间细胞的“恢复”可归因于假定修复因子的重构或再合成，因此阐明这种“恢复”的机制需要一种与用于探索“亚致死性损伤”的性质或其修复机制的方法不同的方法——这些尝试尚未取得成功。甚至哺乳动物细胞也能产生指数存活曲线；但这一事实在一些关于辐射诱导细胞杀伤机制的提议以及基于肩部存活曲线的多亚致死性损伤模型的“相对生物效应理论”中被忽视了。然而，根据修复模型，一般来说细胞基本上是单次打击探测器。修复能力正常的细胞与其缺陷突变体对辐射质量变化的反应之间的比较支持了这样一种假设，即随着传能线密度（LET）增加，相对生物效应（RBE）的增加归因于某种修复模式的能力降低；但有证据表明，即使在LET值非常高时，仍保留一些能力。
