Alper T, Cramp W A
Cell Mutation Unit, RPMS, Hammersmith Hospital, London, England.
Experientia. 1989 Jan 15;45(1):21-33. doi: 10.1007/BF01990449.
Apart from cancer and mutation induction, radiobiological effects on mammals are mostly attributable to cell 'death', defined as loss of proliferative capacity. Survival curves relate retention of that capacity to radiation dose, and often manifest a quasi-threshold ('shoulder'). The shoulder is attributable to an initial mechanism of repair ('Q-repair') which is gradually depleted as dose increases. Another form of repair, which is not depleted ('P-repair'), increases the dose required to deliver an average of one lethal event per cell (dose 'D0'). Neither form of repair can unambiguously be linked with repair of defects in isolated DNA. An important initial lesion may well be disruption of the complex structural relationship between the DNA, nuclear membrane and associated proteins. One form of P-repair may be restoration of that structural relationship.
除了癌症和诱变作用外,对哺乳动物的放射生物学效应主要归因于细胞“死亡”,细胞“死亡”定义为增殖能力的丧失。存活曲线将这种能力的保留与辐射剂量相关联,并且常常表现出一个准阈值(“坪区”)。坪区归因于一种初始修复机制(“Q修复”),随着剂量增加,这种机制会逐渐耗尽。另一种不会耗尽的修复形式(“P修复”),会增加使每个细胞平均发生一次致死事件所需的剂量(剂量“D0”)。这两种修复形式都无法明确地与分离DNA中缺陷的修复联系起来。一个重要的初始损伤很可能是DNA、核膜和相关蛋白质之间复杂结构关系的破坏。P修复的一种形式可能是该结构关系的恢复。