Pollycove Myron, Feinendegen Ludwig E
School of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Hum Exp Toxicol. 2008 Feb;27(2):169-75. doi: 10.1177/0960327107083411.
Four decades of genomic, cellular, animal and human data have shown that low-dose ionizing radiation stimulates positive genomic and cellular responses associated with effective cancer prevention and therapy and increased life span of mammals and humans.( 1-8) Nevertheless, this data is questioned because it seems to contradict the well demonstrated linear relation between ionizing radiation dose and damage to DNA without providing a clear mechanistic explanation of how low-dose radiation could produce such beneficial effects. This apparent contradiction is dispelled by current radiobiology that now includes DNA damage both from ionizing radiation and from endogenous metabolic free radicals, and coupled with the biological response to low-dose radiation. Acceptance of current radiobiology would invalidate long established recommendations and regulations of worldwide radiation safety organizations and so destroy the basis of the very expensive existing system of regulation and remediation. More importantly, current radiobiology would facilitate urgently needed clinical trials of low dose radiation (LDR) cancer therapy.
四十年来的基因组、细胞、动物和人体数据表明,低剂量电离辐射会激发与有效预防和治疗癌症以及延长哺乳动物和人类寿命相关的积极基因组和细胞反应。(1 - 8) 然而,这些数据受到质疑,因为它似乎与电离辐射剂量和DNA损伤之间已得到充分证明的线性关系相矛盾,却又没有对低剂量辐射如何产生这种有益效果给出明确的机制解释。当前的放射生物学消除了这一明显的矛盾,因为它现在既考虑了电离辐射造成的DNA损伤,也考虑了内源性代谢自由基造成的DNA损伤,并结合了对低剂量辐射的生物学反应。接受当前的放射生物学将使全球辐射安全组织长期确立的建议和规定失效,从而破坏现有非常昂贵的监管和补救系统的基础。更重要的是,当前的放射生物学将促进迫切需要的低剂量辐射(LDR)癌症治疗临床试验。