Tyrrell R M
Acta Biol Med Ger. 1979;38(9):1259-69.
There is clear evidence that significant quantities of lesions are induced in DNA by near-UV radiation and that these lesions, although susceptible to repair, may lead to cell death because of the simultaneous disruption of DNA repair systems by the same wavelengths. No particular DNA lesion can be linked to cell death in wild type strains. However, there are good grounds for speculating that a type of near-UV lesion exists which is rapidly "fixed" as a lethal event in cells as a result of the oxygen-dependent disruption of repair. There is a strong indication that the relative ability of various near-UV wavelengths to sensitize cells to heat, chemicals or other radiations is directly related to their efficiency in disrupting DNA repair systems in general. Some important specific questions remain. For example, it is important to ask why breaks formed at 365 nm and 405 nm, although apparently requiring a pol dependent pathway for their repair, do not produce the predicted lethal biological action in the strains tested. In general terms it is hoped to provide more comprehensive physico-chemical data in support of, or contradicting, the proposed model.
有明确证据表明，近紫外线辐射会在DNA中诱导产生大量损伤，并且这些损伤尽管易于修复，但由于相同波长同时破坏DNA修复系统，可能导致细胞死亡。在野生型菌株中，没有特定的DNA损伤可与细胞死亡相关联。然而，有充分理由推测，存在一种近紫外线损伤类型，由于修复过程中依赖氧气的破坏，这种损伤在细胞中会迅速“固定”为致死事件。有强烈迹象表明，各种近紫外线波长使细胞对热、化学物质或其他辐射敏感的相对能力，总体上与它们破坏DNA修复系统的效率直接相关。一些重要的具体问题仍然存在。例如，重要的是要问为什么在365纳米和405纳米处形成的断裂，尽管显然需要依赖pol的途径进行修复，但在测试的菌株中却没有产生预期的致死生物学作用。一般来说，希望提供更全面的物理化学数据来支持或反驳所提出的模型。
