Billen D
Radiat Res. 1987 Aug;111(2):354-60.
When cells are exposed to ionizing radiation, they suffer lethal damage (LD), potentially lethal damage (PLD), and sublethal damage (SLD). All three forms of damage may be caused by direct or indirect radiation action or by the interaction of indirect radiation products with direct DNA damage. In this report I examine the expression of LD and PLD caused by the indirect action of X rays in isogenic, repair-deficient Escherichia coli. The radiosensitivity of a recA mutant, deficient both in pre- and post replication recombination repair and SOS induction (inducible error-prone repair), was compared to that of a recB mutant which is recombination deficient but SOS proficient and to a previously studied DNA polymerase 1-deficient mutant (polA) which lacks the excision repair pathway. Indirect damage by water radicals (primarily OH radicals) was circumvented by the presence of 2 M glycerol during irradiation. Indirect X-ray damage by water radicals accounts for at least 85% of the PLD found in exposed repair-deficient cells. The DNA polymerase 1-deficient mutant is most sensitive to indirect damage with the order of sensitivity polA1 greater than recB greater than or equal to recA greater than wild type. For the direct effects of X rays the order of sensitivity is recA greater than recB greater than polA1 greater than wild type. The significance of the various repair pathways in mitigating PLD by direct and indirect damage is discussed.
当细胞受到电离辐射时，会遭受致死性损伤（LD）、潜在致死性损伤（PLD）和亚致死性损伤（SLD）。这三种损伤形式都可能由直接或间接辐射作用引起，或者由间接辐射产物与直接DNA损伤的相互作用导致。在本报告中，我研究了X射线间接作用在同基因、修复缺陷型大肠杆菌中所引起的LD和PLD的表达情况。将一个recA突变体（在复制前和复制后重组修复以及SOS诱导方面均有缺陷，即诱导性易错修复缺陷）的辐射敏感性，与一个recB突变体（重组缺陷但SOS功能正常）以及一个先前研究过的缺乏切除修复途径的DNA聚合酶1缺陷型突变体（polA）的辐射敏感性进行了比较。在照射过程中加入2M甘油可避免水自由基（主要是OH自由基）造成的间接损伤。水自由基造成的间接X射线损伤至少占暴露的修复缺陷型细胞中发现的PLD的85%。DNA聚合酶1缺陷型突变体对间接损伤最为敏感，其敏感性顺序为polA1大于recB大于或等于recA大于野生型。对于X射线的直接效应，敏感性顺序为recA大于recB大于polA1大于野生型。文中讨论了各种修复途径在减轻直接和间接损伤所导致的PLD方面的意义。
