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盘基网柄菌营养细胞的紫外线照射

Ultraviolet irradiation of the vegetative cells of Dictyostelium discoideum.

作者信息

Freim J O, Deering R A

出版信息

J Bacteriol. 1970 Apr;102(1):36-42. doi: 10.1128/jb.102.1.36-42.1970.

Abstract

Experiments on the effect of ultraviolet (UV) light on the survival of vegetative Dictyostelium discoideum cells indicate that this is a relatively UV-resistant organism. Several factors suggest the presence of some type of repair process. Experiments to test for liquid-holding recovery and simple photoreactivation yielded negative results. Acriflavine and caffeine were utilized to possibly interfere with dark repair. Acriflavine produced no UV sensitization, but caffeine did cause a concentration-dependent decrease in survival of irradiated cells. When UV-irradiated cells were illuminated with photoreactivating light while suspended in caffeine, the survival increased above that for cells treated with caffeine alone, suggesting an overlap between lesions repaired by photorepair and dark repair. Growth experiments showed that UV light induced a dose-dependent division delay, followed by a period of retarded growth characterized by the presence of a constant fraction of nonviable cells in the irradiated population. The delayed exposure of cells to caffeine after irradiation showed that the magnitude of the caffeine sensitization diminished throughout the division-delay period. An action spectrum indicated probable nucleoprotein involvement in the induction of division delay. UV light retarded ribonucleic acid and protein synthesis and temporarily blocked deoxyribonucleic acid synthesis. However, synthesis of all three accelerated prior to the end of the division-delay period and then closely paralleled the increase in cell number.

摘要

关于紫外线(UV)对盘基网柄菌营养细胞存活影响的实验表明,这是一种对紫外线相对有抗性的生物体。有几个因素表明存在某种类型的修复过程。测试持液复苏和简单光复活的实验结果为阴性。吖啶黄素和咖啡因被用于可能干扰暗修复。吖啶黄素未产生紫外线致敏作用,但咖啡因确实导致受辐照细胞的存活率呈浓度依赖性下降。当紫外线照射的细胞悬浮在咖啡因中并用光复活光照射时,其存活率高于仅用咖啡因处理的细胞,这表明光修复和暗修复所修复的损伤之间存在重叠。生长实验表明,紫外线诱导剂量依赖性的分裂延迟,随后是一段生长迟缓期,其特征是受辐照群体中存在一定比例的非存活细胞。辐照后延迟给细胞施加咖啡因表明,在整个分裂延迟期内,咖啡因致敏的程度逐渐降低。一个作用光谱表明核蛋白可能参与了分裂延迟的诱导。紫外线延迟了核糖核酸和蛋白质的合成,并暂时阻断了脱氧核糖核酸的合成。然而,在分裂延迟期结束前,所有这三种物质的合成均加速,然后与细胞数量的增加密切平行。

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