Tomiyama H, Tachibana A, Yonei S
Int J Radiat Biol Relat Stud Phys Chem Med. 1986 Dec;50(6):973-81. doi: 10.1080/09553008614551391.
Experiments were performed to investigate the involvement of the cell membrane in the excision DNA repair process in Escherichia coli. Two membrane-binding drugs, procaine and phenethyl alcohol (PEA), inhibited liquid-holding recovery (LHR) in u.v.-irradiated E. coli wild-type and recA strains. In uvrB and polA strains where, after u.v.-irradiation, LHR was absent the two drugs had no effect. Both drugs markedly reduced the removal of u.v.-induced thymine dimers in the DNA of wild-type cells (H/r30). Analysis by alkaline sucrose gradients revealed that PEA inhibited the incision step in excision repair. In contrast, procaine had no effect on incision but apparently inhibited the late steps in excision repair. PEA dissociated DNA from the cell membrane, whereas procaine did not. The results suggest that the two drugs PEA and procaine inhibit LHR and the excision repair process operating on u.v.-induced damage in E. coli by at least two different mechanisms each of which may involve the cell membrane.
开展了实验以研究细胞膜在大肠杆菌切除修复过程中的作用。两种膜结合药物,普鲁卡因和苯乙醇(PEA),抑制了紫外线照射后的大肠杆菌野生型和recA菌株中的持液恢复(LHR)。在uvrB和polA菌株中,紫外线照射后不存在LHR,这两种药物没有作用。两种药物均显著减少了野生型细胞(H/r30)DNA中紫外线诱导的胸腺嘧啶二聚体的去除。碱性蔗糖梯度分析表明,PEA抑制切除修复中的切口步骤。相比之下,普鲁卡因对切口没有影响,但明显抑制了切除修复的后期步骤。PEA使DNA与细胞膜解离,而普鲁卡因则不会。结果表明,PEA和普鲁卡因这两种药物通过至少两种不同机制抑制大肠杆菌中LHR以及对紫外线诱导损伤的切除修复过程,每种机制可能都涉及细胞膜。