Kaina B
Mutat Res. 1982 Mar;93(1):195-211. doi: 10.1016/0027-5107(82)90135-x.
Exposure of V79 Chinese hamster cells to a single very low (sub-toxic and sub-clastogenic) dose of MNU or MNNG made these cells resistant to the toxic, mutagenic and clastogenic activities of the same agents given 6 h later. Cell survival was increased nearly 2-fold under optimal conditions when compared with the non-pretreated controls. Aberration frequencies were reduced to nearly half the control values (cells not pretreated). This was observed for a wide range of pretreatment concentrations and at different recovery times. The effect of mutagen pretreatment was most pronounced with respect to the induction of TG resistance, which became drastically reduced. The data indicate the existence of an adaptive repair pathway in V79 cells which may be induced by very low levels of methylating agents and which is error-free in handling lesions responsible, at least partially, for reproductive cell death, mutations and chromosomal aberrations.
将V79中国仓鼠细胞暴露于单一非常低(亚毒性和亚致断裂性)剂量的N-甲基-N-亚硝基脲(MNU)或N-甲基-N'-硝基-N-亚硝基胍(MNNG)后,这些细胞对6小时后给予的相同试剂的毒性、诱变和致断裂活性产生了抗性。在最佳条件下,与未预处理的对照相比,细胞存活率提高了近2倍。畸变频率降低到对照值(未预处理的细胞)的近一半。在广泛的预处理浓度和不同的恢复时间都观察到了这种情况。诱变预处理对诱导胸苷(TG)抗性的影响最为明显,胸苷抗性大幅降低。数据表明V79细胞中存在一种适应性修复途径,该途径可能由极低水平的甲基化剂诱导,并且在处理至少部分导致生殖细胞死亡、突变和染色体畸变的损伤时无错误。