Filippov V D, Lotareva O V, Kuralenko O V
Mol Gen Mikrobiol Virusol. 1991 Jul(7):20-2.
The initial rates of antimutagenic dark repair were measured in Escherichia coli WP2 trpE65 cells irradiated by UV-light (11 J/m2) and then incubated in liquid media of various compositions. Samples were taken from suspension of incubated bacteria every 5 min following irradiation, mixed with acriflavine to block further repair and plated onto the selective medium containing acriflavine (1 micrograms/ml) to score the Trp+ mutations. The initial rate of antimutagenic repair was estimated from the kinetics of disappearance of mutations in several successive probes. It appeared to depend on the composition of a medium, to establish just after placing irradiated bacteria onto the medium and to decrease significantly in irradiated cells incubated under conditions favourable for growth. The decrease was not due to inhibition of postreplicative repair and was not caused by casaminoacids as such, but by combination of growth factors that provided the intensive protein synthesis. The decrease could be responsible for a strong mutational response of bacteria to irradiation because it secures the survival of premutagenic lesions in DNA till mutation fixation. It is suggested that metabolic regulation of the antimutagenic repair activity exists, based on an active switch of the energy flows required for several parallel metabolic pathways that proceed in irradiated cells.
在紫外线(11 J/m²)照射大肠杆菌WP2 trpE65细胞后,将其置于不同成分的液体培养基中孵育,测定抗诱变暗修复的初始速率。照射后每隔5分钟从孵育细菌的悬液中取样,与吖啶黄素混合以阻断进一步修复,然后接种到含有吖啶黄素(1微克/毫升)的选择培养基上,以计数Trp⁺突变。抗诱变修复的初始速率是根据几个连续样本中突变消失的动力学来估计的。结果表明,其似乎取决于培养基的成分,在将照射后的细菌接种到培养基上后立即确立,并在有利于生长的条件下孵育的照射细胞中显著降低。这种降低不是由于复制后修复的抑制,也不是由酪蛋白氨基酸本身引起的,而是由提供大量蛋白质合成的生长因子组合导致的。这种降低可能是细菌对辐射产生强烈突变反应的原因,因为它确保了DNA中诱变前损伤在突变固定之前的存活。基于照射细胞中几个平行代谢途径所需能量流的主动切换,提示存在抗诱变修复活性的代谢调节。