Nyström T
Department of Cell and Molecular Biology - Microbiology, Göteborg University, Box 462, 405 30 Göteborg, Sweden.
Arch Microbiol. 2001 Sep;176(3):159-64. doi: 10.1007/s002030100314.
A number of regulatory networks are functionally integrated in starving cells of Escherichia coli to reduce oxidation of target macromolecules and to enhance the cell's ability to withstand environmental insults. However, despite the fact that starving wild-type E. coli cells enhance their capacity to manage oxidative stress, the proteins of these cells become increasingly oxidized and the cells gradually lose their ability to reproduce. Indeed, it has been argued that starved and growth-arrested bacterial cells show the same signs of senescence as aging cells of higher organisms and that free radicals may be involved in the gradual loss of bacterial culturability observed in a stationary phase culture. Another model suggests that the apparent loss of viability of starved cells is a programmed and adaptive response in which the cells enter a reversible non-culturable state; the theory of the formation of viable but non-culturable cells. Recent data concerning the physiology and biochemistry of starved E. coli cells favor the model that starvation-induced loss of culturability is the result of stochastic deterioration rather than a programmed and adaptive phenomenon, and these data will be reviewed here.
在大肠杆菌的饥饿细胞中，一些调控网络在功能上相互整合，以减少目标大分子的氧化，并增强细胞抵御环境损伤的能力。然而，尽管饥饿的野生型大肠杆菌细胞增强了其应对氧化应激的能力，这些细胞中的蛋白质却越来越多地被氧化，并且细胞逐渐失去繁殖能力。事实上，有人认为饥饿且生长停滞的细菌细胞表现出与高等生物衰老细胞相同的衰老迹象，并且自由基可能参与了在稳定期培养中观察到的细菌可培养性的逐渐丧失。另一种模型认为，饥饿细胞明显的活力丧失是一种程序性的适应性反应，在这种反应中细胞进入一种可逆的不可培养状态，即可培养但不可培养细胞形成的理论。最近关于饥饿大肠杆菌细胞生理生化的数据支持这样一种模型，即饥饿诱导的可培养性丧失是随机退化的结果，而不是一种程序性的适应性现象，本文将对这些数据进行综述。
