Sigler K, Chaloupka J, Brozmanová J, Stadler N, Höfer M
Institute of Microbiology, Academy of Sciences of the Czech Republic, Prague.
Folia Microbiol (Praha). 1999;44(6):587-624. doi: 10.1007/BF02825650.
Oxidative stress in microbial cells shares many similarities with other cell types but it has its specific features which may differ in prokaryotic and eukaryotic cells. We survey here the properties and actions of primary sources of oxidative stress, the role of transition metals in oxidative stress and cell protective machinery of microbial cells, and compare them with analogous features of other cell types. Other features to be compared are the action of Reactive Oxygen Species (ROS) on cell constituents, secondary lipid- or protein-based radicals and other stress products. Repair of oxidative injury by microorganisms and proteolytic removal of irreparable cell constituents are briefly described. Oxidative damage of aerobically growing microbial cells by endogenously formed ROS mostly does not induce changes similar to the aging of multiplying mammalian cells. Rapid growth of bacteria and yeast prevents accumulation of impaired macromolecules which are repaired, diluted or eliminated. During growth some simple fungi, such as yeast or Podospora spp., exhibit aging whose primary cause seems to be fragmentation of the nucleolus or impairment of mitochondrial DNA integrity. Yeast cell aging seems to be accelerated by endogenous oxidative stress. Unlike most growing microbial cells, stationary-phase cells gradually lose their viability because of a continuous oxidative stress, in spite of an increased synthesis of antioxidant enzymes. Unlike in most microorganisms, in plant and animal cells a severe oxidative stress induces a specific programmed death pathway--apoptosis. The scant data on the microbial death mechanisms induced by oxidative stress indicate that in bacteria cell death can result from activation of autolytic enzymes (similarly to the programmed mother-cell death at the end of bacillary sporulation). Yeast and other simple eukaryotes contain components of a proapoptotic pathway which are silent under normal conditions but can be activated by oxidative stress or by manifestation of mammalian death genes, such as bak or bax. Other aspects, such as regulation of oxidative-stress response, role of defense enzymes and their control, acquisition of stress tolerance, stress signaling and its role in stress response, as well as cross-talk between different stress factors, will be the subject of a subsequent review.
微生物细胞中的氧化应激与其他细胞类型有许多相似之处，但也有其特定特征，这些特征在原核细胞和真核细胞中可能有所不同。我们在此综述氧化应激主要来源的性质和作用、过渡金属在氧化应激中的作用以及微生物细胞的细胞保护机制，并将它们与其他细胞类型的类似特征进行比较。其他要比较的特征包括活性氧（ROS）对细胞成分的作用、基于脂质或蛋白质的二级自由基及其他应激产物。简要描述了微生物对氧化损伤的修复以及对无法修复的细胞成分的蛋白水解清除。内源性形成的ROS对需氧生长的微生物细胞的氧化损伤大多不会诱导出与增殖的哺乳动物细胞衰老相似的变化。细菌和酵母的快速生长可防止受损大分子的积累，这些大分子会被修复、稀释或清除。在生长过程中，一些简单真菌，如酵母或柄孢霉属物种，会表现出衰老，其主要原因似乎是核仁碎片化或线粒体DNA完整性受损。酵母细胞衰老似乎会因内源性氧化应激而加速。与大多数生长中的微生物细胞不同，静止期细胞尽管抗氧化酶的合成增加，但由于持续的氧化应激会逐渐丧失活力。与大多数微生物不同，在植物和动物细胞中，严重的氧化应激会诱导一种特定的程序性死亡途径——凋亡。关于氧化应激诱导的微生物死亡机制的现有数据很少，表明在细菌中，细胞死亡可能是自溶酶激活的结果（类似于芽孢杆菌形成芽孢末期的程序性母细胞死亡）。酵母和其他简单真核生物含有促凋亡途径的成分，这些成分在正常条件下处于沉默状态，但可被氧化应激或哺乳动物死亡基因（如bak或bax）的表达激活。其他方面，如氧化应激反应的调节、防御酶的作用及其控制、应激耐受性的获得、应激信号传导及其在应激反应中的作用，以及不同应激因素之间的相互作用，将是后续综述的主题。
