Oxidative stress in microorganisms - I - Microbial vs. higher cells - Damage and defenses in relation to cell aging and death

Oxidative stress in microbial cells shares many similarities with other cel l types but it has its specific features which may differ in prokaryotic an d eukaryotic cells. We survey here the properties and actions of primary so urces of oxidative stress, the role of transition metals in oxidative stres s and cell protective machinery of microbial cells, and compare them with a nalogous features of other cell types. Other features to be compared are th e action of reactive oxygen species (ROS) on cell constituents, secondary l ipid- or protein-based radicals and other stress products. Repair of oxidat ive injury by microorganisms and proteolytic removal of irreparable cell co nstituents are briefly described. Oxidative damage of aerobically growing m icrobial cells by endogenously formed ROS mostly does not induce changes si milar to the aging of multiplying mammalian cells. Rapid growth of bacteria and yeast prevents accumulation of impaired macromolecules which are repai red, diluted or eliminated. During growth some simple fungi, such as yeast or Podospora spp., exhibit aging whose primary cause seems to be fragmentat ion of the nucleolus or impairment of mitochondrial DNA integrity. Yeast ce ll aging seems to be accelerated by endogenous oxidative stress. Unlike mos t growing microbial cells, stationary-phase cells gradually lose their viab ility because of a continuous oxidative stress, in spite of an increased sy nthesis 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 indu ced by oxidative stress indicate that in bacteria cell death can result fro m activation of autolytic enzymes (similarly to the programmed mother-cell death at the end of bacillar sporulation). Yeast and other simple eukaryote s contain components of a proapoptotic pathway which are silent under norma l conditions but can be activated by oxidative stress or by manifestation o f mammalian death genes, such as bak or bax. Other aspects, such as regulat ion 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 t he subject of a subsequent review.