The physiology and genetics of oxidative stress in mycobacteria



  • Redox reactions are essential for life and play a role in both aerobic and anaerobic respiration. In aerobic microorganisms, the oxidants and reactive species are equalized by the antioxidants in order to maintain redox balance (1). Mycobacterium tuberculosis is an obligate aerobe, although it has been demonstrated that it can survive for more than a decade in vitro under anaerobic conditions. In the macrophage and the lung of the host, M. tuberculosis is exposed to a range of complex environments which can profoundly influence the physiology, including the redox homeostasis, of the mycobacterium. Thus, it is likely that the mechanisms to maintain redox homeostasis in M. tuberculosis are vital in determining disease outcome. As in other bacteria, M. tuberculosis has developed pathways that monitor and respond to gaseous signals, such as NO, CO, and O2, and fluctuations in the intra- and extracellular redox status (2 - 4). In this article, we will explore the physiology and genetics of redox homeostasis in mycobacteria by considering the in vivo environments to which M. tuberculosis is exposed, the sensors whereby mycobacteria discern an imbalance in the redox balance both endogenously and in the extracellular environment, mechanisms utilized by mycobacteria to respond to redox stress in order to maintain the intracellular redox balance, and the means currently used to measure the redox state in mycobacteria.
  • Authors

    Digital Object Identifier (doi)

    International Standard Book Number (isbn) 13

  • 9781555818838
  • Start Page

  • 297
  • End Page

  • 322