NO-mediated cytoprotection: instant adaptation to oxidative stress in bacteria

Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13855-60. doi: 10.1073/pnas.0504307102. Epub 2005 Sep 19.


Numerous sophisticated systems have been described that protect bacteria from increased levels of reactive oxygen species. Although indispensable during prolonged oxidative stress, these response systems depend on newly synthesized proteins, and are hence both time and energy consuming. Here, we describe an "express" cytoprotective system in Bacillus subtilis which depends on nitric oxide (NO). We show that NO immediately protects bacterial cells from reactive oxygen species by two independent mechanisms. NO transiently suppresses the enzymatic reduction of free cysteine that fuels the damaging Fenton reaction. In addition, NO directly reactivates catalase, a major antioxidant enzyme that has been inhibited in vivo by endogenous cysteine. Our data also reveal a critical role for bacterial NO-synthase in adaptation to oxidative stress associated with fast metabolic changes, and suggest a possible role for NO in defending pathogens against immune oxidative attack.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptation, Physiological
  • Antioxidants / metabolism
  • Bacillus subtilis / drug effects
  • Bacillus subtilis / genetics
  • Bacillus subtilis / metabolism*
  • Catalase / metabolism
  • Cytoprotection
  • Enzyme Activation
  • Gene Deletion
  • Hydrogen Peroxide / pharmacology
  • Iron / pharmacology
  • Nitric Oxide / pharmacology*
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase / metabolism*
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism
  • Water / pharmacology


  • Antioxidants
  • Fenton's reagent
  • Reactive Oxygen Species
  • Water
  • Nitric Oxide
  • Hydrogen Peroxide
  • Iron
  • Catalase
  • Nitric Oxide Synthase