Biology of nitric oxide signaling

Lucas Liaudet, Francisco Garcia Soriano, Csaba Szabo

Research output: Contribution to journalArticle

261 Scopus citations


The free radical nitric oxide (NO) has emerged in recent years as a fundamental signaling molecule for the maintenance of homeostasis, as well as a potent cytotoxic effector involved in the pathogenesis of a wide range of human diseases. Although this paradoxical fate has generated confusion, separating the biological actions of NO on the basis of its physiologic chemistry provides a conceptual framework which helps to distinguish between the beneficial and toxic consequences of NO, and to envision potential therapeutic strategies for the future. Under normal conditions, NO produced in low concentration acts as a messenger and cytoprotective (antioxidant) factor, via direct interactions with transition metals and other free radicals. Alternatively, when the circumstances allow the formation of substantial amounts of NO and modify the cellular microenvironment (formation of the superoxide radical), the chemistry of NO will turn into indirect effects consecutive to the formation of dinitrogen trioxide and peroxynitrite. These 'reactive nitrogen species' will, in turn, mediate both oxidative and nitrosative stresses, which form the basis of the cytotoxicity generally attributed to NO, relevant to the pathophysiology of inflammation, circulatory shock, and ischemia-reperfusion injury.

Original languageEnglish (US)
JournalCritical Care Medicine
Issue number4 SUPPL.
StatePublished - Apr 2000
Externally publishedYes



  • Cell signaling
  • Cytotoxicity
  • Dinitrogen trioxide
  • Nitration
  • Nitric oxide
  • Nitrosation
  • Nitrosothiols
  • Oxidation
  • Peroxynititee
  • Superoxide radical

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Liaudet, L., Soriano, F. G., & Szabo, C. (2000). Biology of nitric oxide signaling. Critical Care Medicine, 28(4 SUPPL.).