Nitric oxide and hypoxia

Alexander Galkin, A. Higgs, S. Moncada

Research output: Contribution to journalArticlepeer-review

Abstract

NO (nitric oxide) can affect mitochondrial function by interacting with the cytochrome c oxidase (complex IV) of the electron transport chain in a manner that is reversible and in competition with oxygen. Concentrations of NO too low to inhibit respiration can trigger cell defence response mechanisms involving reactive oxygen species and various signalling molecules such as nuclear factor kappa B and AMP kinase. Inhibition of mitochondrial respiration by NO at low oxygen concentrations can cause so-called metabolic hypoxia and divert oxygen towards other oxygen-dependent systems. Such a diversion reactivates prolyl hydroxylases and thus accounts for the prevention by NO of the stabilization of hypoxia-inducible transcription factor. In certain circumstances NO interacts with superoxide radical to form peroxynitrite, which can affect the action of key enzymes, such as mitochondrial complex I, by S-nitrosation. This chapter discusses the physiological and pathophysiological implications of the interactions of NO with the cytochrome c oxidase.
Original languageEnglish
Pages (from-to)29-42
Number of pages14
JournalEssays in Biochemistry
Volume43
Publication statusPublished - 2007

Fingerprint Dive into the research topics of 'Nitric oxide and hypoxia'. Together they form a unique fingerprint.

Cite this