title: Does nitric oxide modulate mitochondrial energy generation and apoptosis?
abstract: The physiological role of nitric oxide (NO) in the maintenance of vascular tone, in synaptic transmission and in cellular defence is now firmly established. Recent evidence indicates that NO can also affect mitochondrial function. Here, we review findings indicating that NO   through its interaction with components of the electron-transport chain   might function not only as a physiological regulator of cell respiration, but also to augment the generation of reactive oxygen species by mitochondria, and thereby trigger mechanisms of cell survival or death.
authors: The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. s.moncada@ucl.ac.uk
authors: Salvador
authors: S
authors: Moncada
authors: Jorge D
authors: JD
authors: Erusalimsky
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D004579:Electron Transport; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D009569:Nitric Oxide / Q000502:physiology*; D018384:Oxidative Stress; D010101:Oxygen Consumption
chemical_list: D009569:Nitric Oxide; D003576:Electron Transport Complex IV