title: Reactive oxygen species in the cellular pathophysiology of shock.
abstract: Reactive oxygen species (ROS) mediate the fine balance between cellular physiology and pathophysiology. Accordingly it is not surprising that cellular redox homeostasis is disrupted by shock events related to ischemia-reperfusion and inflammation. ROS may initiate as well as amplify the shock cellular insult in a number of ways which include important contributions to inflammation as well as lytic and apoptotic cell death. In addition, ROS in the setting of shock represent important antecedents to cellular proliferation, differentiation, and adaptation by virtue of altered transcription and translation of antioxidant enzymes, stress proteins, and a variety of cytokines. It is likely that an eventual important biochemical therapeutic goal in the setting of shock will involve re-establishing cellular redox homeostasis not only to ensure cellular structural integrity, but also to re-establish normal secondary cellular signal transduction mechanisms.
authors.affiliation: University of Wisconsin Children's Hospital, Division of Critical Care Medicine, Madison 53792-4108, USA.
authors.forename: F
authors.initials: F
authors.lastname: Flowers
authors.forename: J J
authors.initials: JJ
authors.lastname: Zimmerman
mesh_terms: D006801:Humans; D007511:Ischemia / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000502:physiology*; D015427:Reperfusion Injury / Q000378:metabolism; D012769:Shock / Q000209:etiology / Q000503:physiopathology*
chemical_list: D017382:Reactive Oxygen Species; D009569:Nitric Oxide