title: Oxidative stress in severe acute illness.
abstract: The overall redox potential of a cell is primarily determined by oxidizable/reducible chemical pairs, including glutathione-glutathione disulfide, reduced thioredoxin-oxidized thioredoxin, and NAD(+)-NADH (and NADP-NADPH). Current methods for evaluating oxidative stress rely on detecting levels of individual byproducts of oxidative damage or by determining the total levels or activity of individual antioxidant enzymes. Oxidation-reduction potential (ORP), on the other hand, is an integrated, comprehensive measure of the balance between total (known and unknown) pro-oxidant and antioxidant components in a biological system. Much emphasis has been placed on the role of oxidative stress in chronic diseases, such as Alzheimer's disease and atherosclerosis. The role of oxidative stress in acute diseases often seen in the emergency room and intensive care unit is considerable. New tools for the rapid, inexpensive measurement of both redox potential and total redox capacity should aid in introducing a new body of literature on the role of oxidative stress in acute illness and how to screen and monitor for potentially beneficial pharmacologic agents.
authors: Swedish Medical Center, Englewood, CO, USA; St. Anthony Hospital, Lakewood, CO, USA; The Medical Center of Plano, Plano, TX, USA. Electronic address: dbaror@ampiopharma.com.
authors: David
authors: D
authors: Bar-Or
authors: Swedish Medical Center, Englewood, CO, USA; St. Anthony Hospital, Lakewood, CO, USA; The Medical Center of Plano, Plano, TX, USA. Electronic address: rbaror@ampiopharma.com.
authors: Raphael
authors: R
authors: Bar-Or
authors: Swedish Medical Center, Englewood, CO, USA; St. Anthony Hospital, Lakewood, CO, USA; The Medical Center of Plano, Plano, TX, USA. Electronic address: lrael@ampiopharma.com.
authors: Leonard T
authors: LT
authors: Rael
authors: SomaLogic, Inc., Boulder, CO, USA. Electronic address: ebrody@somalogic.com.
authors: Edward N
authors: EN
authors: Brody
mesh_terms: D000208:Acute Disease; D000975:Antioxidants / Q000627:therapeutic use*; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D009104:Multiple Trauma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009243:NAD / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D018805:Sepsis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D020521:Stroke / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism; D013879:Thioredoxins / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D009243:NAD; D013879:Thioredoxins; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione
keywords: 4-Hydroxynonenal; Hypoxia-inducible factor 1; Malondialdehyde; Oxidation reduction potential; Superoxide dismutase; Traumatic brain injury
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