title: Is the autoxidation of catecholamines involved in ischemia-reperfusion injury?
abstract: The autoxidation of catecholamines has been proposed to be a source of oxygen radicals in ischemia-reperfusion injury. However, this autoxidation per se is extremely slow at physiological pH and therefore is unlikely to be a primary source of oxygen radicals in ischemia-reperfusion injury. On the other hand, oxygen radicals from catecholamines are more likely to arise through catalyzed oxidations involving enzymatic systems and/or metal ions. It is these latter reactions that may be of interest with respect to damage associated with ischemia-reperfusion injury.
authors.affiliation: Institute for Toxicology, University of Southern California, Los Angeles 90033.
authors.forename: S L
authors.initials: SL
authors.lastname: Jewett
authors.forename: L J
authors.initials: LJ
authors.lastname: Eddy
authors.forename: P
authors.initials: P
authors.lastname: Hochstein
mesh_terms: D002395:Catecholamines / Q000378:metabolism*; D004837:Epinephrine / Q000378:metabolism; D005609:Free Radicals; D006863:Hydrogen-Ion Concentration; D006892:Hydroxydopamines / Q000378:metabolism; D008954:Models, Biological; D015428:Myocardial Reperfusion Injury / Q000378:metabolism; D010084:Oxidation-Reduction; D016627:Oxidopamine; D010100:Oxygen / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D002395:Catecholamines; D005609:Free Radicals; D006892:Hydroxydopamines; D016627:Oxidopamine; D010100:Oxygen; D004837:Epinephrine