Is the autoxidation of catecholamines involved in ischemia-reperfusion injury?
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.
Jewett
S L
SL
Institute for Toxicology, University of Southern California, Los Angeles 90033.
Eddy
L J
LJ
Hochstein
P
P
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*
D002395:Catecholamines; D005609:Free Radicals; D006892:Hydroxydopamines; D016627:Oxidopamine; D010100:Oxygen; D004837:Epinephrine