Mechanisms of reoxygenation injury in myocardial infarction: implications of a myoglobin redox cycle.
The addition of ascorbate to ischemic rat hearts prevents the myocardial damage associated with reoxygenation. H2O2 oxidizes myoglobin (Mb+2) to higher oxidation states (Mb+4 and Mb+5) which are rapidly reduced by ascorbate. It is proposed that the operation of a myoglobin redox cycle, in which H2O2 causes the two-electron oxidation of myoglobin, is a critical determinant of reperfusion injury. Conversely, the reduction of myoglobin, in one-electron steps, may represent an essential protective mechanism against such injury in the heart.
Galaris
D
D
Institute for Toxicology, University of Southern California, Los Angeles 90033.
Eddy
L
L
Arduini
A
A
Cadenas
E
E
Hochstein
P
P
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D003402:Creatine Kinase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D009211:Myoglobin / Q000378:metabolism*; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains; D013053:Spectrophotometry
D009211:Myoglobin; D006861:Hydrogen Peroxide; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D001205:Ascorbic Acid