Cardiac toxicity of singlet oxygen: implication in reperfusion injury.
Oxygen-derived free radicals (O2.-, H2O2, and .OH) that are produced during postischemic reperfusion are currently suspected to be involved in the pathogenesis of tissue injury. Another reactive oxygen species, the electronically excited molecular oxygen (1O2), is of increasing interest in the area of experimental research in cardiology. In this review are discussed the main potential sources of singlet oxygen in the organism, particularly in the myocardium, the various cardiovascular cytotoxic effects induced by this reactive oxygen intermediate, and the growing evidence of its involvement in ischemia/reperfusion injury.
Toufektsian
M C
MC
Laboratoire Stress Cardiovasculaires et Pathologies Associées, Université Joseph Fourier, Bâtiment Jean Roget, Domaine de la Merci, Grenoble, France.
Boucher
F R
FR
Tanguy
S
S
Morel
S
S
de Leiris
J G
JG
D000818:Animals; D006321:Heart / Q000187:drug effects*; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity*; D017382:Reactive Oxygen Species
D017382:Reactive Oxygen Species; D010100:Oxygen