Cytochrome oxidase activity of mitochondria from ischemic and reperfused myocardium.
Polarographic measurements show that activity of cytochrome oxidase (CO), assayed as ascorbate plus TMPD oxidase, is decreased in the mitochondria (M) from postischemic areas of rabbit heart 1, 6, and 9 days after temporary (1-hr) coronary artery occlusion (CAO). This effect is observable only in the absence of added cytochrome c. Cytochrome oxidase activity in the cytochrome c-containing medium was not different from the control level. Levels of cytochromes c + c1 and a were substantially lower in tissue from postischemic areas and elevated in the intact tissue 1 and 6 days after temporary CAO as compared with control hearts. Stoichiometry of the cytochromes was not changed. After 1 or 4 hr of permanent CAO, CO activity (plus cytochrome c) of ischemic M was equal to that of M from intact area; CO activity (with or without cytochrome c) was reduced after 0.5 and 1 hr but elevated after 3 or 4 hr of in vitro ischemia as compared with control. The changes of CO activity in infarcted human heart M were similar to those in rabbits after temporary CAO; CO activity was restored after addition of cytochrome c. The data suggest that leakage of cytochrome c occurs during isolation of M and is more pronounced in ischemia-damaged M.
D000818:Animals; D003327:Coronary Disease / Q000201:enzymology*; D003576:Electron Transport Complex IV / Q000378:metabolism*; D008929:Mitochondria, Heart / Q000201:enzymology*; D011817:Rabbits; D013938:Thymidine Monophosphate / Q000378:metabolism
D013938:Thymidine Monophosphate; D003576:Electron Transport Complex IV