[Effect of experimental myocardial infarct on the succinate oxidation rate and succinate dehydrogenase activity in the heart mitochondria].
The rate of oxidation of NADH and 3-hydroxybutyrate was studied in heart mitochondria after short-term (60 min) occlusion of coronary artery and the subsequent reperfusion. Addition of NAD increased the rate of 3-hydroxybutyrate oxidation, lowered in mitochondria of impaired tissue, but no complete restoration occurred. The 3-hydroxybutyrate dehydrogenase activity was decreased by 25%. The rate of NADH oxidation in ultrasonicated mitochondria from the infarction zone exceeded 2-fold the rate of 3-hydroxybutyrate oxidation. These data suggest that deficiency of NAD limited primarily the rate of 3-hydroxybutyrate oxidation in heart mitochondria under conditions of experimental myocardial infarction. The level of 3-hydroxybutyrate dehydrogenase activity appears to restrict the rate of 3-hydroxybutyrate oxidation after addition of NAD.
D000818:Animals; D004789:Enzyme Activation / Q000187:drug effects; D008929:Mitochondria, Heart / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism*; D010071:Oxaloacetates / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D011817:Rabbits; D013385:Succinate Dehydrogenase / Q000378:metabolism*; D013386:Succinates / Q000378:metabolism*
D010071:Oxaloacetates; D013386:Succinates; D013385:Succinate Dehydrogenase
Vliianie éksperimental'nogo infarkta miokarda na skorost' okisleniia suktsinata i aktivnost' suktsinatdegidrogenazy v mitokhondiiakh serdtsa.