ubiquinone and Autolysis

The rate of irreversible loss of mitochondrial phosphorylating respiratory function with NAD-linked substrates during zero flow myocardial autolysis at 37 degrees C was gradual and relatively linear with time, progressing at about 1% of the control activity per minute. State 3 respiratory rates and initial rates of inner membrane potential development dropped off in close parallel with one another as well as with NADH-coenzyme Q (CoQ) reductase activity, suggesting that oxygen uptake as well as membrane potential development were rate limited by the increasing impairment of electron flow through complex I. Although the initial rate of membrane potential development dropped off gradually, the time course for the loss of the ability to ultimately develop and hold a full potential was slower still, there being only a moderate impairment of this ability at 80 min of autolysis. This sustained ability to develop and hold a membrane potential after more than 1 h of autolysis suggested that inner membrane leakiness contributed little or not at all to the functional impairment observed. The irreversible loss of mitochondrial inner membrane competence emerged in these studies as a relatively late development in the sequence of cellular alterations which characterize the myocardial ischemic process.

Topics: Animals; Autolysis; Cardiomyopathies; Dogs; Enzyme Activation; Female; Male; Membrane Potentials; Mitochondria, Heart; NAD; Phosphorylation; Time Factors; Ubiquinone

Complex I (NADH-ubiquinone reductase) is a complex system located in the inner mitochondrial membrane and has the ability to catalyse several different enzymatic reactions concerned in electron transport. It is known to be one of the first components of the respiratory chain to be damaged by ischemia. Our results, using autolysis in the rat heart as experimental model, indicate that the NADH dehydrogenase system was impaired relatively early during ischemia while transhydrogenation and NADPH dehydrogenation appeared to be relatively resistant.

Topics: 2,6-Dichloroindophenol; Animals; Autolysis; Coronary Disease; Female; Ferrocyanides; Mitochondria, Heart; NAD(P)H Dehydrogenase (Quinone); NADH, NADPH Oxidoreductases; Oxygen; Oxygen Consumption; Phosphorylation; Quinone Reductases; Rats; Rats, Inbred Strains; Ubiquinone; Vitamin K

Topics: Animal Nutritional Physiological Phenomena; Animals; Antioxidants; Autolysis; Creatine Kinase; Deficiency Diseases; Female; Lipid Metabolism; Male; Membranes; Muscles; Oxidation-Reduction; Peptide Hydrolases; Peroxides; Rats; Ubiquinone; Vitamin E Deficiency