
An injection of ionol-type antioxidants stimulates fast oxidation of extramitochondrial NADH in isolated liver mitochondria via an external pathway, which is sensitive to cyanide and resistant to amital and antimycin A. This activation is accompanied by a decrease in cytochrome a and cytochrome (c + C1) levels in liver homogenate. Part of the cytochrome c pool can be removed by washing the antioxidant-treated mitochondria. It is assumed that the injection of the antioxidants leads to desorption of the cytochrome c bound to the inner membrane into the intermembrane space of mitochondria. This cytochrome acts as a linking agent between NADH cytochrome c reductase of the outer mitochondrial membrane and cytochrome c oxidase of the inner membrane. The Li-derivative of ionol (5 x 10(-4) and 10(-3) M) decreases the transmembrane potential of the submitochondrial particles from bovine heart by 15-20%.
Submitochondrial Particles, Mitochondria, Liver, Butylated Hydroxytoluene, NAD, Antioxidants, Mitochondria, Heart, Membrane Potentials, Rats, Kinetics, Animals, Cytochromes, Cattle, Female, Oxidation-Reduction
Submitochondrial Particles, Mitochondria, Liver, Butylated Hydroxytoluene, NAD, Antioxidants, Mitochondria, Heart, Membrane Potentials, Rats, Kinetics, Animals, Cytochromes, Cattle, Female, Oxidation-Reduction
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