Imada I, Fujita T, Sugiyama Y, Okamoto K, Kobayashi Y
Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.
Arch Gerontol Geriatr. 1989 May;8(3):323-41. doi: 10.1016/0167-4943(89)90014-9.
The oxidation of succinate and NADH in a ubiquinone-depleted canine brain mitochondrial preparation was restored by a low molecular weight benzoquinone, idebenone. Idebenone inhibited NADH(NADPH)/ADP-Fe3+-dependent lipid peroxidation in canine brain mitochondria and protected against the resulting inactivation of NADH-cytochrome c reductase activity. Idebenone did not affect the activities of succinate oxidase in canine and rat brain mitochondria but suppressed the oxygen consumption in NADH oxidation. This suppression might be related to the inhibition of lipid peroxidation. These results suggest that idebenone functions as an electron carrier in the respiratory chains of brain mitochondria and as an antioxidant against membrane damage caused by lipid peroxidation in brain mitochondria.
