[Participation of tocopherol and its analogs in lipid peroxidation processes and electron transport in rat liver mitochondria in vivo].

The effects of vitamin E and its analogs--alpha-tocopheryl acetate with a shortened up to six carbon atoms side chain carrying a saturated and an unsaturated bonds at the chain terminus, alpha-tocopherol and alpha-tocopheryl quinone devoid of the side chain--on the rate of malonic dialdehyde formation, the diene conjugate and total lipid content in the liver as well as the activity of the respiratory chain enzymes--succinate--and NADH-dehydrogenase, succinate- and NADH-ubiquinone reductase, as well as the vitamin E and ubiquinone content in the liver mitochondria of vitamin E-deficient rats in vivo have been investigated. It has been found that alpha-tocopheryl acetate with a shortened (up to C6) side chain carrying a saturated bond at the chain terminus is the most effective analog of tocopherol. Further reduction of the tocopherol side chain or tocopherol conversion into quinone causes a decrease in their tocopherol activity.

[Effect of tocopherol, its analogs and the antioxidant ionol on lipid peroxidation in vitro].

Ionol, alpha-tocopherol and its analogues (tocoferenquinones with C6 and C1 in the side chain, tocopherol without the side chain and two tocopherols with shortened to C6 side chain both with saturated and with unsaturated bond at the end) were studied for their effect on the formation rate of malonaldehyde in the tissue and liver mitochondria of vitamin E-deficient rats in vitro. Preparations were used in two concentrations: 35 mg per 1 ml of the medium--in a dose suppressing processes or lipid peroxidation; and 5 mg per 1 ml of the medium--in a dose activating biosynthesis of ubiquinone in the animal tissues. Tocopherol effect on lipid peroxidation processes in the liver tissue and mitochondria is shown to be different and to depend on its concentration in the medium.

[Vitamin E, ubiquinone and ubiquinone-dependent enzymes in experimental myocarditis].

It is shown that a day after introduction of adrenaline which evokes experimental focal myocarditis the level of ubiquinone and vitamin E content in the myocardial mitochondria increases by 56.8 and 122%, respectively. Succinate-ubiquinone-reductase activity in mitochondria remains practically unchanged, while NADH-ubiquinone-reductase activity considerably falls.

[Comparative study of the effects of alpha-tocopherol and a synthetic antioxidant on respiration and oxidative phosphorylation in rat liver mitochondria].

In order to decide whether vitamin E action on ubiquinone-dependent enzymatic systems of mitochondria and on ubiquinone metabolism consisting in its antioxidative function, the effects of alpha-tocopherol and the most effective synthetic antioxidant, chlorohydrate 2-ethyl-6-methyl-3-hydroxypyridine, were compared. It was shown that the contents of vitamin E and ubiquinone as well as the activities of succinate- and NADH-ubiquinone reductase, succinate- and NADH-dehydrogenases in liver mitochondria are increased and the levels of ATP, adenine nucleotides and phosphate potential in the livers of vitamin E-deficient rats are elevated 3 hours after alpha-tocopherol injection (5 micrograms per 1 g of body weight). The synthetic antioxidant injected under identical conditions at a dose of 50 micrograms per 1 g of body weight did not change the ubiquinone content or the enzymatic activities, but considerably enhanced the ATP level.