Resveratrol and 2-Ethyl-6-Methyl-3-Hydroxypiridine N-Acetyl Cysteinate as Protecting Agents upon the Stress Exposure.

The increased generation of reactive oxygen species (ROS) by mitochondria under stress conditions leads to lipid peroxidation (LPO) as a consequence of the ROS interactions with polyunsaturated fatty acids in the lipid bilayer of cell membranes, causing their damage. It was assumed that chemical preparations that reduce the excessive ROS generation by mitochondria should exhibit protecting properties under oxidative-stress conditions. In this context, the antioxidants resveratrol (RSV) and 2-ethyl-6-methyl-3-hydroxypyridine N-acetylcysteinate (NAC-3-HP) were examined as potential chemical protectors upon the exposure to stress, able to maintain the functional state of mitochondria.

Bis(µ-Tartrato)Di(μ-Hydroxy) Germanate (IV) Triethanolammonium as a Mononuclear Alkaline Phospholipase A Inhibitor.

It was established that the administration of an aqueous solution of bis(µ-tartrato)di(μ-hydroxy) germanate (IV) triethanolammonium to animals daily for 2 months at a dose of the active substance of 10 mg/kg of the animal's weight leads to inhibition of the total activity of the alkaline phospholipase A of mononuclear cells. The results of the study can be used to correct lipid metabolism in the development of disorders in hyperlipidemia. This makes it possible to expand the scope of use of the studied substance and create new pharmaceuticals based on bis(µ-tartrato)di(μ-hydroxy) germanate (IV) triethanolammonium prevent and inhibit the development of hyperlipidemia.

[Anphen and energy status of the animal body].

Energy status of rats was altered after administration of anphen [2,4-(hydroxy-3,5-ditretbutyl phenyl)-2-aminomalonic acid] at a dose of 40 mg/kg. Within 30 min after administration, maximal rates of NAD-dependent substrates and succinate oxidation were detected in liver mitochondria, which appears to occur due to activation of the mitochondrogenesis. The rate of electron transport in respiratory chain of mitochondria was decreased 1.

[Effects of combined action of heavy metal salts and phenol on energetics of isolated rat liver mitochondria].

Experiments were carried out to investigate effects of heavy metal salts and phenol both alone and in different combinations on respiration rate and coupling of respiration and oxidative phosphorylation by rat liver mitochondria. Oxygen consumption measurements were obtained using a Clark electrode and lactate plus glutamate as substrates. It is shown that a 50% decrease of the respiratory rate was achieved in less concentrations of substances in the mixture compared with the effects of the individual substances.

[Activation of lipid peroxidation in the liver mitochondria and acute toxicity of chemical compounds].

The effect of toxic substances on the functional state of liver mitochondria has been studied. It has been shown, that the contact of toxic substances with mitochondria lead to the reduction of the degree of association of oxidation with phosphorylation. EDTA in concentrations necessary to inhibit lipid peroxide oxidation prevents toxic effects.

[Mechanism of action of piracetam on NADH oxidation via the external pathway in rat liver mitochondria].

Activation of the external pathway (amytalantimycine A-resistant) of the exogenous NADH oxidation was studied in rat liver mitochondria after long-term (within 6 days) administration of pyracetame. Stimulation of lipid peroxidation and a decrease in viscosity of mitochondrial membranes accompanied the increase in the rate of oxygen consumption in mitochondria in presence of the exogenous NADH, amytal and antimycine A.

[Fatty acid composition and energy state of liver mitochondria after the administration of antioxidants of the ionol group to albino rats].

Injections of albino rats with antioxidants of the ionol group cause cyclic changes in the energy state of liver mitochondria which are correlated with changes in the fatty acid composition of mitochondrial membranes. The increase in the degree of coupling between oxidation and phosphorylation coincides in time with the increment in the content of saturated fatty acids and a decrease in the unsaturated fatty acid content in the total fraction of mitochondrial membrane lipids. Conversely, the activation of the external pathway of NADH oxidation and a decrease of the respiratory control are correlated with the diminution of the saturated fatty acid content and an increased percentage of unsaturated fatty acids.

[Effect of ionol-type antioxidants on the energetics of liver mitochondria].

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.

Activation of the external pathway of NADH oxidation in liver mitochondria of cold-adapted rats.

15 min cold exposure of rats adapted to cold results in switching on a pathway of the fast oxidation of extramitochondrial NADH in the isolated liver mitochondria. This pathway is sensitive to mersalyl and cyanide, resistant to amytal and antimycin A, and can be stimulated by dinitrophenol. A portion of the endogenous cytochrome c pool can easily be removed by washing mitochondria of the cold-exposed rats.