[Rotenone-sensitive oxidation of NADH and F0F1-ATPase activity in a homogenate of rat skeletal muscles during thermal adaptation]. / Rotenon-chuvstvitel'noe okislenie NADH i aktivnost' F0F1-ATPazy v gomogenate skeletnykh myshts krysy pri termoadaptatsii.

A method has been developed for measuring the rates of rotenone-sensitive oxidation of NADH and oligomycin-sensitive hydrolysis of ATP in rat skeletal muscle homogenates. The method is based on the use of alamethicin which increases the permeability of the inner mitochondrial membrane for NADH and ATP. It has been shown that prolonged cold adaptation of rats (4 weeks, 4 degrees) does not change the activity of rotenone-sensitive NADH-oxidase in rat skeletal muscle homogenates which is equal to 12.4 +/- 4.4 nmol NADH/min/mg protein, but increases threefold that of F0F1-ATPase--from 31.8 +/- 7.4 up to 93.1 +/- 14.3 nmol P(i)/min/mg protein. It is suggested that prolonged cold adaptation induces structural-and-functional changes in the H(+)-ATP-synthetase complex of skeletal muscle mitochondria.

[Status of liver mitochondria and rat tissue creatine kinase during administration of antivitamin K]. / Sostoianie mitokhondrii pecheni i aktivnost' kreatinkinazy tkanei krysy pri vvedenii antivitamina K.

It has been shown that 16-18 days administration of antivitamin K (pelentan) leads to two-fold increase of prothrombin time in adult rats but does not influence the soluble brain, renal, heart, muscle and serum creatine kinase activity. No effect on metabolic function of isolated liver mitochondria has been found in contrast to the vitamin K deficient rats. Mitochondria were characterized by high value of respiration control; substance oxidation rates and internal mitochondrial Ca2+ content do not differ in the level from those of control animals. From the obtained results and data published in literature a conclusion can be drawn about only particular similarity (prothrombin time) between the antivitamin K administration and alimentary vitamin K deficit.

[Metabolic function of isolated liver mitochondria during various conditions of vitamin D and K supply and administration of pelentane]. / Metabolicheskie funktsii izolirovannykh mitokhondrii pecheni pri razlichnoi obespechennosti krys vitaminami D i K i vvedenii pelentana.

Alimentary deficiency of vitamin K caused a decrease in the rate of respiration in presence of ADP and in the rate of oxidative phosphorylation in the presence of succinate. Administration of the antivitamin K pelentane, excess of vikasol and deficiency of vitamin D did not affect these parameters. As distinct from controls and rats treated with pelentane, transport of calcium was decreased in presence of all the substrates studied in mitochondria isolated from liver tissue of animals deprived of vitamins K and D as well as of animals treated with vikasol excess. At the same time, accumulation of calcium led to time-dependent inhibition of respiratory chain if NAD-dependent substrates were used. Possible reasons of dissimilarity observed are discussed; the phenomenon found may occur due to exhaustion of the mitochondrial pyridine nucleotides pool. The data obtained suggest that antivitamins K altered only some parameters of body status (prothrombin time) similarly to the alterations observed in alimentary deficiency of vitamin K.

[Nature of endogenous proton conductance of the inner mitochondrial membrane. Role of Ca2+ transport system in proton transfer]. / Priroda éndogennoi protonnoi provodimosti vnutrennei membrany mitokhondrii. Uchastie Ca2+-transportiruiushchei sistemy v perenose protona.

In order to elucidate the nature of endogenous proton conductance of rat liver inner mitochondrial membrane, the dependence of the rate of Ca2+ transport on pH was studied. It was found that the inhibiting effect of H+ is independent of protonation of functional groups of hypothetical Ca2+ carrier, but results from electrogenic transfer of H+ across the membrane, which is highly permeable for the proton. The adsorption of H+ by mitochondria is inhibited by ruthenium red and other specific inhibitors of Ca2+ transport. It is concluded that endogenous proton conductance of the inner mitochondrial membrane depends on the functioning of the same transport system essential for membrane permeability for Ca2+ and other bivalent cations. The correlation observed between the rates of H+ and Ca2+ transport in mitochondria and the ratio of cation mobilities in aqueous solutions is in favour of a "porous" mechanism of cation transport across the mitochondrial membrane.

[Role of planar cobalt chelate complexes as shunting agents in the electron transport chain of mitochondria]. / Ploskie khelatnye kompleksy kobal'ta kak shuntiruiushchie agenty v elektrontransportnoi tsepi mitokhondrii.

It was shown that planar cobalt chelate complexes catalyze oxidation of NADH and hexahydroubiquinole Q4H2 by air oxygen. The most active agent--perchlorate of the cobalt complex 1, 2, 3, 7, 8, 12, 13, 17, 18, 19-decamethyloctadehydrocorrin--is capable of shunting the electron transfer chain of rat liver mitochondria and beef heart submitochondrial particles, catalyzing electron transfer from CoQ directly to the oxygen.