[Effect of negative hydro-aero ions on the structure and functional properties of mitochondria]. / Vliianie otritsatel'nykh gidroaéroionov na strukturu i funktsional'nye svoistva mitokhondrii.

Studies were carried out of the physical mechanism of biological effect of natural stimulant of the living activity--light negative hydroaeroions. The latter are a hydroxyl separated from water ions and designated here as electrically noncompensated hydroxyl OH-. Unique effect of OH-, i.e. fast restoration and prevention of fine damage of native mitochondria (NM) at storage was revealed on mitochondria preparations by specific procedure, providing preservation of the ability of self-organization--formation of aggregated and denser packing--native mitochondria. This effect of OH- is conditioned by increased formation of native mitochondria aggregates and is concerned with better ADP phosphorylation and Ca2- release. The effect of the air current OH- is produced by water action presaturated with OH-. OH- induces in water cooperative structure formation preserved for many days, which is indicated by an increase of its heat capacity and decrease of surface tension. The principal factor in OH- effect both on mitochondria and water seems to be a decrease of local positive changes. It is of more advantage in NM water suspensions to order (structurate) NM with disordering water, which explains formation of NM stable aggregates. OH- effect supports the main function of the organism struggling with proton excess which destroys biological self-organization. Strengthened structural self-organization under the effect of OH- found in NM seems to be of universal importance for biological macromolecules and membranes and is a primary effect of OH- on the living objects.

[Changes in the stimulation of mitochondrial respiration by adrenaline depending upon the dose]. / Izmenenie stimuliatsii dykhaniia mitokhondrii adrenalinom v zavisimosti ot dozy.

Effects of low and high 25 and 100 micrograms per 100 g of body weight doses of adrenaline on respiration and oxidative phosphorylation in rat liver mitochondria are compared. The high dose of adrenaline is shown to decrease activation of respiration and phosphorylation typical of the low doses. This decrease is caused by inhibition of succinate dehydrogenase and is accompanied by uncoupling of respiration and phosphorylation in mitochondria.

[Acetylcholine activation of alpha-ketoglutarate oxidation in liver mitochondria]. / Aktivatsiia atsetilkholinom okisleniia alpha-ketoglutarata v mitokhondriiakh pecheni.

Activation of alpha-ketoglutarate oxidation in the rat liver mitochondria takes place 15 and 30 min after intraperitoneal injection of acetyl choline. This mediator in doses of 25, 50 and 100 micrograms per 100 g of body weight causes a pronounced stimulation of phosphorylation respiration rate and calcium capacity of mitochondria with alpha-ketoglutarate oxidation. Acetyl choline is found to have a moderate inhibitory action on oxidation of lower (physiological) concentrations of succinate. Its stimulating action on alpha-ketoglutarate oxidation is associated with activation of M-cholinoreceptors; atropine, a choline-blocker, removes completely this effect. It is supposed that alpha-ketoglutarate and succinate are included into the composition of two reciprocal hormonal-substrate nucleotide systems.

[Effect of animal serum on mitochondrial respiration in stress]. / Vliianie syvorotki krovi zhivotnykh pri stresse na dykhanie mitokhondrii.

Effect of small amounts of rat blood serum on respiration of the animal brain mitochondria was studied. The following conditions were shown to be critical: the rats had to be kept undisturbed to avoid the effects of stress, high concentrations of mitochondrial suspension had to be used, incubation of the suspension at 26 degrees and use of succinate as a substrate of oxidation were also essential. Low concentrations of blood serum obtained from rats, maintained in tranquil state and, especially, under conditions of immobilization stress, increased the respiration rate in active state (V3) as well as in inactive state (V4). An increase in concentration of blood serum caused an inhibition of the V3 and activation of the V4 states as well as complete uncoupling of oxidative phosphorylation in mitochondria.

[High adrenaline sensitivity of the mitochondrial processes in the mucosa of the small intestine in rats]. / Vysokaia chuvstvitel'nost' k adrenalinu mitokhondrial'nykh protsessov v slizistoi obolochki tonkoi kishki krysy.

Higher adrenalin sensitivity of mitochondrial processes in the small intestinal mucosa compared to that in liver mitochondria, was revealed under specially devised conditions of work with isolated mitochondria retaining their natural properties. Fifteen minutes after intraperitoneal injection of adrenalin into rats in a dose of 5 micrograms/100 bw an increase in Ca2+ capacity was seen only in intestinal mucosa mitochondria. The adrenalin-induced activation of oxidative phosphorylation was more remarkable in intestinal than in liver mitochondria at the initial stages of adrenalin action. The effect of adrenalin was completely reversed by the beta-blocker propranolol only in liver mitochondria. After 3 hours the adrenalin-induced activation of phosphorylation in the mitochondria ceases, whereas in the small intestinal mucosa it still persists.

[Isolation and features of the functioning of mitochondria of the small intestine mucosa in the rat]. / Vydelenie i osobennosti funktsionirovaniia mitokhondrii slizistoi obolochki tonkogo kishechnika krysy.

A modification is suggested for the method of intact mitochondria isolation from rat thin intestine mucosa. Mitochondria are obtained which can in vitro transport Ca2+ simultaneously with phosphorylation of the added ADP. Kinetic advantages of succinate in providing oxidative phosphorylation as compared with NAD-dependent substrates are much more pronounced in mitochondria of the thin intestine mucosa than in other tissues, and Ca2+ transport occurred only under succinate oxidation. As compared with liver mitochondria these mitochondria are shown to be more sensitive to adrenaline and calcium action.

[Effect of adrenaline on calcium transport and oxidative phosphorylation in mitochondria]. / Vliianie adrenalina na transport kal'tsiia i okislitel'noe fosforilirovanie v mitokhondriiakh.

Intraperitoneal adrenaline injection induces in 15 and 30 min an increase in the phosphorylation rate, calcium capacity and Ca2+ retention time in the rat liver mitochondria. A rise of the phosphorylation rate is inhibited by inderal, a beta-adreno-blocker. Energy metabolism grows considerably with succinate exchange intensification.