[Regulation of thyroid hormones of the interaction of mitochondria with low-molecular weight cytoplasmic mediators, induced by phosphate- dependent transport of K+ and H+ ions through the mitochondrial inner membrane]. / Reguliatsiia tireoidnymi gormonami vzaimodeistviia mitokhondrii s nizkomolekuliarnymi tsitoplazmaticheskimi mediatorami, indutsiruiushchimi fosfatzavisimyi transport ionov K+ i H+ cherez membranu mitokhondrii.

In vivo thyroid hormones control the binding to mitochondria of low molecular weight water-soluble cytoplasmic mediators that are capable to induce oxidative phosphorylation uncoupling, by increasing the sensitivity of mitochondria to the effects of these mediators. In hyperthyroid rat liver mitochondria cytoplasmic mediators stimulate the phosphate-dependent transport of K+ and H+ in a greater degree than in liver mitochondria of control rats. The increase in the oxidative phosphorylation uncoupling by cytoplasmic mediators is one of mechanisms of thermogenesis stimulation by thyroid hormones.

[Regulation of oxidative phosphorylation, K+ ions transport and the volume of mitochondrial matrix by cytoplasmic glycopeptide and Ca2+ ions]. / Reguliatsiia okislitel'nogo fosforilirovaniia, transporta ionov K+ i ob''ema matriksa mitokhondrii tsitoplazmaticheskim glikopeptidom i ionami Ca2+.

A thermostable low molecular weight glycopeptide containing syalic acids, which uncouples mitochondrial oxidative phosphorylation, has been detected, isolated and purified from rat liver cytoplasm. In the presence of the glycopeptide, oxidative phosphorylation in rat liver mitochondria is uncoupled by low physiological concentrations of Ca2+, which otherwise do not have any appreciable effect on the mitochondria. Oxidative phosphorylation uncoupling by the glycopeptide is accompanied by an increase of the mitochondrial volume. This process has a limited amplitude and is regulated by changes in Ca2+ concentration in the extramitochondrial space. The glycopeptide has been shown to induce K+ transport across the inner mitochondrial membrane, this effect is enhanced by Ca2+.

[Induction of electrogenic phosphate transport through the mitochondrial membrane by a thermostable cytoplasmic factor in hyperthyroidism]. / Induktsiia élektrogennogo transporta fosfata cherez membranu mitokhondrii termostabil'nym tsitoplazmaticheskim faktorom pri gipertireoze.

Addition of a thermostable cytoplasmic fraction leads to the uncoupling of oxidative phosphorylation of the mitochondria. In hyperthyrosis such an effect manifests itself more powerfully than in the control. Addition of the thermostable cytoplasmic fraction induces electrogenic phosphate transport via the mitochondrial membrane. In hyperthyrosis, the activity of the thermostable inducer of phosphate transport in the cytoplasm increases. The functioning of the phosphate cycle may be the cause of the uncoupling of oxidative phosphorylation of the mitochondria during the disease in question.

[Regulation of pyruvate transport in mitochondria by thyroid hormones]. / Reguliatsiia transporta piruvata v mitokhondriiakh tireoidnymi gormonami.

During thyroidectomy, the stimulating action of the catalytic amounts of a thermostable fraction of rat liver and diaphragm cytoplasm on Ca2+ transport in mitochondria, which indicates the decrease of the activity of an insulin-dependent cytoplasmic regulator (IDR) in insulin target organs. Thyroidectomized rats also manifested a decrease in blood insulin and glucose concentrations. Administration of the physiological doses of thyroxine produced an increase in both blood glucose concentration and IDR activity in the liver and diaphragm of thyroidectomized rats. Experiments with measuring the kinetics of the swelling of deenergized mitochondria in isoosmotic solution of ammonium pyruvate demonstrated the inhibition of liver mitochondrial swelling in thyroidectomized rats.

[Effect of thyroidectomy and hyperthyroidism on Ca2+/2H+-antiporter activity in rat liver mitochondria]. / Vliianie tireoidéktomii i gipertireoza na aktivnost' Ca2+/2H+-antiportera v mitokhondriiakh pecheni krysy.

The manifestation of Ca2+/2H+ antiporter activity in rat liver mitochondria was shown to be inhibited in thyroidectomy and stimulated in hyperthyroidosis. Experiments with measuring the kinetics of the swelling of deenergized mitochondria in isoosmotic solutions Ca (NO3)2, pH 8.1 demonstrated inhibition of the swelling of liver mitochondria during thyroidectomy and stimulation because of administering thyroid hormones in vivo. During thyroidectomy, the phosphate-induced swelling of rat liver mitochondria was powerfully inhibited. Meanwhile administration of thyroxine to rats stimulated the swelling of mitochondria.

[Placental permeability in rats and rabbits for thyroid hormones at different periods of pregnancy]. / Pronitsaemost' platsenty krys i krolikov dlia tireoidnykh gormonov na raznykh srokakh beremennosti.

Upon the introduction of 14C-thyroxine in the rats on the 20th day of pregnancy, about 1/7 of the introduced radioactivity is found in the blood serum of the foetus; the labelled hormone is found in the foetus organs. The permeability of placenta at different times of pregnancy was also studied in rabbits. The placenta was shown to be permeable on the 23rd and 28th days of pregnancy, whereas earlier (16-17th days of development) negligible amounts of the labelled thyroxine introduced in the mother are found in the foetus organs.

[Development of the response of rabbit fetal tissues to thyroxine]. / Razvitie reaktsii tkanei plodov krolikov na tiroksin.

Development of rabbit fetal tissues sensitivity to thyroxin was studied on the basis of changes in alpha-glycerophosphate oxidase activity in the liver mitochondria of pregnant rabbits and their fetuses to which thyroxin was administered at different stages of pregnancy. T4 administration up to the 23rd day of gestation caused an increase in the enzyme activity in the maternal liver mitochondria only, whereas in the fetus it was at the control level. From the 24th day of pregnancy an increase of the alpha-glycerophosphate oxidase activity was seen in the fetal liver mitochondria. This can be explained by the appearance of rabbit fetal tissues sensitivity to maternal thyroxin at this period of gestation, increasing by the end of pregnancy.

[Effect of potassium iodide and perchlorate on the process of thyroid hormone secretion]. / Vliianie iodida i perkhlorata kaliia na protsess sekretsii tireoidnykh gormonov.

The influence of potassium iodide and perchlorate on the parameters characterizing the thypoid hormones secretion, such as the cAMP level in the gland tissue and the number of intracellular colloid droplets under condition of stimulation by thyrotropic hormone was studied. It was shown that the abovementioned parameters were depressed by an excess of iodide, but perchlorate administration prevented the inhibitory effect of iodide. The results obtained favour the conception on the sensitivity of the thyroid adenylate cyclase system to the organic iodine concentration. Apparently and excess of iodide depressed the capacity of perchlorate to influence its concentration in the gland, and thereby the process of iodine organification and of the thyroid hormone secretion maintained at the optimal leve.