The Effect Of NO Donor on Calcium Uptake and Reactive Nitrogen Species Production in Mitochondria.

Background/aims: NO and reactive nitrogen species (RNS) are thought to be physiologically important effectors of mitochondrial calcium transport, but this issue was not studied in a living organism. According to literature, the modulation of Ca2+ uptake could influence RNS production via the action on mitochondrial NO synthase (mtNOS). The aim of this work was to study the effect of in vivo administration of NO donor nitroglycerine (NG) on matrix Ca2+ accumulation, RNS production and mtNOS activity.

siRNA-induced silencing of hypoxia-inducible factor 3α (HIF3α) increases endurance capacity in rats.

Molecular mechanisms of adaptation to exercise despite a large number of studies remain unclear. One of the crucial factors in this process is hypoxia inducible factor (HIF) that regulates transcription of many target genes encoding proteins that are implicated in molecular adaptation to hypoxia. Experiments were conducted on 24 adult male Fisher rats.

The effect of atp-dependent potassium uptake on mitochondrial functions under acute hypoxia.

The opening of mitochondrial K(+) АТР-channel (mtK(+) АТР-channel) is supposed to be important in the modulation of mitochondrial functions under hypoxia, but the underlying mechanisms have not been clarified yet. The aim of this work was to study the effect of acute hypoxia on mtK(+) АТР-channel activity and to estimate the contribution of the channel in the modulation of mitochondrial functions. MtK(+) АТР-channel activity was assessed polarographically from the rate of State 4 respiration and by potentiometric monitoring of potassium efflux from deenergized mitochondria.

[The effect of uridine on the endurance of animals with different resistance to physical stress: the role of mitochondrial ATP-dependent potassium channel].

The effect of a metabolic precursor of natural activator of mitochondrial ATP-dependent potassium channel (mitochondrial K+(ATP))--uridine on animal's endurance to physical stress was studied. The endurance was determined by recording the time period during which the rat loaded with a plummet of 20% of body weight can swim until physical exhaustion at 32 degrees C. It was found that highly resistant animals swam until exhaustion for 7.

Tissue oxygenation and mitochondrial respiration under different modes of intermittent hypoxia.

We compared the results of five modes of intermittent hypoxia training (IHT) on gastrocnemius muscle Po2 and heart and liver mitochondrial respiration in rats. Minutes of hypoxia, %O2, and recovery minutes on air in each mode were: 1) 5, 12%, 5; 2) 15, 12%, 15; 3) 5, 12%, 15; 4) 5, 7%, 5; and 5) 5, 7%, 15. Mode 1 proved best in that Pmo2 dropped minimally at the end of every hypoxic bout and recovered quickly after each bout.

HIF-3α mRNA expression changes in different tissues and their role in adaptation to intermittent hypoxia and physical exercise.

The role of HIF-3α in response to intermittent hypoxia and physical exercise was investigated in Fisher rats using reverse transcription, real-time PCR and RNA interference. Under acute hypoxia (12% O(2), 2h), the level of HIF-1α, HIF-2α, and HIF-1β mRNA did not significantly change in the heart, lung, kidney and muscle tissues, but HIF-3α mRNA expression was strongly elevated in all tissues investigated. Five weeks of intermittent hypoxic training (IHT) led to an increase of HIF-3α mRNA in all studied tissues, but under the influence of acute hypoxia after IHT, the expression of HIF-3α mRNA did not increase in all tissues excluding skeletal muscle.