Bioenergetic parameters of the brain in rats with different resistance to hypoxia

Dudchenko, A. M.; Chernobaeva, G. N.; Белоусова, В. В.; Vlasova, I. G.; Luk’yanova, L. D.

doi:10.1007/bf00836406

Cited by 18 publications

(24 citation statements)

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“…Kinetic parameters (K m and V max ) of mitochondrial enzymes in the cerebral cortex of low and highly resistant rats (rotenone-sensitive NADH-cytochrome C reductase [8], succinate-cytochrome C reductase [9], and cytochrome C oxidase [1]) were measured 2 h and 1 day after the 1st training session under conditions of INH/O 20 or INH/O 30 . Otherwise, these parameters were evaluated 1 day after the course of training with 8, 15, or 21 training sessions.…”

Section: Methodsmentioning

confidence: 99%

“…The mitochondrial respiratory chain plays a signal role and modulates oxygen consumption and rate of oxygen release from the extracellular medium to mitochondria. Opposite changes in activity of mitochondrial enzyme complexes I and II were found at the early stage of hypoxia [1,[4][5][6][7][10][11][12]. They provide the maintenance of electron transport function in the cytochrome region of the respiratory chain.…”

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Effect of intermittent normobaric hypoxia on kinetic properties of mitochondrial enzymes

et al. 2007

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We studied the effect of intermittent normobaric hypoxia on the formation of adaptive signs and state of mitochondrial enzymes in the cerebral cortex of rats with different resistance to hypoxia. Kinetic parameters for mitochondrial enzymes in the substrate region of the respiratory chain of the cerebral cortex underwent various changes in low resistant and highly resistant rats over the first 2 h after 1-h intermittent normobaric hypoxia. Low resistant animals were characterized by more effective functioning of rotenone-sensitive NADH-cytochrome C reductase and succinate-cytochrome C reductase under conditions of increased reduction status of the cell. These features correlated with the increase in the general resistance of animals. Significant changes in kinetic properties of mitochondrial enzymes and signs of the development of resistance were not found in highly resistant rats. Reciprocal relations between mitochondrial enzyme complexes in the substrate region of the respiratory chain probably play a role of the signal regulatory mechanism, which mediates tissue-specific and general resistance of rats under conditions of intermittent normobaric hypoxia. These effects did not depend on oxygenation of the inhaled gas mixture during the inter-hypoxic period.

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Section: Methodsmentioning

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Effect of intermittent normobaric hypoxia on kinetic properties of mitochondrial enzymes

et al. 2007

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“…Consequently, the stable regime of ATP synthesis in the hepatocytes in the 890-50 ~tM O 2 range is maintained not so much by glycolysis as by aerobic oxidation, the suppression of which at low P0~ causes the ATP concentration to decline. This may be due to inactivation of the first enzyme complex in the respiratory chain under the conditions of oxygen deficiency; the leading role of this complex in the regulation of the energy-synthesizing function in various cell types was demonstrated previously [3,6]. Prolonged adaptation of animals to periodic hypoxia changed the dynamics of lactate formation during incubation of hepatocytes of HR rats.…”

Section: Resultsmentioning

confidence: 85%

“…This damage is not compensated by the activation of glycolysis. As already mentioned, suppression of the NAD-dependent oxidation in the respiratory chain, probably due to hypercalcemia and inhibition of Ca-dependent enzymes of the Krebs cycle under the conditions of acute hypoxia [3,6,10], may be one of these mechanisms.…”

Section: Resultsmentioning

confidence: 95%

Role of glycolysis in the maintenance of the energy-synthesizing function of hepatocytes from rats adapted and nonadapted to hypoxia at different oxygen concentrations

1995

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It is demonstrated that the lactate-P0:dependence is the same in hepatocytes of rats with high and low resistance to hypoxia and does not correlate with phasic changes in the ATP concentration in the 890-50 ~tM 02 region. Strong activation of lactate formation against the background of ATP decrease indicates that glycolysis is not the major mechanism determining the steady-state ATP level in the cell and affecting the ATP-P0~ relationship in a wide range of oxygen concentrations. The intensity of glycolysis in hepatocytes of rats with high resistance to hypoxia is markedly increased after periodic adaptation to hypoxia but remains practically unchanged in the hepatocytes of low-resistance rats. This indicates that fundamentally different compensatory mechanisms are involved in this process in the liver of high-and low-resistance rats.Key Words: hepatocytes; glycolysis; lactate; ATP; adaptation; hypoxia Glycolysis and oxidative phosphorylation are two regulatory mechanisms controlling and determining the energy-synthesizing function of the cell. Under conditions of oxygen deficiency, the reduction in the intensity of the aerobic component is compensated by the activation of glycolysis. Therefore, increased lactate production at lowered oxygen concentration in the medium reflects the intensity of glycolysis and can be employed as a prognostic criterion for the evaluation of hypoxia, characterizing the contribution of the anaerobic process to energy formation. Analysis of the dynamics of this process in oxygen deficiency is hence of prime importance. Since brain tissues are highly sensitive to hypoxia, the role of glycolysis in hypoxia has been studied predominantly in the brain. On the other hand, the specific features of alterations Laboratory of Bioenergetics, Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow in the energy-synthesizing function of the liver and the role of glycolysis in this process in hypoxia have been poorly investigated, even though hepatic ischemia is a major cause of liver pathologies. In view of all this, we decided to explore how glycolysis aids in allowing the energy-synthesizing function of isolated hepatocytes incubated under varied conditions of oxygenation develop resistance to oxygen deficiency.

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“…These were run separately in homogenates and in isolated mitochondrial and microsomal fractions because, as shown earlier [16], the results for homogenates may differ from those for isolated fractions. The homogenates and isolated mitochondria were prepared as previously described [2], while isolated liver microsomes were prepared as detailed by Karuzina and Archakov [3]. Cy-0007-4888195/0012-1193 $ !…”

Section: Methodsmentioning

confidence: 99%

Effects of adaptation to hypoxia on cytochrome levels in the brain and liver of rats

Dudchenko

Luk’yanova

1995

Bull Exp Biol Med

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After a prolonged (for 30 days) adaptation of rats to intermittent hypoxia, their brains contained lowered levels of mitochondrial cytochromes, despite an increase in the number of mitochondria in the brain tissue mass, along with similar levels of high-energy compounds and more protein as compaired to the brains of unadapted controls. A mitochondrial population with novel properties presumably emerged in the brain. These effects were all more strongly marked in rats with an initially low resistance to hypoxia. In the liver of hypoxiaadapted animals, unlike in their brain, cytochrome levels in the mitochondrial and microsomal redox chains were lowered and the biogenesis of mitochondria was much less intensive. Key Words: adaptation; hypoxia; cytochromes; brain; liver; individual resistanceLong-term (LT) adaptation of animals to hypoxia has been shown to cause mitochondrial hyperplasia [4,15], activate protein synthesis [7,11], and raise mitochondrial cytochrome c [19] and cytochrome c oxidase levels [15] and the concentration of functional respiratory units [18] in the myocardium. Such changes may boost the power of the cardiac energysynthesizing system, reduce the ATP and creatine phosphate deficits in the cardiac tissue [7,13], and mitigate the damaging effects of hypoxia on the functional and metabolic homeostasis of cardiac cells. As regards brain and liver cells, the existing information on changes which their mitochondrial enzyme systems undergo during LT adaptation to hypoxia is highly inconclusive [1,15], probably because the respiratory chain in animals with an initially low resistance to hypoxia works differently than in highly resistant animals [5], making it hard to unravel the mechanisms by which adaptive changes occur in the energy-synthesizing system of the brain and liver. In view of this, the purpose of the present study was to examine and compare the effects of LT adaptation to intermittent hypoxia on respiratory chain cytoIxaboratory of Bioenergetics, Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow chromes and on cytochromes of other redox chains in rats with high and low resistance to acute hypoxia. MATERIALS AND METHODSThe study was conducted on random-bred male rats (body weight 180-200 g) pretested for responsiveness to acute hypobaric hypoxia in a pressure chamber (at an "altitude" of 11,000 m) [5] and considered, on the basis of test results, to be highly resistant (HR) or lowresistant (LR) to acute hypoxia. Thereafter, a proportion of rats from both groups were adapted, in daily 5-h sessions for a total of 30 days, to an "altitude" of 5000 m in the pressure chamber; after 25 days of the adaptation period, they were retested for their ability to survive at 11,000 m. The remaining HR and LR rats served as unadapted controls. One day after the last session, all rats were sacrificed to remove the brain and liver and obtain material for assays. These were run separately in homogenates and in isolated mitochondrial and microsomal fractions because, as shown earlier [16],...

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Bioenergetic parameters of the brain in rats with different resistance to hypoxia

Cited by 18 publications

References 3 publications

Effect of intermittent normobaric hypoxia on kinetic properties of mitochondrial enzymes

Effect of intermittent normobaric hypoxia on kinetic properties of mitochondrial enzymes

Role of glycolysis in the maintenance of the energy-synthesizing function of hepatocytes from rats adapted and nonadapted to hypoxia at different oxygen concentrations

Effects of adaptation to hypoxia on cytochrome levels in the brain and liver of rats

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