Effects of adaptation to intermittent hypoxia on oxidative phosphorylation in brain mitochondria of rats with different sensitivities toward oxygen deficiency

Luk’yanova, L. D.; Chernobaeva, G. N.; Romanova, V. E.

doi:10.1007/bf02445567

Cited by 10 publications

(9 citation statements)

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“…The large number of small mitochondria in the cerebral cortex in tolerant-to-hypoxia rats is an indicator of increased metabolic mitochondrial activity and higher intensity of oxidative phosphorylation in these rats in comparison to susceptible rats. This is in accordance with the results of earlier studies that demonstrated different intensities of oxidative phosphorylation in the cerebral cortex in rats with tolerant and susceptible hypoxia resistance [ 214 , 215 ]. Thus, under normoxia, phenotypic ultrastructural, functional and metabolic differences are observed between the mitochondria of cerebral cortex cells of tolerant- and susceptible-to-hypoxia rats.…”

Section: Physiological Biochemical and Molecular-biological Charsupporting

confidence: 93%

Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics

Джалилова

Makarova

2020

Biomedicines

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Hypoxia plays an important role in the development of many infectious, inflammatory, and tumor diseases. The predisposition to such disorders is mostly provided by differences in basic tolerance to oxygen deficiency, which we discuss in this review. Except the direct exposure of different-severity hypoxia in decompression chambers or in highland conditions, there are no alternative methods for determining organism tolerance. Due to the variability of the detection methods, differences in many parameters between tolerant and susceptible organisms are still not well-characterized, but some of them can serve as biomarkers of susceptibility to hypoxia. At the moment, several potential biomarkers in conditions after hypoxic exposure have been identified both in experimental animals and humans. The main potential biomarkers are Hypoxia-Inducible Factor (HIF)-1, Heat-Shock Protein 70 (HSP70), and NO. Due to the different mechanisms of various high-altitude diseases, biomarkers may not be highly specific and universal. Therefore, it is extremely important to conduct research on hypoxia susceptibility biomarkers. Moreover, it is important to develop a method for the evaluation of organisms’ basic hypoxia tolerance without the necessity of any oxygen deficiency exposure. This can contribute to new personalized medicine approaches’ development for diagnostics and the treatment of inflammatory and tumor diseases, taking into account hypoxia tolerance differences.

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Section: Physiological Biochemical and Molecular-biological Charsupporting

confidence: 93%

Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics

Джалилова

Makarova

2020

Biomedicines

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“…Hypoxia in mammalian cells is often correlated with a reduction in cytochrome levels and mitochondrial enzyme activities. In addition, respiration rates decrease in brain mitochondria of rats and mice exposed to intermittent hypobaric hypoxia (10,17,35,38). However, the resting and active respiration rates of liver and heart mitochondria isolated from rats acclimatized to hypobaric hypoxia did not differ from those of control rats (11), not even when measured at more physiological low oxygen concentrations (12).…”

Section: Discussionmentioning

confidence: 96%

Metabolic depression and enhanced O₂affinity of mitochondria in hypoxic hypometabolism

St‐Pierre

Tattersall

Boutilier

2000

American Journal of Physiology-Regulatory, Integrative and Comp

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This study examined whether the steady-state hypometabolism seen in overwintering frogs (Rana temporaria) is reflected at the mitochondrial level either by a reduction in their resting (state 4) and active (state 3) respiration rates and/or by increases in O(2) affinity. We isolated mitochondria from the skeletal muscle of cold-submerged frogs at different stages during their hibernation in normoxic and hypoxic water. A modest metabolic depression at the whole animal level (normoxic submergence) was not associated with a reduction in mitochondrial state 4 and state 3 respiration rates. However, mitochondria isolated from frogs that were submerged for 1 mo manifested an increase in their O(2) affinity compared with controls and with animals submerged for 4 mo. Hypometabolism was more pronounced at the whole animal level during hypoxic submergence and was accompanied by 1) a reduction in mitochondrial state 4 and state 3 rates and 2) an increase in the O(2) affinity of mitochondria. These findings demonstrate that metabolic depression can be reflected at all levels of biological organization in hypoxia-tolerant animals.

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“…Similar, though less pronounced differences in values of kinetic parameters are typical for cytochrome oxidase in BC of HR and LR animals. Therefore, in the LR BC, these enzymes faster become saturated with the enzyme-specific substrates (NADH or cyt- c ) and slower oxidize them, which may result in lower activity and faster inactivation of C-I (Dudchenko and Luk'yanova, 1995 , 1996 ; Luk'yanova et al, 1995 ).…”

Section: Features Of Respiratory Chain Reprogramming In Hypoxic Brainmentioning

confidence: 99%

“…For this reason, the suppression of BC C-I activity occurs earlier and is more marked in LR rats than in HR rats. Therefore, in different forms of hypoxic exposure, the switching of oxidation pathways for respiratory chain substrates from the NAD-dependent pathway to the succinate pathway is due to kinetic reasons (Luk'yanova et al, 1995 ). The existence of different kinetic properties of respiratory chain enzymes in HR and LR rat BC, a target for hypoxia, suggests that this phenomenon is genetically predetermined, and the energy metabolism is involved as a major factor determining formation of individual resistance.…”

Section: Features Of Respiratory Chain Reprogramming In Hypoxic Brainmentioning

confidence: 99%

Mitochondria-controlled signaling mechanisms of brain protection in hypoxia

2015

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The article is focused on the role of the cell bioenergetic apparatus, mitochondria, involved in development of immediate and delayed molecular mechanisms for adaptation to hypoxic stress in brain cortex. Hypoxia induces reprogramming of respiratory chain function and switching from oxidation of NAD-related substrates (complex I) to succinate oxidation (complex II). Transient, reversible, compensatory activation of respiratory chain complex II is a major mechanism of immediate adaptation to hypoxia necessary for (1) succinate-related energy synthesis in the conditions of oxygen deficiency and formation of urgent resistance in the body; (2) succinate-related stabilization of HIF-1α and initiation of its transcriptional activity related with formation of long-term adaptation; (3) succinate-related activation of the succinate-specific receptor, GPR91. This mechanism participates in at least four critical regulatory functions: (1) sensor function related with changes in kinetic properties of complex I and complex II in response to a gradual decrease in ambient oxygen concentration; this function is designed for selection of the most efficient pathway for energy substrate oxidation in hypoxia; (2) compensatory function focused on formation of immediate adaptive responses to hypoxia and hypoxic resistance of the body; (3) transcriptional function focused on activated synthesis of HIF-1 and the genes providing long-term adaptation to low pO2; (4) receptor function, which reflects participation of mitochondria in the intercellular signaling system via the succinate-dependent receptor, GPR91. In all cases, the desired result is achieved by activation of the succinate-dependent oxidation pathway, which allows considering succinate as a signaling molecule. Patterns of mitochondria-controlled activation of GPR-91- and HIF-1-dependent reaction were considered, and a possibility of their participation in cellular-intercellular-systemic interactions in hypoxia and adaptation was proved.

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Effects of adaptation to intermittent hypoxia on oxidative phosphorylation in brain mitochondria of rats with different sensitivities toward oxygen deficiency

Cited by 10 publications

References 2 publications

Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics

Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics

Metabolic depression and enhanced O₂affinity of mitochondria in hypoxic hypometabolism

Mitochondria-controlled signaling mechanisms of brain protection in hypoxia

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Effects of adaptation to intermittent hypoxia on oxidative phosphorylation in brain mitochondria of rats with different sensitivities toward oxygen deficiency

Cited by 10 publications

References 2 publications

Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics

Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics

Metabolic depression and enhanced O2affinity of mitochondria in hypoxic hypometabolism

Mitochondria-controlled signaling mechanisms of brain protection in hypoxia

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Metabolic depression and enhanced O₂affinity of mitochondria in hypoxic hypometabolism