Signaling Role of Mitochondrial Enzymes and Ultrastructure in the Formation of Molecular Mechanisms of Adaptation to Hypoxia

This study was the first comprehensive investigation of the dependence of mitochondrial enzyme response (catalytic subunits of mitochondrial complexes (MC) I-V, including NDUFV2, SDHA, Cyt b, COX1 and ATP5A) and mitochondrial ultrastructure in the rat cerebral cortex (CC) on the severity and duratio...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-08, Vol.22 (16), p.8636
Main Authors: Lukyanova, Ludmila, Germanova, Elita, Khmil, Natalya, Pavlik, Lybov, Mikheeva, Irina, Shigaeva, Maria, Mironova, Galina
Format: Article
Language:English
Subjects:
Adaptation
adaptation to hypoxia
Animals
Catalytic subunits
catalytic subunits of mitochondrial complexes (MC- I-V)
Cerebral cortex
Electron transport
Enzymes
Exposure
Homeostasis
Hypoxia
Low resistance
Metabolism
Mitochondria
mitochondrial dynamics
mitochondrial enzymes
Molecular modelling
Oxygen probes
Respiration
Ultrastructure
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Summary:This study was the first comprehensive investigation of the dependence of mitochondrial enzyme response (catalytic subunits of mitochondrial complexes (MC) I-V, including NDUFV2, SDHA, Cyt b, COX1 and ATP5A) and mitochondrial ultrastructure in the rat cerebral cortex (CC) on the severity and duration of in vivo hypoxic exposures. The role of individual animal’s resistance to hypoxia was also studied. The respiratory chain (RC) was shown to respond to changes in environmental [O2] as follows: (a) differential reaction of mitochondrial enzymes, which depends on the severity of the hypoxic exposure and which indicates changes in the content and catalytic properties of mitochondrial enzymes, both during acute and multiple exposures; and (b) ultrastructural changes in mitochondria, which reflect various degrees of mitochondrial energization. Within a specific range of reduced O2 concentrations, activation of the MC II is a compensatory response supporting the RC electron transport function. In this process, MC I develops new kinetic properties, and its function recovers in hypoxia by reprograming the RC substrate site. Therefore, the mitochondrial RC performs as an in vivo molecular oxygen sensor. Substantial differences between responses of rats with high and low resistance to hypoxia were determined.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22168636