Moderate intermittent hypoxia/hyperoxia: implication for correction of mitochondrial dysfunction

The purpose of this study was to appreciate the acute hypoxia-induced mitochondrial oxidative damage development and the role of adaptation to hypoxia/hyperoxia (H/H) in correction of mitochondrial dysfunction. It was demonstrated that long-term sessions of moderate H/H [5 cycles of 5 min hypoxia (1...

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Bibliographic Details
Published in:Central European journal of biology 2012-10, Vol.7 (5), p.801-809
Main Authors: Gonchar, Olga A, Mankovska, Irina N
Format: Article
Language:English
Subjects:
Acute hypoxia
Biochemistry
Biomedical and Life Sciences
Biotechnology
Cell Biology
gene expression
glutathione peroxidase
Human Genetics
hydrogen peroxide
hyperoxia
hypoxia
Immunology
Intermittent hypoxia/hyperoxia
Life Sciences
lipid peroxidation
liver
messenger RNA
mitochondria
Mitochondrial dysfunction
Mn-SOD expression
oxygen
post-translational modification
protective effect
proteins
rats
Research Article
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Summary:The purpose of this study was to appreciate the acute hypoxia-induced mitochondrial oxidative damage development and the role of adaptation to hypoxia/hyperoxia (H/H) in correction of mitochondrial dysfunction. It was demonstrated that long-term sessions of moderate H/H [5 cycles of 5 min hypoxia (10% O2 in N2) alternated with 5 min hyperoxia (30% O2 in N2) daily for two weeks]_attenuated basal and Fe2+/ascorbate-induced lipid peroxidation (LPO) as well as production of carbonyl proteins and H2O2 in liver mitochondria of rats exposed to acute severe hypoxia (7% O2 in N2, 60 min) in comparison with untreated animals. It was shown that H/H increases the activity of glutathione peroxidase (GPx), reduces hyperactivation of Mn-SOD, and decreases Cu,Zn-SOD activity as compared with untreated rats. It has been suggested that the induction of Mn-SOD protein expression and the coordinated action of Mn-SOD and GPx could be the mechanisms underlying protective effects of H/H, which promote the correction of the acute hypoxia-induced mitochondrial dysfunction. The increase in Mn-SOD protein synthesis without changes in Mn-SOD mRNA level under H/H pretreatment indicates that the Mn-SOD activity is most likely dependent on its posttranslational modification or on the redox state of liver mitochondria.
ISSN:1895-104X
2391-5412
1644-3632
2391-5412
DOI:10.2478/s11535-012-0072-x