Effects of intermittent hypoxia different regimes on mitochondrial lipid peroxidation and glutathione-redox balance in stressed rats

Gonchar, Olga

doi:10.2478/s11535-008-0016-7

Cited by 7 publications

(9 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our previous study, we demonstrated a decline in the MnSOD activity after severe hypoxia that is in accordance with an enhancement of superoxide production in mitochondria [8]. Consistent with the decreased MnSOD protein expression/activity found in our study, some authors [30] also observed that severe hypoxia in sessions of intermittent hypoxia causes a decrease in MnSOD protein expression in vivo with a marked diminution in the dismutating capacity in the liver, heart and brain tissues of animals subjected to intense intermittent hypoxia.…”

Section: Fig 4 Effect Of Short-and Long-term Hypoxia/reoxygenation supporting

confidence: 74%

“…MnSOD and GPxthe key antioxidant defense enzymes that function in concert to prevent ROS reactions in response to oxidative stress [5]. There are plenty of reports concerning the role of MnSOD and GPx in the cellular redox homeostasis involved in the adaptive responses against oxidative stress [6][7][8][9], although the mechanisms associated with protein expression and specific activity of MnSOD as well as GPx during H/R of different duration are not fully understood. In the past years, a number of transcription factors and signaling pathways have been identified and outlined to mediate critical transcriptional responses to oxidative stress [10].…”

mentioning

confidence: 99%

“…The effect of hypoxia/reoxygenation seems to be cell type specific [5,8,20], therefore, the organ that was considered was the heart as a site with the largest density/volume of mitochondria and an elevated rate of oxygen consumption under the nonstandard situa tion. H/R-induced tissues injury is of significance in cardiovascular pathophysiology because it occurs in a wide variety of clinical conditions, such as myocardial infarction, stroke, shock, cancer, and organ transplantation [1].…”

mentioning

confidence: 99%

See 2 more Smart Citations

Changes in proHB-EGF expression after functional activation of the immune system cells

Gonchar¹,

Mankovskaya²

2017

Ukr.Biochem.J.

View full text Add to dashboard Cite

The intensity of oxidative stress, protein expression of antiapoptotic Bcl-2 as well as antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GPx) and their regulator p53 were studied in the mitochondria of rat heart. Sessions of repeated hypoxia/reoxygenation ((h/r) A large body of experimental data indicates that reactive oxygen species (ROS) play a fundamental role in hypoxia/reoxygenation injury of cells and subcellular structures [1]. Mitochondria are considered an important locus of ROS production mainly at the level of complexes I and III of the respiratory chain and hence a potential contributor to cells damage during hypoxia [2]. At the same time, mitochondria could be major targets of ROS attack. These events result in mitochondrial dysfunction with superoxide leakage, the formation of other aggressive ROS which attack lipids, proteins and other cell constituents, lead to energy and metabolic disorders, deplete of cellular antioxidant defense, and induce the apoptotic cascade [1,2].In general, mitochondrial oxidative stress is determined by the balance between ROS generation and their elimination by antioxidants [3]. The antioxidants and free radical scavenging enzymes, including MnSOD, peroxiredoxin 3 and 5, thioredoxin, glutathione, and glutathione peroxidase, not only constitute the first line of defense against oxidative damage within the mitochondria but also are essential for maintaining the critical cellular redox balance and play key role in modulating cellular responses to external stimuli [4]. MnSOD and GPxthe key antioxidant defense enzymes that function in concert to prevent ROS reactions in response to oxidative stress [5]. There are plenty of reports concerning the role of MnSOD and GPx in the cellular redox homeostasis involved in the adaptive responses against oxidative stress [6][7][8][9], although the mechanisms associated with protein expression and specific activity of MnSOD as well as GPx during H/R of different duration are not fully understood.

show abstract

Section: Fig 4 Effect Of Short-and Long-term Hypoxia/reoxygenation supporting

confidence: 74%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Changes in proHB-EGF expression after functional activation of the immune system cells

Gonchar¹,

Mankovskaya²

2017

Ukr.Biochem.J.

View full text Add to dashboard Cite

show abstract

“…Investigations performed in our and other laboratories have shown that adaptation to IHT as well as hyperbaric oxygenation (HO) could reduce the oxidative stress-induced damage caused by extremal influences such as ischemia, exhaustive physical exercise, more severe and sustained hypoxia, and emotional stress [11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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

Gonchar

Mankovskaya

2012

Open Life Sciences

Self Cite

View full text Add to dashboard Cite

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.

show abstract

“…The second one includes enzymes maintaining redox homeostasis within the cell [glutathione reductase (GSR), thioredoxins (TXNs) and its reductases (TXRD)], and the third one includes antioxidants related to iron metabolism [heme oxygenase (HMOX) and aconitase (ACO1)]. Apparently, different components of the cardiac antioxidant system may participate in the antioxidant response to diverse hypoxic conditions (10,11,30,42).Studies dealing with antioxidant responses of the heart to chronic hypoxic stress provide only fragmented information, and heterogeneous data obtained in diverse models and protocols of hypoxia under different experimental conditions do not offer a clear view on this issue. In the present study we aimed to assess the level of oxidative stress and mRNA transcripts of 20 antioxidant genes and related regulatory proteins in rat myocardium after adaptation to three regimens of chronic hypoxia that differ in their ability to reduce I/R injury.…”

mentioning

confidence: 99%

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems

Kasparova

Neckář

Dabrowská

et al. 2015

Physiological Genomics

View full text Add to dashboard Cite

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems. Physiol Genomics 47: 612-620, 2015. First published October 13, 2015; doi:10.1152/physiolgenomics.00058.2015.-It has been documented that adaptation to hypoxia increases myocardial tolerance to ischemia-reperfusion (I/R) injury depending on the regimen of adaptation. Reactive oxygen species (ROS) formed during hypoxia play an important role in the induction of protective cardiac phenotype. On the other hand, the excess of ROS can contribute to tissue damage caused by I/R. Here we investigated the relationship between myocardial tolerance to I/R injury and transcription activity of major antioxidant genes, transcription factors, and oxidative stress in three different regimens of chronic hypoxia. Adult male Wistar rats were exposed to continuous normobaric hypoxia (FIO 2 0.1) either continuously (CNH) or intermittently for 8 h/day (INH8) or 23 h/day (INH23) for 3 wk period. A control group was kept in room air. Myocardial infarct size was assessed in anesthetized open-chest animals subjected to 20 min coronary artery occlusion and 3 h reperfusion. Levels of mRNA transcripts and the ratio of reduced and oxidized glutathione (GSH/GSSG) were analyzed by real-time RT-PCR and by liquid chromatography, respectively. Whereas CNH as well as INH8 decreased infarct size, 1 h daily reoxygenation (INH23) abolished the cardioprotective effect and decreased GSH/GSSG ratio. The majority of mRNAs of antioxidant genes related to mitochondrial antioxidant defense (manganese superoxide dismutase, glutathione reductase, thioredoxin/thioredoxin reductase, and peroxiredoxin 2) were upregulated in both cardioprotective regimens (CNH, INH8). In contrast, INH23 increased only PRX5, which was not sufficient to induce the cardioprotective phenotype. Our results suggest that the increased mitochondrial antioxidant defense plays an important role in cardioprotection afforded by chronic hypoxia. adaptation to hypoxia; cardioprotection; ischemia-reperfusion injury; oxidative stress; antioxidant defense ADAPTATION TO CHRONIC HYPOXIA may improve cardiac tolerance to acute ischemia-reperfusion (I/R) injury under certain conditions. Whereas chronic continuous hypoxia induces a protective cardiac phenotype, a brief daily interruption of hypoxic adaptation for 1 h eliminates the protective effect (31). Tissue damage caused by I/R insult is tightly related to the excess of reactive oxygen species (ROS), but the exact molecular mechanism underlying these adverse effects is still not fully elucidated. Intracellular ROS initiate a sequence of oxidation reactions that can seriously damage cell structures. ROS differ in their reactivity, as well as in mechanisms and sites of their production. These harmful species can be eliminated by specific scavengers. If production of ROS exceeds the capacity limit of antioxidant systems or if the systemic capacity is insufficient, the level of ROS in individual cell compartments increases and generates ...

show abstract

Effects of intermittent hypoxia different regimes on mitochondrial lipid peroxidation and glutathione-redox balance in stressed rats

Cited by 7 publications

References 40 publications

Changes in proHB-EGF expression after functional activation of the immune system cells

Changes in proHB-EGF expression after functional activation of the immune system cells

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

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems

Contact Info

Product

Resources

About