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Moderate Intermittent Hypoxia/Hyperoxia: Implication for Correction of Mitochondrial Dysfunction

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Moderate Intermittent Hypoxia/Hyperoxia: Implication for Correction of Mitochondrial Dysfunction Cent. Eur. J. Biol. • 7(5) • 2012 • 801-809 DOI: 10.2478/s11535-012-0072-x Central European Journal of Biology Moderate intermittent hypoxia/hyperoxia: implication for correction of mitochondrial dysfunction Research Article Olga A. Gonchar*, Irina N. Mankovska Department of Hypoxic States, Bogomoletz Institute of Physiology National Academy of Sciences of Ukraine, 01024 Kiev, Ukraine Received 26 January 2012; Accepted 06 June 2012 Abstract: 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 2+ basal and Fe /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. Keywords: Intermittent hypoxia/hyperoxia • Acute hypoxia • Mitochondrial dysfunction • Mn-SOD expression © Versita Sp. z o.o. 1. Introduction of mitochondrial free radical oxidation and antioxidant capacity as well as the influence of these processes Oxidative stress is a common and fundamental cause on the functional and structural integrity of mitochondria of a wide range of pathophysiologic conditions [1]. and on the redox regulation of many cellular functions. Mitochondria can represent a significant source of Although O2- is generated from several sites in the reactive oxygen species (ROS), which in addition to mitochondria, the main source of mitochondrial O2- cytosolic NAD(P)H oxidase and xanthine oxidase appears to be within the inner mitochondrial membrane, contribute to the vicious cycle of ROS production [2]. at complexes I and III of the electron transport chain in Recent findings pointed out that severe hypoxia could particular [6]. Superoxide is transformed to hydrogen cause cellular oxidative stress with consequent damage peroxide by the detoxification enzymes (Mn-SOD in matrix to lipids, proteins, and DNA [3,4]. Oxidative damage to or CuZn-SOD in intermembrane space [7]) and then to mitochondrial membranes, enzymes, electron transport water by glutathione peroxidase (GPx) or peroxiredoxin chain components, ATP production, permeability III and V. However, when these enzymes cannot convert transition pore opening, and imbalance in the ROS fast enough or act not in concordance, oxidative antioxidant systems lead to mitochondrial dysfunction damage occurs and accumulates in the mitochondria [8]. [5]. Dysfunctional mitochondria will produce more Mitochondrial ROS generation and antioxidant ROS and cause additional damage [4]. The monitoring capacity are potential targets for pharmacological and of the changes in mitochondrial pro-and anti-oxidant molecular approaches to correct oxidative stress- balance deserves special attention, due to the intensity induced injuries, including mitochondrial dysfunction. * E-mail: [email protected] 801 Moderate intermittent hypoxia/hyperoxia: implication for correction of mitochondrial dysfunction In this study, we suggested an alternative approach 2. Experimental Procedures instead of the standard antioxidant therapy. This approach was to induce the own protective antioxidant system of an 2.1 Materials organism by applying a new regime of adaptive training, All chemicals were purchased from Sigma, Fluka and which combines periods of hypoxia and hyperoxia (H/H). Merck and were of the highest purity. Clinical and experimental studies have confirmed beneficial effects of intermittent hypoxic training 2.2 Animals and study design (IHT) on hypoxic ventilatory response, an increase Male Wistar rats weighing 220-260 g were used. in the red blood cell mass, erythropoietin level, and The experimental animals were housed in Plexiglas aerobic capacity as well as enhance mRNA myoglobin, cages (4 rats per cage) and kept in an air-filtered and hypoxia-inducible factor-1, and vascular endothelial temperature-controlled (20-22°C) room. Rats received a growth factor expression in human muscle after acute standard pellet diet and water ad libitum and were kept exercise [9,10]. Investigations performed in our and under an artificial light-dark cycle of 12 h. The present other laboratories have shown that adaptation to study was approved by the Animal Ethics Committee at IHT as well as hyperbaric oxygenation (HO) could the Bogomoletz Institute of Physiology, Kiev, Ukraine reduce the oxidative stress-induced damage caused (Protocol No 5/17). Rats were randomly divided into by extremal influences such as ischemia, exhaustive four groups (eight animals in each). Animals of group physical exercise, more severe and sustained hypoxia, 1 were kept under normoxic conditions and served as and emotional stress [11-15]. a control. In group 2, rats were exposed to a single The basis of these effects is moderate periodic action of acute hypoxia by breathing with the hypoxic generation of free radical signal during changes in the gaseous mixture (7% O2 in N2) for 60 min. Group 3 oxygen level which induced the activation of various included animals subjected to sessions of intermittent metabolic processes and may be an important trigger hypoxia/hyperoxia. We applied repeated short-term for specific adaptation [16]. It is known that the periodic 5-min inhalation of gaseous mixture containing 10% O2 activation of ROS during IHT and HO is involved in a in N2 with 5-min intervals of hyperoxia (breathing with cascade of intracellular redox signaling with subsequent the hyperoxic gaseous mixture containing 30% O2 in activation of redox-sensitive transcription factors and N2) under normobaric condition in a special chamber genes controlling the synthesis of protective components where the temperature and humidity were maintained at (including antioxidants), which improves the organism’s 21-26ºC and 55-60%, respectively. Rats had five similar resistance to oxidative stress [17]. H/H is characterized sessions daily for 14 days. The gaseous mixtures with by upregulation of adaptive ROS signals compared low and high content of O2 were obtained with the help to classical IHT and HO and therefore represents an of a device (“Metaks” Co) operating on the membrane interesting approach for the formation of protective gas partition principle with on-line computer control reactions. of O2 levels in isolated animal cages. Rats of group 4 Many studies have explained the important role of were exposed to acute hypoxia on the first day after Mn-SOD in the prevention of oxidative stress [18-20]. cessation of the intermittent hypoxia/hyperoxia training However, little is known about the gene and protein course. Animals were decapitated immediately after the expression of Mn-SOD during H/H and its participation experiment. At the time of sacrifice, the rats were lightly in correction of mitochondrial dysfunction. anesthetized with ether. The present study was thus designed to evaluate the effect of prolonged intermittent moderate H/H on 2.3 Mitochondria isolation prooxidant/antioxidant balance in liver mitochondria of Rat liver mitochondria were isolated by differential rats exposed to acute severe hypoxia. Investigation of centrifugation as described by Jonson and Lardy [21], the indices of lipid peroxidation (LPO), protein carbonyl with some modifications. Liver was collected in isolation content, H2O2 production, as well as the activity of medium A (250 mM sucrose, 10 mM Tris/HCI (pH 7.6) key antioxidant enzymes such as Cu,Zn-, Mn-SOD, and 1 mM EGTA) and homogenized. After centrifugation and GPx permit us to appreciate the acute hypoxia- of the homogenate at 1000xg for 5 min, the supernatant induced mitochondrial oxidative damage development was strained on gauze and recentrifuged at 12000xg and the role of adaptation to H/H in correction of for 15 min. The resulting pellet was resuspended in mitochondrial dysfunction. In the present study mRNA, ice-cold isolation medium B (250 mM sucrose, 10 mM protein expression, and the specific activity of Mn-SOD Tris/HCI (pH 7.6) and 0.1 mM EGTA) and a new series at different oxygen levels as important biomarkers of of centrifugation was performed. The final washing oxidative stress were analyzed. and resuspension of mitochondria was in medium B 802 O.A. Gonchar, I.N. Mankovska without EGTA. Mitochondrial protein concentration was 7.4) for 1 h at 37ºC. Mn-SOD proteins were detected estimated by the Lowry method, using bovine serum using primary monoclonal antibody for Mn-SOD albumin as a standard. (Sigma-Aldrich Co) at a dilution 1:1000 for 2 h at 37ºC, followed by incubation with horseradish peroxidase- 2.4 Biochemical assays conjugated secondary antibody (Sigma-Aldrich
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