Hyperglycemia is known to cause oxidative stress that leads mainly to enhanced production of mitochondrial reactive oxygen species (ROS). It has been demonstrated that hyperbaric oxygen (HBO) treatment also increases the formation of ROS. There are, however, no comprehensive evaluations of such oxidative effects in diabetes which requires HBO treatment. The purpose of this study is to investigate the influence of a clinically-recommended HBO treatment on glucose homeostasis and oxidative stress in rats with streptozotocin (STZ)-induced diabetes. Under the clinically-used HBO exposure protocol, the levels of blood glucose, thiobarbituric acid reactive substances (TBARS) as a lipid peroxidation marker, and the activity of superoxide dismutase (SOD) as an antioxidant enzyme marker were investigated in the erythrocytes, liver, pancreas, skeletal muscle, and brain of rats with STZ-induced diabetes. The levels of blood glucose and TBARS increased significantly (p<0.05), and the activity of SOD decreased significantly (p<0.05) in the erythrocytes and all organs of rats with diabetes subjected to HBO exposure. These results suggested that HBO exposure might boost glucose autoxidation and increase ROS production in STZ-induced diabetes as side-effects of administering HBO treatment for the first time., T. Matsunami ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
As a consequence of enhanced production of oxygen free radicals, lipid peroxidation leads to the degradation of membrane lipids and disturbances of membrane permeability. Lipid peroxidation increases under stress conditions such as hypoxia, ischemia or acidosis as well as in metabolic diseases, e.g. diabetes mellitus. We have shown that subcomatous doses of insulin (6.0 IU/kg) significantly increase thiobarbituric acid reactive substances (TBARs), especially malondialdehyde (MDA) - the endproduct of lipid peroxidation, in the brain and heart of mice. In our model of insulin-induced hypoglycemia, mice were treated with the neuroprotective, peptide-containing drug Cerebrolysin (100 mg/kg b.w.). Animals were sacrificed by decapitation two or three hours after the injection of tested substance and samples were taken to determine several serum parameters (glucose, total protein, triglycerides and lactic acid) and TBARs in the brain and heart. Although Cerebrolysin was not able to affect serum parameters after subcomatous insulin injection, the drug significantly influenced lipid peroxidation. A single injection of Cerebrolysin already decreased TBARs levels in the brain and heart tissue. Presuming that an increase of TBARs reflects disturbances of the cell membrane, we have documented a promising effect of Cerebrolysin on cell integrity., J. Patočková, M. Kršiak, P. Marhol, E. Tůmová., and Obsahuje bibliografii
Considering the preexisting influence of the process of natural aging on antioxidant enzymes activity and the level of lipid peroxidation, the age of the rats at which D-galactose (D-gal) treatment is started could strongly impact the development of D-gal induced senescence. To eval uate this, we subjected 1, 3 and 15 months old rats to D-gal treatment in parallel with having appropriate placebos (0.9 % saline). Our results showed elevated glutathione peroxidase (GPx) acti vity and no significant changes in superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) activity or malondialdehyde (MDA) levels in relation to natural aging. In mature and aged senescent livers we observed positive correlation between increased ratio R=SOD/(GPx+CAT) and increased MDA concentration. MDA levels seemed to correlate positively with the age of the animals at which D-gal treatment had started. In the case of 3 and 15 months old rats there was D-gal induced decrease in SOD and GR activity, but this effect of the treatment was not observed in 1 month old rats. Our results imply that the changes in the antioxidant enzyme activities are not only under the influence of the D-gal overload, but also depend on the developmental stage of the rats. According to our resu lts, with regard to enzymatic antioxidant capacity and the level of lipid peroxidation, the best age for induction of senescence is somewhere after the third month., N. Hadzi-Petrushev, V. Stojkovski, D. Mitrov, M. Mladenov., and Obsahuje bibliografii
Despite the demonstrated exercise -induced increase in reactive oxygen species (ROS) production, growing epidemiological evidence indicates that habitual, moderate physical activity reduces the incidence of several oxidative stress-based diseases. This apparent paradox can be explained taking into account that ROS produced during repeated ex ercise bouts may act as mild stressors able to trigger physiological and biomolecular hormetic responses through a number of redox-sensitive transcription pathways. Unfortunately, much more limited information is available from general population-based research, which could better reflect the condition of common people interested in achieving and maintaining good fitness levels. The present work aimed at investigatin g whether and how exercise-related habits in non-professional regular runners (n=33) can affect the systemic anti-oxidative capacity, and the resting serum levels of typical lipid peroxidation-related by-products and oxidatively- damaged proteins, in comparison with untrained sedentary individuals (n=25). We also anal yzed in both groups the redox response elicited by a modified Bruce-based maximal exercise test on the same parameters. Our findings indicated that long- term regular and moderate practice of aerobic physical activity can increase antioxidant defense systems, lower the resting protein oxidation processes and reduce the immediate up- regulation of lipid-targeting oxidative stress in response to an acute bout of exercise., S. Falone, A. Mirabilio, A. Pennelli, M. Cacchio, A. Di Baldassarre, S. Gallina, A. Passerini, F. Amicarelli., and Obsahuje bibliografii
Hypoxic exposure triggers a generation of reactive oxygen species that initiate free radical damage to the lung. Hydrogen peroxide is the product of alveolar macrophages detectable in the expired breath. We evaluated the significance of breath H2O2 concentration for the assessment of lung damage after hypoxic exposure and during posthypoxic period. Adult male rats were exposed to normobaric hypoxia (10 % O2) for 3 hours or 5 days. Immediately after the hypoxic exposure and then after 7 days or 14 days of air breathing, H2O2 was determined in the breath condensate and in isolated lung macrophages. Lipid peroxidation was measured in lung homogenates. Three-hour hypoxia did not cause immediate increase in the breath H2O2; 5-day hypoxia increased breath H2O2 level to 458 %. After 7 days of subsequent air breathing H2O2 was elevated in both groups exposed to hypoxia. Increased production of H2O2 by macrophages was observed after 5 days of hypoxia and during the 7 days of subsequent air breathing. Lipid peroxidation increased in the periods of enhanced H2O2 generation by macrophages. As the major increase (1040 %) in the breath H2O2 concentration found 7 days after 3 hours of hypoxia was not accompanied by lipid peroxidation, it can be concluded that the breath H2O2 is not a reliable indicator of lung oxidative damage., J. Wilhelm, M. Vaňková, H. Maxová, A. Šišková., and Obsahuje bibliografii
The present study was designed to evaluate the plasma markers of reactive oxygen species (ROS) activity and cytokines, and their relationship with thiol redox status of basketball players during training. Sixteen professional players of the Polish Basketball Extraleague participated in the study. The study was performed during the preparatory period and the play-off round. Markers of ROS activity (lipid peroxidation TBARS, protein carbonylation PC) and reduced glutathione (GSH) demonstrated regularity over time, i.e. TBARS, PC and GSH were elevated at the beginning and decreased at the end of training periods. Oxidized glutathione (GSSG) was not affected by exercise training. Thiol redox status (GSHtotal-2GSSG/GSSG) correlated with TBARS and PC in both training periods. The level of interleukin-6 (IL-6) was increased and positively correlated with thiol redox (r=0.423) in the preparatory period, whereas tumor necrosis factor α (TNFα) was increased and inversely correlated with thiol redox (r=-0.509) in the play-off round. The present study showed significant shifts in markers of ROS activity, thiol redox status and inflammatory mediators (IL-6, TNFα) following professional sport training as well as correlation between changes in thiol redox and cytokine response., A. Zembron-Lacny, M. Slowinska-Lisowska, A. Ziemba., and Obsahuje bibliografii a bibliografické odkazy
Hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) play an important role in brain control of blood pressure (BP). One of the important mechanisms involved in the pathogenesis of hypertension is the elevation of reactive oxygen species (ROS) production by nicotine adenine dinucleotide phosphate (NADPH) oxidase. The aim of our present study was to investigate NADPH oxidase -mediated superoxide (O 2 - ) production and to search for the signs of lipid peroxidation in hypothalamus and medulla oblongata as well as in renal medulla and cortex of hypertensive male rats transgenic for the murine Ren -2 renin gene (Ren -2 TGR) and their age -matched normotensive controls ‒ Hannover Sprague Dawley rats (HanSD) . We found no difference in the activity of NADPH oxidase measured as a lucigenin -mediated O 2 - production in the hypothalamus and medulla oblongata. However, we observed significantly elevated NADPH oxidase in both renal cortex and medulla of Ren -2 TGR com pared with HanSD. Losartan (LOS) treatment (10 mg/kg body weight/day) for 2 months (Ren -2 TGR+LOS) did not change NADPH oxidase -dependent O 2 - production in the kidney. We detected significantly elevated indirect m arkers of lipid peroxidation measured as th iobarbituric acid -reactive substance s (TBARS) in Ren -2 TGR, while they were significantly decreased in Ren -2 TGR +LOS. In conclusion, the present study shows increased NADPH oxidase activities in renal cortex and medulla with significantly increased TBARS in renal cortex. No significant changes of NADPH oxidase and markers of lipid peroxidation were detected in the studied brain regions., M. Vokurková, H. Rauchová, L. Řezáčová, I. Vaněčková, J. Zicha., and Obsahuje bibliografii
Enhanced production of superoxide radicals by nicotinamideadenine dinucleotide phosphate (NADPH) oxidase in the brain and/or kidney of salt hypertensive Dahl rats has been proposed to participate in the pathogenesis of this form of experimental hypertension. Most information was obtained in young Dahl saltsensitive (DS) rats subjected to high salt intake prior to sexual maturation. Therefore, the aim of our study was to investigate whether salt hypertension induced in adult DS rats is also accompanied with a more pronounced oxidative stress in the brain or kidney as compared to Dahl salt-resistant (DR) controls. NADPH oxidase activity as well as the content of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (oxidative index), which indicate a degree of lipid peroxidation, were evaluated in two brain regions (containing either hypothalamic paraventricular nucleus or rostral ventrolateral medulla) as well as in renal medulla and cortex. High salt intake induced hypertension in DS rats but did not modify blood pressure in DR rats. DS and DR rats did not differ in NADPH oxidase-dependent production of ROS, TBARS content or oxidative index in either part of the brain. In addition, high-salt diet did not change significantly any of these brain parameters. In contrast, the enhanced NADPH oxidase-mediated ROS production (without significant signs of increased lipid peroxidation) was detected in the renal medulla of salt hypertensive DS rats. Our findings suggest that there are no signs of enhanced oxidative stress in the brain of adult Dahl rats with salt hypertension induced in adulthood., M. Vokurková, H. Rauchová, L. Řezáčová, I. Vaněčková, J. Zicha., and Obsahuje bibliografii
This study was designed to investigate effect of alpha-lipoic acid (LA) on lipid peroxidation, nitric oxide production and antioxidant systems in rats exposed to chronic restraint stress. Twenty four male Wistar rats, aged three months, were divided into four groups: control (C), the group treated with LA (L), the group exposed to restraint stress (S) and the group exposed to stress and treated with LA (LS). Restraint stress was applied for 21 days (1 h/day) and LA (100 mg/kg/day) was injected intraperitonally to the L and LS groups for the same period. Restraint stress significantly decreased brain copper/zinc superoxide dismutase (Cu,Zn-SOD) and brain and retina glutathione peroxidase (GSH-Px) and catalase (CAT) activities compared with the control group. Thiobarbituric acid reactive substances (TBARS), nitrite and nitrate levels were significantly increased in the tissues of the S group compared with the C group. LA produced a significant decrease in brain and retina TBARS, nitrite and nitrate levels of the L and LS groups compared to their corresponding control groups. LA increased all enzyme activities in the tissues of the LS group compared to the S group. Our study indicated that LA is an ideal antioxidant candidate for the prevention of stress-induced lipid peroxidation., D. Akpinar, P. Yargiçoğlu, N. Derin, Y. Alicigüzel, A. Ağar., and Obsahuje bibliografii a bibliografické odkazy
Cytochrome oxidase activity from the retina can be enhanced or depressed by free radical-mediated reactions both in positive and negative aspect. The greatest effect was exerted by ischemia/reperfusion, which significantly increased the fluorescent products of lipid peroxidation (358 %, P<0.01) and inhibited the enzyme activity (14 %, P<0.001). After hyperoxia the fluorescent products slightly increased (192 %, P< 0.05) as well as the enzyme activity (133 %, P<0.05). Hypoxia had no effect on any of these parameters. Specific changes in the composition of fluorophores after ischemia/reperfusion were revealed in the fluorescence spectra. The fact that increased lipid peroxidation after hyperoxia and after ischemia/reperfusion does not produce the same effect upon cytochrome oxidase activity might be explained by changes in the kinetic behavior of cytochrome oxidase. In the control enzyme preparation, two binding sites for cytochrome c were observed. One was of the low-affinity (Km=60 mM) and the other of the high-affinity (Km=1.12 mM). After in vitro-initiated lipid peroxidation, the low-affinity binding site was lost and the activity measured under "optimum" conditions at a single cytochrome concentration was higher than in the controls. This implies that oxidative damage to cytochrome oxidase in vivo can be site-specific and its extent should be estimated by performing detailed kinetic analysis as otherwise the results might be misleading., A. Šišková, J. Wilhelm., and Obsahuje bibliografii