Effect of Long-Term Normobaric Hyperoxia on Oxidative Stress in Mitochondria of the Guinea Pig Brain

Tatarková, Zuzana; Engler, Ivan; Čalkovská, Andrea; Mokrá, Daniela; Drgová, A; Hodas, Peter; Lehotský, Ján; Dobrota, Dušan; Kaplán, Peter

doi:10.1007/s11064-011-0473-7

Cited by 25 publications

(24 citation statements)

References 30 publications

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“…Hyperoxia has been long known to increase the generation of reactive oxygen species (Jamieson et al, 1986), which could cause oxidative damage to lipids and proteins (Tatarkova et al, 2011). Reactive oxygen species may in turn decrease enzymatic activities in aerobic metabolism pathways via inhibition of pyruvate dehydrogenase (Bogaert et al, 1994), a critical enzyme in transforming pyruvate into acetyl-CoA for the citric acid cycle.…”

Section: Physiological Considerationsmentioning

confidence: 99%

Effect of Hypoxia and Hyperoxia on Cerebral Blood Flow, Blood Oxygenation, and Oxidative Metabolism

Liu

Pascual

et al. 2012

J Cereb Blood Flow Metab

152

182

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Characterizing the effect of oxygen (O 2 ) modulation on the brain may provide a better understanding of several clinically relevant problems, including acute mountain sickness and hyperoxic therapy in patients with traumatic brain injury or ischemia. Quantifying the O 2 effects on brain metabolism is also critical when using this physiologic maneuver to calibrate functional magnetic resonance imaging (fMRI) signals. Although intuitively crucial, the question of whether the brain's metabolic rate depends on the amount of O 2 available has not been addressed in detail previously. This can be largely attributed to the scarcity and complexity of measurement techniques. Recently, we have developed an MR method that provides a noninvasive (devoid of exogenous agents), rapid ( < 5 minutes), and reliable (coefficient of variant, CoV < 3%) measurement of the global cerebral metabolic rate of O 2 (CMRO 2 ). In the present study, we evaluated metabolic and vascular responses to manipulation of the fraction of inspired O 2 (FiO 2 ). Hypoxia with 14% FiO 2 was found to increase both CMRO 2 (5.0±2.0%, N = 16, P = 0.02) and cerebral blood flow (CBF) (9.8±2.3%, P < 0.001). However, hyperoxia decreased CMRO 2 by 10.3 ± 1.5% (P < 0.001) and 16.9 ± 2.7% (P < 0.001) for FiO 2 of 50% and 98%, respectively. The CBF showed minimal changes with hyperoxia. Our results suggest that modulation of inspired O 2 alters brain metabolism in a dose-dependent manner.

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Section: Physiological Considerationsmentioning

confidence: 99%

Effect of Hypoxia and Hyperoxia on Cerebral Blood Flow, Blood Oxygenation, and Oxidative Metabolism

Liu

Pascual

et al. 2012

J Cereb Blood Flow Metab

152

182

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“…21 Several factors can account for these conflicting results, which include timing and the duration of oxygen therapy. 25 Tatarkova et al 26 demonstrated that prolonged NBO treatment is accompanied by a significant increase in mitochondrial oxidative damage. This is consistent with findings that prolonged exposure to hyperoxia can activate apoptosis.…”

Section: Strokementioning

confidence: 99%

Synergetic Neuroprotection of Normobaric Oxygenation and Ethanol in Ischemic Stroke Through Improved Oxidative Mechanism

et al. 2013

Stroke

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Background and Purpose— Normobaric oxygenation (NBO) and ethanol both provide neuroprotection in stroke. We evaluated the enhanced neuroprotective effect of combining these 2 treatments in a rat stroke model. Methods— Sprague-Dawley rats were subjected to middle cerebral artery occlusion for 2 hours. Reperfusion was then established and followed by treatment with either (1) an intraperitoneal injection of ethanol (1.0 g/kg), (2) NBO treatment (2-hour duration), or (3) NBO plus ethanol. The extent of brain injury was determined by infarct volume and motor performance. Oxidative metabolism was determined by ADP/ATP ratios, reactive oxygen species levels, nicotinamide adenine dinucleotide phosphate oxidase activity, and pyruvate dehydrogenase activity. Protein expression of major nicotinamide adenine dinucleotide phosphate oxidase subunits (p47 phox , gp91 phox , and p67 phox ) and the enzyme pyruvate dehydrogenase was evaluated through Western immunoblotting. Results— NBO and ethanol monotherapies each demonstrated reductions as compared to stroke without treatment in infarct volume (36.7% and 37.9% vs 48.4%) and neurological deficits (score of 6.4 and 6.5 vs 8.4); however, the greatest neuroprotection (18.8% of infarct volume and 4.4 neurological deficit) was found in animals treated with combination therapy. This neuroprotection was associated with the largest reductions in ADP/ATP ratios, reactive oxygen species levels, and nicotinamide adenine dinucleotide phosphate oxidase activity, and the largest increase in pyruvate dehydrogenase activity. Conclusions— Combination therapy with NBO and ethanol enhances the neuroprotective effect produced by each therapy alone. The mechanism behind this synergistic action is related to changes in cellular metabolism after ischemia reperfusion. NBO plus ethanol is attractive for clinical study because of its ease of use, tolerability, and tremendous neuroprotective potential in stroke.

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“…•+ ) for 60 h as described previously (Tatarkova et al 2011). The O 2 concentration was monitored periodically by an oxygen analyzer (Permolyt 3, Veb Junkalor, Germany).…”

Section: Animals and Nbo Treatmentmentioning

confidence: 99%

“…The molecular mechanisms responsible for side effects of hyperoxia are not yet fully understood, however, excessive formation of reactive oxygen species (ROS) has been proposed as one of potential factors mediating damaging effects (Narkowicz et al 1993). In animal studies, it was shown that oxygenation treatment significantly increases lipid and protein oxidative damage in the heart, brain and other organs and tissues (Hensley et al 1995;Chavko and Harabin 1996;Ay et al 2007; Kaplan et al 2009;Tatarkova et al 2011). However, few studies that have investigated the efficacy of antioxidant treatment are controversial.…”

Section: Introductionmentioning

confidence: 99%

“…Controversy exists also regarding the effects of hyperoxia on endogenous antioxidants. HBO and NBO treatments were shown to stimulate activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in brain and skeletal muscle (Gregorevic et al 2001;Ay et al 2007;Tatarkova et al 2011). On the other hand, SOD, GPx and catalase activities in erythrocytes were not affected by HBO (Dennong et al 1999;Eken et al 2005).…”

Section: Introductionmentioning

confidence: 99%

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Effect of normobaric oxygen treatment on oxidative stress and enzyme activities in guinea pig heart

Tatarková¹,

Engler²,

Čalkovská³

et al. 2012

gpb

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Abstract. Normobaric oxygen (NBO) therapy is commonly applied for the treatment of various diseases, including myocardial infarctions, but its effectiveness is controversial. Potential adverse effects of hyperoxia are related to excessive formation of free radicals. In the present study we examined the effect of 60-h NBO treatment on lipid peroxidation (LPO), activity of manganese superoxide dismutase (Mn-SOD) and mitochondrial enzymes of energy metabolism in guinea pig heart. NBO treatment resulted in significant accumulation of thiobarbituric acid reactive substances and loss of Mn-SOD activity despite slight elevation of Mn-SOD protein content. Activity of electron transport chain complex III decreased significantly, while activity of complex IV was slightly elevated and citrate synthase was unchanged. LPO, inhibition of Mn-SOD and complex III activities were more pronounced when inhaled oxygen was partially enriched with superoxide radical. In contrast, when O 2 was enriched with oxygen cation (O 2•+ ), LPO and loss of Mn-SOD activity were prevented. Complex III activity in the O 2•+ -treated group remained depressed but activities of complex IV and citrate synthase were elevated. These data suggest that NBO treatment is associated with myocardial oxidative damage and attenuation of antioxidant defense, but these adverse effects can be partially attenuated by inhalation of O 2 enriched with oxygen cation.

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Effect of Long-Term Normobaric Hyperoxia on Oxidative Stress in Mitochondria of the Guinea Pig Brain

Cited by 25 publications

References 30 publications

Effect of Hypoxia and Hyperoxia on Cerebral Blood Flow, Blood Oxygenation, and Oxidative Metabolism

Effect of Hypoxia and Hyperoxia on Cerebral Blood Flow, Blood Oxygenation, and Oxidative Metabolism

Synergetic Neuroprotection of Normobaric Oxygenation and Ethanol in Ischemic Stroke Through Improved Oxidative Mechanism

Effect of normobaric oxygen treatment on oxidative stress and enzyme activities in guinea pig heart

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Effect of Long-Term Normobaric Hyperoxia on Oxidative Stress in Mitochondria of the Guinea Pig Brain

Cited by 25 publications

References 30 publications

Effect of Hypoxia and Hyperoxia on Cerebral Blood Flow, Blood Oxygenation, and Oxidative Metabolism

Effect of Hypoxia and Hyperoxia on Cerebral Blood Flow, Blood Oxygenation, and Oxidative Metabolism

Synergetic Neuroprotection of Normobaric Oxygenation and Ethanol in Ischemic Stroke Through Improved Oxidative Mechanism

Effect of normobaric oxygen treatment on oxidative stress and enzyme activities in guinea pig heart

Contact Info

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Resources

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Effect of normobaric oxygen treatment on oxidative stress and enzyme activities in guinea pig heart