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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukemia inhibitory factor (LIF) and tumor necrosis factor (TNF) have been shown to protect animals from radiation, hyperoxia, and endotoxic shock. TNF is also known to induce the expression of manganese superoxide dismutase (MnSOD) in vitro and in vivo. We therefore examined the effects of these cytokines on reperfusion injury in the isolated rabbit heart model. Rabbits were injected intravenously with 10 micrograms of either human TNF-alpha or lymphotoxin (TNF-beta), or murine TNF-alpha or murine LIF dissolved in saline. Control animals were injected with an equal volume of saline. After 24 h, hearts were isolated and perfused. Following an equilibration period, the hearts were subjected to 1 h ischemia and 1 h of reperfusion. All treated groups showed significant increases in percent recovery of developed tension (% preischemic) when compared to saline-treated control hearts. In addition there were significant decreases in lactate dehydrogenase release (LDH), accumulation of thiobarbituric acid reactive substances (TBARS), and accumulation of carbonyl proteins. These results correlate with increases in myocardial MnSOD activity. Thus, the protection from myocardial reperfusion injury seen in the pretreated group may be due to a mechanism that involves the induction of MnSOD.
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PMID:Leukemia inhibitory factor and tumor necrosis factor induce manganese superoxide dismutase and protect rabbit hearts from reperfusion injury. 776 Mar 46

A new micromethod for the determination of sphingomyelin in samples suspended in aqueous solutions, and modified micromethods for determining phosphatidylcholine and phosphatidylglycerol were used to determine phosphatidylcholine and sphingomyelin (detection limits of 1.8 mumol/l), and phosphatidylglycerol (detection limit of 2.3 mumol/l) in lipid dispersions, membranes from sheep erythrocytes and platelets, and pulmonary surfactants from rats of different ages and rats maintained under normobaric hyperoxia for 2 days prior to their sacrifice. The procedures are easy to perform, accurate, require less sample than conventional methods and can also be applied directly to aqueous samples. Phospholipase C and sphingomyelinase were used to release phosphorylcholine from phosphatidylglycerol and sphingomyelin, respectively. The choline released from phosphorylcholine by alkaline phosphatase is reconverted to phosphorylcholine by ATP and choline kinase. In the phophatidylglycerol determination, phospholipase D was used to release glycerol and phosphatidate. The glycerol formed was converted to glycerolphosphate using ATP and glycerol kinase. In all cases, the ADP thus formed was determined by following the enzymatic conversion of NADH to NAD at 340 nm in an coupled pyruvate kinase/lactate dehydrogenase system. Significant variations in the phospholipid composition of rat pulmonary surfactant were found during development; in particular there was an increase in the phosphatidylglycerol content of adult rats as compared with younger rats. Hyperoxia produced changes in the phosphatidylglycerol content of surfactant from adult rats, but not from 2-day old rats.
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PMID:Enzymatic determination of phosphatidylcholine, sphingomyelin and phosphatidylglycerol in lipid dispersions, blood cell membranes and rat pulmonary surfactant. 870 43

Brain reperfusion and/or reoxygenation may be of particular importance in the etiology of neuronal damage after hypoxic-ischemic insult in neonates, especially with reference to the generation of free radicals. To investigate this issue, the influence of either standard reoxygenation or transient hyperoxia was studied on the consequences of severe hypoxia in a model of cultured neurons isolated from the fetal rat brain. Culture dishes were exposed for 6 h to hypoxia (95% N2/5% CO2). They were then placed under normoxia (95% air/5% CO2) or hyperoxia (95% O2/5% CO2) for 3 h, and finally returned to normoxia. Control cultures were kept under normoxic conditions. Cell morphology, protein concentrations, lactate dehydrogenase leakage, energy metabolism, as reflected by specific transport and incorporation of 2-D-[3H]deoxyglucose, as well as superoxide radical formation were analyzed as a function of time. Po2 values in the cell incubating medium were decreased by 78% by hypoxia and increased by 221% by hyperoxia. No morphologic alteration could be noticed before 72 h posthypoxia, when cell degeneration became apparent, with a concomitant reduction in protein contents. Hypoxia-reoxygenation induced a transient cellular hypermetabolism, as shown by a 36% increase in 2-D-[3H]deoxyglucose uptake 24 h after hypoxia, and then a 23% decrease below control values at 72 h. It also led to a sharp increase in the formation of superoxide radicals (+108%). Transient hyperoxia during reoxygenation did not exacerbate these events, and thus would not enhance their deterimental effects on cell integrity.
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PMID:Influence of post-hypoxia reoxygenation conditions on energy metabolism and superoxide production in cultured neurons from the rat forebrain. 884 31

Epithelial cells are prone to oxidant injury, which could change epithelial cell homeostasis and lead to degenerative diseases. We examined the effects of hyperoxia on death and proliferation off Madin-Darby canine kidney (MDCK) epithelial cells and antioxidant vitamin protection. Subconfluent and near-confluent MDCK cells were cultured under normoxia or hyperoxia for two days. We measured cell number and viability, mitochondria enzymatic activity, thymidine incorporation, necrosis [lactate dehydrogenase (LDH) release], and apoptosis (DNA fragmentation and morphological changes). When the cells were subconfluent, hyperoxia decreased the number of adherent cells, mitochondrial enzymatic activity, and thymidine incorporation, but neither LDH release nor apoptotic changes increased compared with normoxic controls. In normoxia, near-confluent cells had lower nonadherent cell numbers, mitochondrial enzymatic activity, and thymidine incorporation than subconfluent cells; hyperoxia further decreased the latter two parameters and increased apoptotic changes and LDH release in near-confluent cells. Vitamin E protected mitochondrial enzymatic activity, apoptotic changes, and LDH release against hyperoxic injury but did not affect changes in thymidine incorporation with hyperoxia. Vitamin C partially protected the mitochondrial enzymatic activity and thymidine incorporation in subconfluence, but not in near confluence. These results indicate that cell density is a major determinant of the effects of hyperoxic injury and the profile of antioxidant vitamin protection.
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PMID:Cell density and antioxidant vitamins determine the effects of hyperoxia on proliferation and death of MDCK epithelial cells. 929 Jan 15

Although the antioxidant properties of N-acetylcysteine (NAC) in vitro are widely accepted, the efficacy of NAC in the prevention of O2 toxicity in vivo is poorly documented. The aim of our study was to investigate the presumed protective effect of NAC on hyperoxic lung injury, focusing on gamma-glutamyltransferase (gamma-GT) activity and glutathione (GSH) levels in lung tissue, epithelial lining fluid (ELF), and isolated rat type II cells immediately after their isolation and 48 h later when kept in culture in normoxia. Thirty-four male Wistar rats were divided in three groups (n = 10-14) and were exposed to air or to 60 or 85% O2 for 7 days. One-half of the rats in each group received 200 mg/kg NAC intraperitoneally one time per day from 3 days before exposure until the end of the experiment, and the other one-half received the vehicle. In the 85% O2-exposed animals, NAC led to more respiratory distress and weight loss. NAC did not prevent the rise in bronchoalveolar lavage lactate dehydrogenase and alkaline phosphatase, but it did prevent the rise in calculated ELF volume. NAC decreased GSH levels (1.4-fold) and gamma-GT activity (1.8-fold) in the air-exposed type II cells. In the 60% O2-exposed group, no effects of NAC were seen (except for a decrease in gamma-GT mRNA expression), but, in the 85% O2-exposed group, NAC gave rise to higher GSH (2.6-fold) and higher gamma-GT activity (2.9-fold) in the ELF and lower GSH (6.9-fold) and higher gamma-GT activity (3.6-fold) in the type II cells. Even in culture, GSH levels remained 1.5-fold lower than in the cells from the air-exposed animals and 2-fold lower than in the cells from the 85% O2-exposed animals. There was increased DNA damage (as assessed by thymidine incorporation) and apoptosis after hyperoxia, especially after 60% O2, and this effect was amplified after NAC treatment. Although protective at the endothelial side, NAC treatment led to adverse effects at the epithelial side, despite, or probably because of, restoration of the ELF GSH levels in the presence of high O2 levels. Because NAC is rapidly metabolized to cysteine, it is plausible that the effects of NAC are manifested through the toxic effects of cysteine.
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PMID:N-acetylcysteine does not protect against type II cell injury after prolonged exposure to hyperoxia in rats. 931 88

To determine whether glucose depletion is a principal determinant of hyperoxic cell death in vitro, human lung epithelial-like cells (A549) were exposed to hyperoxia (95% O2) in either 10, 30, or 50 ml of medium (Ham's F-12K). Glucose was depleted in the medium after 36, 60, or 96 h, respectively. Medium lactate dehydrogenase (LDH) activity increased only after glucose was depleted. To confirm that glucose depletion was critical to cell death, cells exposed to 95% O2 were supplemented with glucose at regular intervals to reestablish initial medium glucose concentrations. Other cells received no supplements. Without supplementation, glucose was depleted within 48 h, followed within 12 h by an almost complete loss of cell ATP and elevated medium LDH activity. Glucose-supplemented cells appeared normal microscopically and did not release LDH activity despite an extracellular pH of 6.5 due to fermentation. Additional experiments at sea-level pressure confirmed that glucose supplementation prevents extensive cell death in hyperoxia in cultured A549 cells.
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PMID:Glucose modulates cell death due to normobaric hyperoxia by maintaining cellular ATP. 945 14

A rat clonal pheochromocytoma cell line (PC12) was cultured under normoxic (21% O2) and hyperoxic (50% O2) conditions. PC12 cells underwent apoptotic cell death when they were cultured in charcoal-stripped medium in a high-oxygen atmosphere. Vitamin E homologs, alpha-tocopherol (alphaT), beta-tocopherol (betaT), gamma-tocopherol (gammaT), and delta-tocopherol (deltaT), were added to the culture medium to study their biological activities. AlphaT was more effective than gammaT and deltaT in preventing hyperoxia-induced cell death. Addition of exogenous alphaT to charcoal-treated medium prevented lactate dehydrogenase (LDH) leakage from PC12 cells and also inhibited the apoptosis, which was accompanied by DNA fragmentation. Additional alphaT was rapidly concentrated in PC12 cells, suggesting that it exerts antioxidant effects. Our data show that PC12 cell death under high-oxygen conditions is due to apoptosis and that, among the vitamin E homologs, alphaT most effectively prevents hyperoxic apoptosis.
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PMID:alpha-Tocopherol protects PC12 cells from hyperoxia-induced apoptosis. 957 8

This work examines the hypothesis that beetle bioluminescent reactions may primarily have evolved to provide an auxiliary O2 detoxifying mechanism. The activities of antioxidant enzymes and of luciferase in the prothorax (bright) and abdomen (dim) of luminous larval Pyrearinus termitilluminans (Coleoptera: Elateridae) were measured after previous challenge with either hyperoxia, hypoxia, or the firefly luciferase inhibitor luciferin 6'-methyl ether (LME). Upon exposure to pure O2 for 72 h, the prothorax activities of total superoxide dismutase (SOD) and catalase were found to increase by 85% and 50%, respectively. Concomitantly, levels of luciferase and luciferin increased 80% and 50%. Assays of thiobarbituric acid reactive substances (TBARS) showed significantly augmented lipid peroxidation only in the abdomen (30%) where levels of antioxidant enzymes and especially luciferase are low. In contrast, exposure to hypoxia (2% O2) led to significant increases in prothorax citrate synthase (85%), succinate dehydrogenase (25%), and lactate dehydrogenase (30%) activities, but not in luciferase or antioxidant enzyme levels. LME administration alone decreased luciferase activities 20% but did not alter prothorax SOD activity. Prothorax SOD activity was increased by concomitant LME and hyperoxia treatments (30%), along with higher levels of TBARS (25%) and protein reactive carbonyl groups (50%). Altogether these data suggest that in elaterids, bioluminescence and reactions catalyzed by antioxidant enzymes may cooperate to minimize oxidative stress.
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PMID:Bioluminescence as a possible auxiliary oxygen detoxifying mechanism in elaterid larvae. 958 7

Bronchial epithelial cells are the first cells to encounter high concentrations of inspired oxygen, and their damage is a typical feature in many airway diseases. The direct effect of oxygen on the expression of the main antioxidant enzymes (AOEs) in human bronchial epithelial cells is unknown. We investigated the messenger RNA (mRNA) levels of manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), catalase (CAT), and glutathione peroxidase (GPx), as well as the specific activities of MnSOD, CuZnSOD, CAT, GPx, and glutathione reductase, in BEAS-2B bronchial epithelial cells exposed to hyperoxia (95% O2, 5% CO2) for 16 to 48 h. We also assessed the resistance of cells preexposed to hyperoxia to subsequent oxidant stress. Significant cell injury was observed after 72 h exposure to hyperoxia; release of lactate dehydrogenase (LDH) from control cells and cells exposed to hyperoxia for 72 h was 7.0 +/- 1.0% and 22.0 +/- 1.0%, respectively. Hyperoxia for 16 h, 24 h, or 48 h had no effect on the mRNA levels or specific activities of any of these enzymes. Despite their unchanged AOE levels, cells exposed to hyperoxia for 48 h showed increased resistance to H2O2 and menadione. Total glutathione content of the cells increased by 55% and 58% after 24 h and 48 h, respectively, compared with normoxic controls. However, glutathione depletion with buthionine sulfoximine (BSO) did not diminish the oxidant resistance of hyperoxia-exposed cells. We conclude that AOEs in human bronchial epithelial cells are not directly upregulated by high oxygen tension, and that increases in AOE-specific activities or glutathione are not necessary for the development of increased oxidant resistance in these cells.
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PMID:Antioxidant enzyme regulation and resistance to oxidants of human bronchial epithelial cells cultured under hyperoxic conditions. 969 1

Previously it was reported that hyperoxia induced death of the human lung adenocarcinoma cell line (A549 cells) by necrosis, not by apoptosis. This study examined proliferation and death of untransformed human small airway epithelial (SAE) cells in normoxia or hyperoxia in comparison with A549 cells. We tested the hypothesis that SAE cells respond differently to hyperoxic injury than do A549 cells. We measured total cell number and viability, thymidine incorporation (SAE cells only), lactate dehydrogenase (LDH) release, and apoptotic changes as markers for cell proliferation and death. Protective effects of antioxidant vitamins also were examined in SAE cells. In normoxia, subconfluent SAE cells had less apoptosis and fewer detached cells, but higher thymidine incorporation than did near-confluent cells. Hyperoxia suppressed thymidine incorporation and augmented apoptosis in both subconfluent and near-confluent SAE cells. Hyperoxia decreased the total cell number only in subconfluence, whereas SAE cell viability declined with hyperoxia in near confluence, but not in subconfluence. For SAE cells, necrosis assessed by LDH release was minimal in all conditions and was not augmented by hyperoxia in SAE cells. In contrast, normoxic A549 cells proliferated more rapidly than did SAE cells with a large number of cells detached during the culture. A549 cells underwent necrotic cell death under confluent or in hyperoxic conditions, but had much less apoptotic cell death. In SAE cells, vitamin E partially prevented the decline of thymidine incorporation with hyperoxia in subconfluence and protected against apoptotic changes with hyperoxia in both subconfluent and near-confluent conditions. Vitamin C prevented apoptosis with hyperoxia only in near-confluent SAE cells. Thus, SAE cells maintained balanced apoptosis and cell proliferation that were altered by cell density and hyperoxia and demonstrated very little necrosis with hyperoxia. Although A549 cells underwent cell death mainly by necrosis, they also were influenced by cell density and hyperoxia. Cell density also determined specific antioxidant vitamin protection in SAE cells.
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PMID:The effects of hyperoxic injury and antioxidant vitamins on death and proliferation of human small airway epithelial cells. 973 Aug 70


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