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

The rate of lipid peroxidation (by content of the lipid peroxide transformation end product--malonic dialdehyde) in homogenates of rat brain was studied as affected by hyperoxia and with a protective effect of urea in experiments in vivo and in vitro. In both cases an increase is observed in the malonic aldehyde yield with the effect of oxygen under higher pressure. Urea in physiological concentrations lowers the yield under the effect of hyperoxia in vitro. In experiments in vivo introduction of urea also evokes a decrease in the rate of peroxidation. It is established that hyperoxia and urea affect mainly the ascorbate-dependent system of peroxidation. The compositon of phospholipids in the rat brain was studied under the effect of hyperoxia and urea. No changes were found in the number of fractions under the effect of 6at oxygen, only quantitative changes are observed. With introduction of urea before hyperoxia there occurs a normalization in the phospholipid composition. The authors suppose the protective effect of urea to be due to its influence on membranes.
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PMID:[Change in peroxidation and in the phospholipid content in the brain in hyperoxia and the protective action of urea]. 94 11

The effects of oxygen on ascorbic acid concentration and transport were studied in chick embryo (Gallus gallus domesticus). During normoxic incubations, plasma ascorbic acid concentration peaked on fetal day 12 and then fell, before increasing again on day 20 when pulmonary respiration began. In contrast, cerebral ascorbic acid concentration rose after day 6, was maintained at a relatively high level during days 8-18, and then fell significantly by day 20. Exposure of day 16 embryos for 48 h to 42% ambient O2 concentration decreased ascorbic acid concentration by four-fifths in plasma and by one-half in brain, compared to values in normoxic (21% O2) or hypoxic (15% O2) controls. Hyperoxic preincubation of embryos also inhibited ascorbic acid transport, as evidenced by decreased initial rates of saturable and Na(+)-dependent [14C]ascorbic acid uptake into isolated brain cells. It may be concluded that changes in ascorbic acid concentration occur in response to oxidative stress, consistent with a role for the vitamin in the detoxification of oxygen radicals in fetal tissues. However, changing O2 levels have less effect on ascorbic acid concentration in brain than in plasma, indicating regulation of the vitamin by brain cells. Furthermore, the effect of hyperoxia on cerebral vitamin C may result, in part, from inhibition of cellular ascorbic acid transport.
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PMID:Effect of oxygen on ascorbic acid uptake and concentration in embryonic chick brain. 160 63

The development of acute lung injury in rats following the intravenous injection of bleomycin was assessed by measuring the total pulmonary extravascular albumin space. Intravenous bleomycin alone produced no evidence of lung injury, yet when combined with a simultaneous exposure to hyperoxia or simultaneous tracheal instillation of ferric iron or ascorbate a severe lung injury evolved. Neither ferric iron or ascorbate alone produced lung injury when assessed in this manner, and ferrous iron, ferritin and haemoglobin did not potentiate bleomycin induced lung injury. A continuous subcutaneous infusion of desferrioxamine enhanced hyperoxia induced lung injury, and had no modulating effect on the lung injury produced by combined intravenous bleomycin and hyperoxia. These results indicate that ferric iron can potentiate bleomycin induced lung injury, and that the metal chelator desferrioxamine can have adverse effects on the development of acute lung injury.
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PMID:The effects of iron and desferrioxamine on the lung injury induced by intravenous bleomycin and hyperoxia. 246 85

Hyperoxia inhibited concanavalin A stimulated O2- release (respiratory burst) of alveolar macrophages obtained by bronchoalveolar lavage from rats. After 36 h of normobaric 100% O2, a partial reversal (48%) of the inhibition was produced by addition of glucose. Since oxidant-induced, reversible NADPH depletion correlates with reversible inhibition of the respiratory burst, intracellular NADPH was assayed to determine whether irreversible inhibition of the respiratory burst was related to persistent changes in this metabolite. The cellular concentrations of ATP, glutathione, and ascorbate were also measured. After 36 h of hyperoxia, NADPH concentration in alveolar macrophages rose slightly while ATP and glutathione content remained at control levels. Ascorbate levels fell significantly but were not responsible for respiratory burst inhibition. Thus, irreversible loss of cellular function in hyperoxia is not due to persistent alterations in these metabolites. Significant amounts of both glutathione and ascorbate were found in extracellular fractions of lung washings, indicating high concentrations in the aqueous subphase in the lung fluid lining. There was no change in total content of these extracellular antioxidants following O2 exposure.
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PMID:Oxygen toxicity: loss of lung macrophage function without metabolite depletion. 301 77

Hyperoxia induced cellular damage was used as an experimental model system for examining the ameliorative role of antioxidants. Multiplication of HEp-2 cells in monolayer culture was inhibited after exposure to 100% O2 either hyperbarically at 3 atm absolute (atma) or normobarically at 1 atma for periods from 15 s to 4 h. The inhibition was characterized by a slower rate of replication for a period from 1 to 3 d after exposure than in unexposed cultures, and then massive cellular death. Less killing followed exposure to normobaric O2 than to hyperbaric O2, and the shorter the period of exposure to hyperoxia the less killing. Addition of 100 micrograms/ml of sodium L-ascorbate to unexposed cultures enhanced growth (cell number at 6 d) almost twofold. When added ascorbate was present only during hyperoxic exposure (but not afterward), subsequent growth in air was enhanced 1.6-fold. However, when cells were exposed without added ascorbate, there was from 2 to 12-fold greater growth in air in the presence of the added ascorbate (as compared to exposed controls). This greater growth was always only a partial reversal of the lethal effect resulting from hyperoxia. Addition of 25 micrograms/ml catalase did not affect control or exposed cultures. Addition of ascorbate plus catalase was not as effective as ascorbate alone in promoting growth; the catalase moiety antagonized some of the growth enhancing influence of ascorbate. This suggests that extracellular H2O2 was not a factor in the lethal effect resulting from hyperoxia.
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PMID:Partial reversal by sodium ascorbate of hyperoxia-induced damage to HEp-2 cell cultures. 685 35

The efficacy of niacin in protecting rats from normobaric hyperoxia was evaluated in vivo by exposing niacin treated animals and controls to greater than 95% O2 for 96 hours. The vitamin was also evaluated as a possible free radical scavenger in vitro using an Fe-ascorbate initiated microsomal lipid peroxidation system. No protective effects were observed in vivo either in mortality or in differences in lung wet and dry weights of the niacin treated rats when compared to controls. Niacin in varying concentrations also did not decrease lipid peroxidation in the microsomal systems. Although this vitamin has been reported to protect animals from paraquat toxicity when given intraperitoneally once daily, niacin administered in similar doses does not appear to protect rats from hyperoxia.
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PMID:Inability of niacin to protect from in vivo hyperoxia or in vitro microsomal lipid peroxidation. 718 25

It was demonstrated that the processes of lipid peroxidation in brain tissues of rats induced by hyperoxia and Fe-ascorbate system in vivo and in vitro significantly influence specific binding of serotonin and diazepam. Lipid peroxidation caused various changes in the ability to bind utilized ligands: 3H-serotonin binding decreased by 53%, while that of 3H-diazepam increased by 30%. Preliminary administration of the synthetic antioxidant 4-methyl-2,6-ditretbutylphenol prevented these changes.
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PMID:[Binding of 3H-serotonin, 3H-diazepam and lipid peroxidation in brain membranes]. 731 29

Pulmonary oxygen toxicity results from disruption of the usual antioxidant defenses of the body. We therefore investigated whether mice that suffer from oxygen toxicity show significant alterations in the redox status of ascorbate, an important antioxidant, as reflected by changes in the relative amounts of its oxidized and reduced forms. Mice were exposed to air or hyperoxia (> 97% O2, 760 mmHg). After 5 days, plasma and saline-perfused lungs were removed and levels of ascorbate (AA), oxidized ascorbate [dehydroascorbate (DHAA)], and total ascorbate species ([AA+DHAA]) were determined by a sensitive and specific high-performance liquid chromatography assay; lungs were also assayed for total glutathione and glutathione disulfide (GSSG), an established marker of oxidative stress. We found that with hyperoxic exposure plasma AA increased by 32%, plasma DHAA increased substantially from previously undetectable levels, and the DHAA-to-[AA+DHAA] ratio increased. In contrast, in lung, [AA+DHAA] decreased by 41%. Plasma AA, DHAA, and [AA+DHAA] each correlated inversely with lung [AA+DHAA] and directly with lung GSSC. We conclude that alterations in plasma ascorbate redox status reflect pulmonary oxygen toxicity in mice. Our results suggest that further investigations are warranted to determine whether similar findings occur in humans and have clinical utility.
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PMID:Pulmonary oxygen toxicity in mice is characterized by alterations in ascorbate redox status. 859 40

The generation of reactive oxygen species (ROS) is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drug or alcohol, exposure to UV or therapeutic radiation, and deficiency in antioxidant vitamins. Uncontrolled production of ROS often leads to damage of cellular macromolecules (DNA, protein, and lipids) and other small antioxidant molecules. A number of major cellular defense mechanisms exist to neutralize and combat the damaging effects of these reactive substances. The enzymic system functions by direct or sequential removal of ROS (superoxide dismutase, catalase, and glutathione peroxidase), thereby terminating their activities. Metal binding proteins, targeted to bind iron and copper ions, ensure that these Fenton metals are cryptic. Nonenzymic defense consists of scavenging molecules that are endogenously produced (GSH, ubiquinols, uric acid) or those derived from the diet (vitamins C and E, lipoic acid, selenium, riboflavin, zinc, and the carotenoids). These antioxidant nutrients occupy distinct cellular compartments and among them, there are active recycling. For example, oxidized vitamin E (tocopheroxy radical) has been shown to be regenerated by ascorbate, GSH, lipoic acid, or ubiquinols. GSH disulfides (GSSG) can be regenerated by GSSG reductase (a riboflavin-dependent protein), and enzymic pathways have been identified for the recycling of ascorbate radical and dehydroascorbate. The electrons that are used to fuel these recycling reactions (NADH and NADPH) are ultimately derived from the oxidation of foods. Sickle cell anemia, thalassemia, and glucose-6-phosphate-dehydrogenase deficiency are all hereditary disorders with higher potential for oxidative damage due to chronic redox imbalance in red cells that often results in clinical manifestation of mild to serve hemolysis in patients with these disorders. The release of hemoglobin during hemolysis and the subsequent therapeutic transfusion in some cases lead to systemic iron overloading that further potentiates the generation of ROS. Antioxidant status in anemia will be examined, and the potential application of antioxidant treatment as an adjunct therapy under these conditions will be discussed.
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PMID:Interaction of antioxidants and their implication in genetic anemia. 1060 86

High arterial blood oxygen tension increases vascular resistance, possibly related to an interaction between reactive oxygen species and endothelium-derived vasoactive factors. Vitamin C is a potent antioxidant capable of reversing endothelial dysfunction due to increased oxidant stress. We tested the hypotheses that hyperoxic vasoconstriction would be prevented by vitamin C, and that acetylcholine-mediated vasodilation would be blunted by hyperoxia and restored by vitamin C. Venous occlusion strain gauge plethysmography was used to measure forearm blood flow (FBF) in 11 healthy subjects and 15 congestive heart failure (CHF) patients, a population characterized by endothelial dysfunction and oxidative stress. The effect of hyperoxia on FBF and derived forearm vascular resistance (FVR) at rest and in response to intra-arterial acetylcholine was recorded. In both healthy subjects and CHF patients, hyperoxia-mediated increases in basal FVR were prevented by the coinfusion of vitamin C. In healthy subjects, hyperoxia impaired the acetylcholine-mediated increase in FBF, an effect also prevented by vitamin C. In contrast, hyperoxia had no effect on verapamil-mediated increases in FBF. In CHF patients, hyperoxia did not affect FBF responses to acetylcholine or verapamil. The addition of vitamin C during hyperoxia augmented FBF responses to acetylcholine. These results suggest that hyperoxic vasoconstriction is mediated by oxidative stress. Moreover, hyperoxia impairs acetylcholine-mediated vasodilation in the setting of intact endothelial function. These effects of hyperoxia are prevented by vitamin C, providing evidence that hyperoxia-derived free radicals impair the activity of endothelium-derived vasoactive factors.
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PMID:Vitamin C prevents hyperoxia-mediated vasoconstriction and impairment of endothelium-dependent vasodilation. 1200 53


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