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

A rise of hemoglobin concentration accompanied by an increase of the total iron in the blood serum of white mice was found under oxygen pressure of 4 atm for an hour (preconvulsive state) and 6 atm (convulsive state). Changes in correlations of hemoglobin fractions in the blood serum were detected in both stages of oxygen poisoning by disc-electrophoresis in 7.5% polyacrylamide gel. A rise of transferrin concentration under these conditions (hyperoxia) was observed. The deflections occurred were less pronounced following administration of urea to the animals before hyperbaric oxygenation.
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PMID:[Hemoglobin, transferrin and total iron content in the blood serum in hyperoxia and during the protective action of urea]. 46 81

Normal and iron-deficient rats were exposed to 90% O2 at 760 Torr for 24 or 48 h. Erythrocyte response to hyperoxia was monitored by potassium (rubidium) influx studies, by storage stress, and by ultrastructural studies. Normal rat erythrocytes exhibited morphological changes and decrease of ouabain-sensitive potassium influx compared to unexposed controls. Both components of erythrocyte potassium influx were affected by iron deficiency. Erythrocytes from unexposed iron-deficient rats showed a 50% increase in ouabain-sensitive potassium influx compared to controls. Iron-deficient rats exposed to hyperoxia for 24 or 48 h, had erythrocytes with morphological changes. Erythrocytes of iron-deficient rats exposed for 24 h showed no influx change; those exposed for 48 h showed a decrease of ouabain-sensitive influx compared to erythrocytes of controls.
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PMID:Response of the iron-deficient erythrocyte in the rat to hyperoxia. 64 73

The iron chelators o-phenanthroline and desferrioxamine were tested for their ability to protect Chinese hamster ovary cells against the cytotoxic and genotoxic effects of normobaric hyperoxia. Desferrioxamine added at sub-toxic concentrations (up to 2.5 microM) over a period of several days had no protective effect on hyperoxia-induced clonogenic cell killing and growth inhibition. The clastogenic effect of hyperoxia was strongly potentiated by desferrioxamine, while the induction of sister-chromatid exchanges (SCEs) by hyperoxia was unaffected. Similarly, o-phenanthroline (up to 0.25 microM) had no protective effect on hyperoxia-induced cell killing, growth inhibition, and SCE induction, while also this compound potentiated the clastogenic effect of hyperoxia. These results do not support a critical role for cellular iron in the mechanism of toxicity by normobaric hyperoxia in CHO cells. However, the results may still be consistent with a critical involvement of particular iron fraction(s) not susceptible to the chelators used. Furthermore, our results show that concentrations of iron chelators known to protect against short-term (up to 1 h) toxic exposure to oxidative stress become toxic themselves when applied chronically, i.e., in the order of days.
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PMID:Effect of iron chelators on the cytotoxic and genotoxic action of hyperoxia in Chinese hamster ovary cells. 137 85

Histological and ultrastructural studies were made of the lungs of rats that were exposed to 100% oxygen for 60 h and were treated with either normal saline or with ICRF-187, a bis-diketopiperazine derivative of EDTA that has the capacity to chelate iron. This metal is thought to be needed to catalyze the formation of toxic oxygen free radicals. ICRF-187 (20 mg/kg) was given intraperitoneally at approximately 12 h intervals (5 doses) during the 60 h exposure. Seven of the ten saline-treated rats exposed to oxygen died prior to the end of the study whereas only one of the 10 rats in the ICRF-187-treated group died. This difference in mortality is found to be statistically significant (P less than 0.05). All saline-treated rats showed light and electron microscopic evidence of pulmonary damage. ICRF-187 attenuated the morphologic alterations observed by light microscopy (intra-alveolar edema, inflammatory exudates and bronchiolar epithelial cell swelling and hyperplasia; P less than 0.05). In addition, electron microscopic evaluation revealed that capillary thrombi, endothelial cell alterations and alveolar epithelial cell damage also were less severe in ICRF-187-treated rats. It is concluded that ICRF-187 may provide a new and useful approach for the prevention of hyperoxia-induced pulmonary damage.
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PMID:Effect of ICRF-187 on the pulmonary damage induced by hyperoxia in the rat. 151 41

Mutants of Escherichia coli lacking superoxide dismutase (SOD) activity were used to explore the sensitivity of aconitase toward O2 and O2-. The aconitase activity in SOD-free extracts was rapidly lost under aerobic conditions and exogenous SOD afforded a concentration-dependent protection. The rate of the inactivating reaction between O2- and aconitase was estimated to be of the order of 10(9) M-1 s-1. The competitive inhibitors fluorocitrate and tricarballylate provided some protection, and at saturating concentrations, they decreased the rate of the inactivating reaction by 100- and 10-fold, respectively. Aconitase was markedly less sensitive to O2 than it was to O2-. Aerobic growth on succinate involves a greater dependence upon aconitase than does growth on glucose and, as expected, the deleterious consequences of SOD deficiency were more pronounced on succinate than on glucose. Moreover, aconitase activity was lower in extracts of aerobically grown SOD mutants, than it was in the parental strain. We suppose that inactivation of aconitase by O2- involves oxidative attack on the prosthetic iron-sulfur cluster. The extreme sensitivity of aconitase to inactivation by O2- suggests that its inactivation will be an early event in the oxidative stress imposed by hyperoxia, ultraviolet irradiation or redox-cycling agents, such as viologens or quinones.
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PMID:Superoxide sensitivity of the Escherichia coli aconitase. 165 83

Brief hypoxia or hyperoxia has been shown to affect growth and metabolism of chick embryos during the late stages of development. The objective of this study was to alter the availability of oxygen to chick embryos developing in ovo and to determine the effects on tissue zinc, copper, iron and manganese levels. On day 15 of incubation fertile chicken eggs were divided into three groups: 15% O2 (hypoxic), 60% O2 (hyperoxic) and 21% O2 (normoxic) and incubated under these conditions for 72 h to day 18. Hypoxia reduced embryo, heart, brain and liver wet weights, whereas hyperoxia increased embryo, heart, lung and liver wet weights compared to normoxic controls. Chorioallantoic membrane (CAM) wet weight was increased by hypoxia and reduced by hyperoxia. Livers from hyperoxic embryos contained more zinc, iron and manganese and less copper than livers from hypoxic or normoxic embryos. Tissue concentrations of zinc, copper, iron and manganese were reduced in brains from hyperoxic compared to hypoxic or normoxic embryos. Hyperoxia increased the zinc and copper concentrations in CAM, whereas hypoxia reduced zinc and iron levels. The contents of zinc and copper were increased in hyperoxic compared to normoxic or hypoxic lungs. Hearts from hyperoxic embryos had more zinc, copper and manganese than hypoxic or normoxic hearts. Hypoxic yolk sac contained more zinc and manganese than hyperoxic or normoxic yolk sac. Except for yolk sac, the trace element content of tissues from normoxic embryos increased from day 15 to day 18 of incubation in concert with tissue growth. We conclude that the availability of oxygen to the developing chick embryo affects tissue trace element levels through its effects on tissue growth, as a result of adaptation by specific tissues to different oxygen tensions, or via effects on the regulation of trace element uptake and assimilation by the tissues.
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PMID:Effects of brief hypoxia and hyperoxia on tissue trace element levels in the developing chick embryo. 166 14

Prolonged exposure to hyperoxia markedly inhibits normal lung development (alveolarization and respiratory surface area expansion) in immature animals. Since (a) hyperoxia results in excess hydroxyl radical (OH.) formation, (b) (OH.) is implicated in O2-induced lipid peroxidation and DNA alterations, and (c) both OH. formation and its interaction with DNA are Fe++ dependent; chelation of Fe++ should act to protect against pulmonary O2 toxicity and hyperoxic inhibition of lung development. We therefore treated litters of newborn rats with the iron chelator Deferoxamine mesylate (DES) (150 mg/kg/day) during a 10-day exposure to greater than 95% O2. Morphometric analysis demonstrated that compared to the mean airspace size in air control rat pups (Lm = 44.5 microns), hyperoxic exposure resulted in a 34% larger mean air space diameter in O2-saline rat lungs (59.5 microns) versus only an 11% enlargement in O2-DES lungs (51.1 microns*). Lung internal surface area (cm2) per 100-g body weight were air control = 4480, O2-saline = 3570 (decreases 20.3%), and O2-DES = 4125* (decreases 7.9%) (*p less than 0.05 versus O2-saline group). DES-treated animals also had significantly decreased lung conjugated diene levels during hyperoxic exposure and increased lung elastin content (reflective of preserved lung alveolar formation) compared to O2-saline rats. These results indicate that DES treatment substantially ameliorated the inhibitory effects of neonatal hyperoxic exposure on normal lung development.
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PMID:Hyperoxic inhibition of newborn rat lung development: protection by deferoxamine. 179 22

The ability of niacin to relieve the growth-inhibiting effect of hyperoxia on Escherichia coli can be attributed to the dioxygen sensitivity of quinolinate synthetase. The activity of this enzyme within E. coli was diminished by exposure of the cells to 4.2 atm O2, while the activity in extracts was rapidly decreased by 0.2 atm O2. Neither catalase nor superoxide dismutase afforded detectable protection against the inactivating effect of O2, indicating that H2O2 and O2- were not significant intermediates in this process. Nevertheless, H2O2 at 1.0 mM did inactivate quinolinate synthetase, even under anaerobic conditions and in the absence of catalatic activity which might have generated O2. Addition of paraquat to aerobic cultures of E. coli caused an inactivation of quinolinate synthetase, which may be explained in terms of an increase in the production of H2O2. The O2-dependent inactivation of quinolinate synthetase in extracts was gradually reversed during anaerobic incubation and this reactivation was blocked by alpha, alpha'-dipyridyl or by 1,10-phenanthroline. The sequence of the quinolinate synthetase "A" protein contains a--cys-w-x-cys-y-z-cys--sequence, which is characteristic of (Fe-S)4-containing proteins. This sequence, together with the effect of the Fe(II)-chelating agents, suggests that the O2-sensitive site of quinolinate synthetase is an iron-sulfur cluster which is essential for the dehydration reaction catalyzed by the A protein.
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PMID:Quinolinate synthetase: the oxygen-sensitive site of de novo NAD(P)+ biosynthesis. 184 9

Reactive oxygen species are a major cause of damage occurring in ischemic tissue after reperfusion. During reperfusion transitional metals such as iron are required for reactive oxygen species to mediate their major toxic effects. Xanthine oxidase is an important source of reactive oxygen species during ischemia-reperfusion injury, but not in all organs or species. Because cytochrome P-450 enzymes are an important pulmonary source of superoxide anion (O2-.) generation under basal conditions and during hyperoxia, and provide iron catalysts necessary for hydroxyl radical (.OH) formation and propagation of lipid peroxidation, we postulated that cytochrome P-450 might have a potential role in mediating ischemia-reperfusion injury. In this report, we explored the role of cytochrome P-450 enzymes in a rabbit model of reperfusion lung injury. The P-450 inhibitors 8-methoxypsoralen, piperonyl butoxide, and cimetidine markedly decreased lung edema from transvascular fluid flux. Cimetidine prevented the reperfusion-related increase in lung microvascular permeability, as measured by movement of 125I-albumin from the vascular space into lung water and alveolar fluid. P-450 inhibitors also prevented the increase in lung tissue levels of thiobarbituric acid reactive products in the model. P-450 inhibitors did not block enhanced O2-. generation by ischemic reperfused lungs, measured by in vivo reduction of succinylated ferricytochrome c in lung perfusate, but did prevent the increase in non-protein-bound low molecular weight chelates of iron after reperfusion. Thus, cytochrome P-450 enzymes are not likely a major source of enhanced O2-. generation, but serve as an important source of iron in mediating oxidant injury to the rabbit lung during reperfusion. These results suggest an important role of cytochrome P-450 in reperfusion injury to the lung and suggest potential new therapies for the disorder.
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PMID:Role of cytochrome P-450 in reperfusion injury of the rabbit lung. 217 18

Commercial infant formulas, human milk, and lipid emulsions were analyzed for evidence of naturally occurring lipid peroxidation and for susceptibility to an in vitro oxidative challenge using neonatal rat lung, liver, or intestine homogenates. Peroxidation was assessed by quantitation of TBA reactants, diene conjugates, lipid peroxides, and ethane and pentane hydrocarbons. The peroxidation of commercial formulas and human milk was influenced by the nutrient composition, as PUFA and iron enhanced while vitamin E inhibited one or more of the peroxidation pathways. Formulas and lipid emulsions differed in their response to a biological oxidant challenge. Neither neonatal rat lung nor liver tissue were effective in peroxidizing the formula or human milk in vitro, but both formula and human milk were peroxidized by exposure to neonatal rat intestinal tissue. The lipid emulsion was readily peroxidized by neonatal rat lung, liver, and intestinal tissue. The influence of nutrition on survival in hyperoxia was also studied by exposing newborn rat pups to either air or greater than 95% oxygen in the course of feeding Ringer's lactate, Similac 24 + iron, human milk, or Intralipid 10%. The survival of newborn rat pups exposed to air or greater than 95% oxygen was affected by the type of diet received.
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PMID:In vitro and in vivo assessment of lipid peroxidation of infant nutrient preparations: effect of nutrition on oxygen toxicity. 235 14


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