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

Two major lines of defense exist against oxidant lung injury: tissue antioxidants and antioxidant enzymes. We studied pretreatment with the antioxidants, vitamin E and butylated hydroxyanisole (BHA), and the antioxidant enzymes, superoxide dismutase (SOD) and catalase, in rabbits exposed to 100% O2 for 48 h. BHA (200 mg/kg ip) or vitamin E (50-100 mg/kg po) were given for 2 or 3 days, respectively, before O2 exposure. Combined therapy with polyethylene glycol- (PEG) conjugated SOD (12 mg/kg) and catalase (200,000 U/kg) was given intraperitoneally 1 h before and 24 h after beginning 100% O2. Hyperoxia significantly increased the pulmonary content of malondialdehyde, indicating enhanced lipid peroxidation. One hundred percent O2 also increased lung weight gain and alveolar-capillary permeability to aerosolized 99mTc-labeled diethylenetriaminepentaacetate (99mTc-DTPA, 500 mol wt) and fluorescein isothiocyanate-labeled dextran (7,000 mol wt). Pretreatment with vitamin E, BHA, or the combination of PEG-SOD and PEG-catalase prevented the increase in malondialdehyde, lung weight gain, and alveolar-capillary permeability caused by hyperoxia. These results indicate that augmenting either tissue antioxidants or antioxidant enzymes can prevent the pulmonary injury caused by 48 h of 100% O2 in rabbits.
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PMID:Antioxidants and antioxidant enzymes protect against pulmonary oxygen toxicity in the rabbit. 234 49

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

Peroxidation of lung membrane lipids in vitro produces very specific changes in lung membrane fatty acid content with some fatty acids being affected more than others. We performed a series of experiments to determine the changes occurring in fatty acid composition in lung microsomes and mitochondria during an in vivo hyperoxic exposure. Hyperoxia did produce specific changes in the relative content of fatty acids present in lung microsomes and mitochondria of both vitamin E-supplemented and vitamin E-deficient rats. Changes were noted to occur in saturated and polyunsaturated fatty acids. The total amount of lung lipids extractable in the microsomal fractions decreased after hyperoxia in both the vitamin E-supplemented and the vitamin E-deficient animals with no changes occurring in extraction of lung mitochondrial total lipids. Decreases in lung mitochondrial fatty acids caused by hyperoxia occurred in the same fatty acids in both the vitamin E-supplemented and the vitamin E-deficient animals with few polyunsaturated fatty acids (PUFA) being affected. Decreases in lung microsomal fatty acids occurring during hyperoxia were different in the vitamin E-supplemented animals from those in the vitamin E-deficient animals with many more PUFA decreasing in the vitamin E-deficient group. The greatest number of PUFA found to decrease after hyperoxia when comparing all the different groups occurred in the microsomal fraction of the vitamin E-deficient rats. These data suggest that vitamin E-deficient animals have increased peroxidation of lung microsomal PUFA or a decrease in production of lung microsomal PUFA in vivo during a hyperoxic exposure.
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PMID:Effects of hyperoxia and vitamin E on the fatty acid composition of rat lung microsomes and mitochondria. 276 78

We examined the digitonin-stimulated release of superoxide by alveolar macrophages (AMs) from young rats exposed to greater than 95% oxygen for 24-168 h. AMS were obtained by lung lavages, and the release of superoxide stimulated by digitonin was measured by using cytochrome C reduction. The total cell count of lung lavages decreased at 24 and 168 h of oxygen exposure (p less than 0.05 for both). The contamination of polymorphonuclear cells (PMNs) was less than 1% up to 120 h of oxygen exposure, and at 168 h PMNs increased to 5% of total cells in lung lavages. The viability of AMs was greater than 95% up to 72 h and then decreased to 90% at 120 h of oxygen exposure and 87% at 168 h. Digitonin-stimulated superoxide release by AMs recovered from lung lavages in rats exposed to hyperoxia showed a slight increase during the first 48 h. However, oxygen exposure for 72 h or more caused a significant decrease of the stimulated superoxide release of AMs compared to AMs from control rats. This decline in stimulated superoxide release of AMs resulting from hyperoxia was not prevented by vitamin E treatment.
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PMID:Impairment of superoxide release by alveolar macrophage in rats exposed to oxygen and vitamin E. 285 20

Iron administration results in the development of oxidative stress in skeletal muscles, as evidenced by increases in amounts of lipid oxidation fluorescent end products, decreases in vitamin E concentration, and inhibition of calcium transport by sarcoplasmic reticulum. Exhaustive physical loading or hyperoxia, or their combination, does not lead to apparent modification in calcium transport by sarcoplasmic reticulum in skeletal muscle homogenates. However, physical loading or hyperoxia does in fact induce oxidative stress since they magnify the effect of iron loading on the inhibition of calcium transport.
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PMID:Oxidative stress leads to inhibition of calcium transport by sarcoplasmic reticulum in skeletal muscle. 292 49

The development of osteonecrosis after exposure to altered air pressures is consistent with cellular injury brought about by active oxygen species. The syndrome is considered to arise as a result of an unusual combination of circumstances in which hyperoxia itself, together with the additive responses of the endocrine system to hyperoxia, hypothermia and exertion, each appear to play a part; the net result is thought to increase the mitochondrial generation of superoxide. It is suggested that effective prophylaxis may be possible primarily by establishing a nutritional status that is adequate to ensure that the functional activities of radical-scavenging systems are not hampered by deficiencies either of essential trace elements or of vitamin E. Pharmacological pretreatments designed both to decrease excessive levels of superoxide through increased catalysis of anionic dismutation and to attenuate enzyme-dependent peroxidation may provide an additional line of defence.
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PMID:Dysbaric osteonecrosis (caisson disease of bone): are active oxygen species and the endocrine system responsible, and can control of the production of free radicals and their reaction products confer protection? 333 53

Production rates for ethane gas, a hydrocarbon byproduct of lipid peroxidation, measured from the ethane present in the exhaled breath of rats, were used to determine changes in oxygen-free radical activity. Rates of ethane production were measured in rats housed in metabolic chambers and exposed to room air and to high oxygen concentrations. Expired ethane, adsorbed onto activated charcoal and then liberated by heating, was measured by gas chromatography. Ethane production rates in groups of 8 rats increased during 8 h of 100% oxygen exposure from a mean (+/- SE) room air value of 11.30 +/- 1.15 to 27.85 +/- 2.93 pmol/min/100 g rat (p less than 0.005). The mean (+/- SE) percent increases in ethane production after exposure to 100% oxygen in 8 rats pretreated with 0.1 mg/100 g of vitamin E in corn oil vehicle (0.1 ml/100 g) injected intraperitoneally and in a group of 5 rats injected with vehicle alone averaged 157.16 +/- 37.83% and 150.98 +/- 25.19%, respectively. The percent changes noted were not significantly different as measured by analysis of variance. These data indicate that lipid peroxidative activity, hence oxygen-free radical activity, increases in normally fed rats exposed to hyperoxia at a time prior to the previously reported neutrophil influx into the lungs of similarly exposed rats and that it is not attenuated by pretreatment with vitamin E.
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PMID:Ethane production rate in rats exposed to high oxygen concentration. 334 26

We designed experiments using isolated rabbit lungs to determine the effect of hyperoxia on the pulmonary vasoconstriction caused by the infusion of the lipid peroxide tert-butyl hydroperoxide (t-bu-OOH), which produces vasoconstriction by stimulating the pulmonary synthesis of thromboxane. Exposure to 48-60 h of 100% O2 at 1 ATA markedly reduced the increase in pulmonary artery pressure caused by t-bu-OOH infusion. We also investigated whether the mechanism for the attenuated vasoconstriction was due to altered production of arachidonate mediators or oxidant-induced damage to the contractile mechanism. In addition to infusing t-bu-OOH, which selectively stimulates thromboxane production, we also infused Intralipid, an esterified fatty acid emulsion that stimulates production of both thromboxane and prostacyclin. These experiments were done to study the effect of hyperoxia on prostacyclin synthesis. To determine if antioxidant therapy would prevent the changes in mediator production and vascular reactivity caused by hyperoxia, we pretreated animals with the antioxidants butylated hydroxyanisole (BHA) or vitamin E. The lack of vascular reactivity to t-bu-OOH was not due to a decrease in thromboxane synthesis or an increase in prostacyclin synthesis. Hyperoxia did not affect thromboxane synthesis during basal conditions or after stimulation of synthesis by t-bu-OOH. 100% O2 also did not effect the basal synthesis of prostacyclin by the lung. Hyperoxia did, however, markedly reduce prostacyclin synthesis when it was stimulated by Intralipid infusion. Antioxidant pretreatment did not reverse the inhibition of prostacyclin synthesis but did prevent the loss of vascular reactivity caused by hyperoxia. Thus hyperoxia causes vascular paralysis through oxidant-induced injury to the pulmonary vasculature.
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PMID:Mechanism of hyperoxia-induced pulmonary vascular paralysis: effect of antioxidant pretreatment. 405 81

Chow-fed and tocopherol-deficient mice were given aminotriazole (AT), exposed to 100% O(2) at 60 pounds per square inch absolute for 1 hr (OHP), and red blood cells were assayed for catalase activity and lipid peroxide levels. A decrease of catalase activity (CA) in the presence of AT can be taken as evidence of excess formation or accumulation of H(2)O(2). No differences of CA were observed among chow-fed mice, with or without AT and/or OHP. Tocopherol-deficient mice with AT had lower CA (0.174+/-0.040) than chow-fed mice with AT (0.225+/-0.028) P < 0.01. Tocopherol-deficient mice with AT exposed to OHP had even lower CA, 0.137+/-0.024, P < 0.01.The data are consistent with the hypothesis that H(2)O(2) is formed or accumulated in excess in red cells of tocopherol-deficient mice, an effect that is enhanced in the presence of hyperoxia. They imply that tocopherol plays a role in the detoxification of H(2)O(2).
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PMID:In vivo formation of H2O2 in red cells during exposure to hyperoxia. 505 73

Weanling male rats were fed semi-purified diets supplemented with 0, 60, or 600 IU X g-1 vitamin E or 0, 100 or 1000 ppb selenium. One group was injected daily with vitamin E at a rate equivalent to consumption of 60 IU X kg-1. Animals from all groups were sacrificed after exposure to normobaric oxygen or air for 48 h. Lung tissue was analyzed for the combined activity of prostaglandin dehydrogenase and reductase. Using the decline in enzyme activity as an indicator of susceptibility to oxygen poisoning, protection against hyperoxia was directly related to the level of vitamin E supplementation. Selenium supplemented at 100 ppb provided significant protection when compared to 0 ppb or 1000 ppb. The latter dose may have been marginally toxic. We conclude that dietary supplementation of vitamin E and selenium may influence the relative susceptibility of an animal to pulmonary oxygen poisoning.
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PMID:Effect of dietary vitamin E or selenium on prostaglandin dehydrogenase in hyperoxic rat lung. 608 85


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