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

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

The extent of in vivo lipid peroxidation and the in vivo antioxidant effects of alpha-tocopherol and alpha-tocopheryl acetate were studied in newborn rabbits exposed to one of two oxidant stresses: hyperoxia (FIO2 greater than 0.9) or parenteral lipid emulsion infusion. Lipid peroxidation was monitored by measurement of expired ethane and pentane, tissue thiobarbituric acid (TBA) reactants, and tissue lipid peroxides. Seventy-two h of hyperoxia did not increase any of the parameters of lipid peroxidation although mortality was higher in oxygen exposed animals. alpha-Tocopherol (100 mg/kg, intravenous) lowered expired hydrocarbons and tissue TBA reactants, but raised liver lipid peroxides in both air and hyperoxia exposed pups. Infusion of soybean oil emulsion increased production of ethane and pentane, liver TBA reactants, and lung lipid peroxides. Both alpha-tocopherol and alpha-tocopheryl acetate prevented the soybean oil emulsion induced increase in volatile hydrocarbons. alpha-Tocopherol (100 mg/kg, intravenous) administration also prevented the increase in liver TBA reactants and lung lipid peroxides. In identically treated animals, alpha-tocopheryl acetate administration decreased liver TBA reactants but had no effect on lung lipid peroxides. We conclude that alpha-tocopherol reduces lipid peroxidation in newborn rabbits including animals exposed to hyperoxia or infused with lipid emulsions. alpha-Tocopheryl acetate results in lower tissue alpha-tocopherol concentrations and is less effective as an antioxidant in lipid emulsion infused rabbits.
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PMID:Lipid peroxidation in newborn rabbits: effects of oxygen, lipid emulsion, and vitamin E. 371 59

The rate of lipid peroxidation, as determined by expired air pentane and ethane measurements, was assessed in suckled or fasted newborn rats exposed to air or hyperoxia (FIO2 greater than 0.95). Pentane and ethane production in suckled newborn rats did not significantly change with exposure to hyperoxia after birth. Pentane production averaged over a 3-day exposure period was 2.8 pmol/100 g/min in hyperoxia versus 2.5 pmol/100 g/min in air. However, significant increases in ethane production occurred in fasted newborn rats over the first 18 h of life (less than 2.5 pmol/100 g/min increasing to greater than 6 pmol/100 g/min), which were not observed in suckled animals. Although hyperoxia did not cause an increase in pentane or ethane production above air-exposed controls, nutritional deprivation in newborn rats appeared to accelerate lipid peroxidation events and resulted in high mortality in newborn rats exposed to hyperoxia.
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PMID:Lipid peroxidation in the newborn rat: influence of fasting and hyperoxia on ethane and pentane in expired air. 686 3

In recent years a body of data has accumulated, linking the development of bronchopulmonary dysplasia (BPD) to increased oxidative stress in the first few days after birth, since high concentrations of metabolites reflecting increased peroxidation products such as pentane, ethane, protein carbonyl, o-tyrosine, allantoin and F2-isoprostanes, as well as low levels of glutathione and sulfhydryl/total protein ratio, also reflecting increased oxidative load, have been found in the premature infants at risk of or developing BPD. Oxidative stress seems to increase lung antioxidants in some experimental models of BPD and hyperoxia affects foetal lung growth. There are similarities between inflammation and hypoxia/reoxygenation, since both activate a number of inflammatory mediators such as cytokines and adhesion molecules, some of which are found in high concentrations in tracheal aspirate fluid of infants developing BPD. Surfactant production and function are also altered by both hyperoxia and reactive oxygen species per se, making the lungs more vulnerable to injury. This new knowledge may result in new and more efficient therapeutic approaches, hopefully leading to the eradication of BPD in the near future.
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PMID:Bronchopulmonary dysplasia and oxidative stress: are we closer to an understanding of the pathogenesis of BPD? 947

In order to estimate cell damage caused by free radicals during oxygenotherapy, we investigated the time course of two markers of lipoperoxidation: pentane in breath and malondialdehyde (MDA) in blood during brief normobaric hyperoxia. Nine healthy subjects inhaled hydrocarbon-free air (HCFA) for 30 minutes, hydrocarbon-free 100% O2 (HCFO2) for 125 minutes and then HCFA for 70 minutes. After 15 minutes of washout with HCFA, ambient pentane was eliminated. After HCFO2, at T175 versus T30 (i.e., 145 min from the start of 100% HCFO2), pentane production increased (P< 0.05). MDA rose significantly at T155 min (i.e., 125 min from the start of HCFO2), versus T30 (P< 0.01). These results suggest that acute hyperoxia causes a moderate increase in lipid peroxidation in healthy subjects. The increase of pentane and MDA confirms that acute hyperoxia induces lipid peroxidation in healthy subjects.
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PMID:Oxygen toxicity: simultaneous measure of pentane and malondialdehyde in humans exposed to hyperoxia. 1132 14

Long term effects on respiratory function have been found in air divers and have indicated the development of small-airway disease. These effects have been attributed to oxygen toxicity or to venous gas micro emboli (VGM). The airway obstructions observed in air divers raise fundamental questions about whether these alterations exist after one simulated dive. The aim of this report was to study the oxidative stress induced by brief normobaric hyperoxia (FiO2 = 0.6 for 30 min) by measuring breath-exhaled compounds. Oxidative stress was measured by pentane in the expirate of 7 subjects ventilated with hydrocarbon-free air (HFA) before and after the hyperoxic exposure. NO concentration allowed us to determine the inflammatory response in the airway. Venous blood was drawn before and after the O2 breathing period for measurements of malondialdehyde (MDA). In all seven subjects, pentane elimination rates on 60%O2 do not increase after hyperoxia. NO rates during the HFA and hyperoxic exposures are significantly increased (p < 0.05). MDA concentrations are not changed after the hyperoxic exposure. Pulmonary function parameters obtained 225 minutes after hyperoxia are not changed. These results provide evidence that a dry gas and oxygen breathing (FiO2 = 0.6) for 30 min can raise exhaled NO. Oxidative stress assessed by pentane and MDA does not exist. We conclude that dry gas and the mild, 30 minute hyperoxic exposure, frequently encountered by recreational divers may be responsible for an airway inflammation. The consequences of such chronic exposure remains to be established.
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PMID:Effect of air diving exposure generally encountered by recreational divers: oxidative stress? 1250 84