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

Total glutathione levels and the activity of enzymes associated with antioxidant protection in neonatal lung are increased in response to hyperoxia. Glutathione levels in developing rat lung decreased from 24 nmol/mg protein on day 19 of gestation to approximately 12 nmol/mg protein at birth. The initial decrease in glutathione may be due to emergence of other antioxidant systems. Newborn rats placed in 100% oxygen showed a rapid and sustained increase in total glutathione levels which was primarily due to an increase in reduced glutathione. Explants obtained from 16-wk gestation human fetal lung or from 17- to 18-day fetal rat lung also showed increased total and reduced glutathione when cultured in 95% oxygen, 5% CO2 as compared with explants cultured in room air. Type II cells isolated from neonatal rats maintained in oxygen for 6 days also showed glutathione levels twice those found in cells isolated from animals in room air. The activity of antioxidant enzymes (glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase) was increased in lungs of newborn rats exposed to 100% oxygen either at birth or 2 days of age. Antioxidant enzyme activity of lung explants cultured in 95% oxygen, 5% CO2 was also higher than in explants maintained in room air. These results suggest that the increases in glutathione and of antioxidant enzymes in vivo and in vitro are a direct effect of oxygen exposure in lung and that the increase of both glutathione and antioxidant enzyme activity is intrinsic to the lung cell itself. It is likely that increases in glutathione in lung represent an important protective mechanism against oxidant injury.
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PMID:The responses of glutathione and antioxidant enzymes to hyperoxia in developing lung. 403 84

Preexposure of adult rats to ozone (0.8 +/- 0.1 ppm for 7 days) has been found to produce a marked degree of tolerance to hyperoxia (greater than 95% O2). The survival of O3-preexposed rats in hyperoxia for 168 h was 28 of 32 (88%) compared with a rate of 2 of 18 (11%) for nonpreexposed rats. Total lung superoxide dismutase (SOD), glutathione peroxidase (GP), glucose 6-phosphate dehydrogenase (G6-PD), and catalase (CAT) activities were all significantly increased after O3 preexposure and after the subsequent hyperoxic challenge. Probable mechanisms accounting for the markedly improved survival in hyperoxia after O3 preexposure include both increased lung antioxidant enzyme and repair of structural damage by proliferation of alveolar lining cells. The demonstration of cross-tolerance between the atmospheric oxidants O3 and O2 suggests that there are similarities in the lung's adaptation to both oxidants.
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PMID:Ozone-induced tolerance to hyperoxia in rats. 670

The antioxidant enzyme superoxide dismutase (SOD) found in the cytosol of eucaryotic cells and the plasma protein ceruloplasmin are copper containing proteins though to be important in providing protection from oxygen toxicity. To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. Lung SOD activity in the copper-deficient rats was found to be 56% of control and ceruloplasmin content was 6% of control. The copper-deficient rats exhibited increased mortality and enhanced pulmonary toxicity as evidenced by increased pathologic damage and lung edema during the normobaric exposure to 85% O2. Copper-deficient animals also showed increased susceptibility to a hyperbaric exposure of 4 ata of 100% O2 with a decreased time of survival. The copper-deficient rat represents a new model for the study of oxidant injury.
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PMID:Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. 672 91

Because hyperoxia induces early injury to lung endothelial cells and since tolerance to hyperoxia is correlated with increased lung antioxidant enzyme activity, we measured superoxide dismutase, catalase and glutathione peroxidase in both fresh isolates and primary cultures of endothelial cells from pig pulmonary artery and aorta. Cultured endothelial cells were studied at confluency and up to 5 days thereafter under control or hyperoxic conditions. In both types of confluent cell, total and cyanide-insensitive superoxide dismutase increased when compared to fresh cells. The most conspicuous postconfluency change in both types of endothelial cell was a marked decrease in glutathione peroxidase, which could be prevented by the addition of selenomethionine to culture media. A 5-day exposure to hyperoxia resulted in a 2-fold increase in cyanide-insensitive superoxide dismutase in both aortic and pulmonary artery endothelial cells. In view of a similar decrease in DNA in both types of cells despite some differences in enzyme levels, oxygen cytotoxicity could not be related to a particular antioxidant enzyme profile.
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PMID:Effects of culture conditions and hyperoxia on antioxidant enzymes in pig pulmonary artery and aortic endothelium. 711 52

Adult rats preexposed to 10% O2 for 3 days had marked tolerance to hyperoxia-induced lung damage and lethality. The survival of preexposed vs. nonpreexposed rats at 72 h of hyperoxic exposure was 62/62 vs. 7/47 (15%), P less than 0.0001; and after 7 days in 96-98% O2, the comparative survival was 31/33 (94%) vs. 1/20 (5%), P less than 0.0005. Hypoxic exposure produced significant elevations in rat lung superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase activities. In contrast, in adult mice and hamsters, no increased lung antioxidant enzyme levels were produced by preexposure to hypoxia and no significant tolerance to high O2 was realized. (Lethal time50 values for hypoxia-preexposed and nonpreexposed mice, 5.2 and 4.4 days, respectively; and for hamsters, 6.4 and 6.1 days, respectively.) Thus the protective effect of hypoxic preexposure is correlated with adaptive changes in lung antioxidant enzyme activity. Evidence in the literature suggests that superoxide anion (O-2) and H2O2 production may increase under hypoxic conditions. Increased cellular concentrations of their normal substrates could stimulate antioxidant enzyme rises during the preexposure period in hypoxia.
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PMID:Protection from O2 toxicity by preexposure to hypoxia: lung antioxidant enzyme role. 711 67

Undernutrition was found to compromise the tolerance of newborn rat pups to hyperoxia (greater than 95% O2 for 7 days). Survival rate for the normally nourished pups (11 pups/dam) was 56 of 77 (73%) but only 47 of 108 (44%) for the undernourished (18 pups/dam) group (P less than 0.005). Body growth, lung growth, and lung DNA content were significantly reduced by undernutrition. Hyperoxia inhibited these same parameters in both groups of pups. The growth inhibitory effects of O2 and undernutrition were additive, with an especially marked depression of lung DNA content (decreases 65%). Lung maturation was also markedly inhibited by O2 but to a similar extent in both nutrition groups. Despite the disparity in their O2 tolerance, 18/litter and 11/litter pups in O2 responded with equivalent increases in lung antioxidant enzymes. We suggest that the additive depressive effects of neonatal undernutrition and hyperoxia on lung DNA may compromise repair of ongoing O2-induced lung damage and help account for the compromised O2-tolerance we consistently observed even in the presence of significantly elevated antioxidant enzyme defenses.
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PMID:Oxygen toxicity in newborn rats: the adverse effects of undernutrition. 717 19

To determine whether prenatal corticosteroid therapy had adverse effects on the tolerance of the newborn lung to prolonged high O2 exposure, pregnant rats were given injections of dexamethasone (0.2 mg/kg) at 48 and 24 hours prior to parturition, and the newborn pups were placed in 96% to 98% O2 for the first seven days of life. Dexamethasone treatment resulted in significant decreases in body weight (-17%), lung weight (-30%), lung weight/body weight (-22%), and lung DNA (-18%) compared to untreated rat pups. Despite this growth inhibition, the dexamethasone-treated pups had improved survival in hyperoxia (36/48 = 75% vs 29/48 = 60% for untreated rats, P = .055). In addition, substantial "catch-up" lung growth had occurred by seven days and was complete in 28-day-old rats. Dexamethasone did not interfere with normal pulmonary antioxidant enzyme responses to hyperoxia. Thus, prenatal dexamethasone did not compromise the relative tolerance of the newborn to pulmonary O2 toxicity.
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PMID:The effect of prenatal dexamethasone treatment on oxygen toxicity in the newborn rat. 718 11

To examine the dose-response relationships of oxygen-induced lung changes, newborn rats were exposed to various patterns of concentrations of hyperoxia (0.4, 0.8, and greater than 0.95 FiO2) for up to 12 days. Prominent findings included microscopic evidence of lung injury and retarded alveolar development (secondary septal development delayed by as much as 88%), lower whole lung DNA (50% of control), lung-to-body-weight ratios (by as much as 18%), and significantly less compliance in the lungs afer exposures of 6 or 12 day duration to all concentrations of hyperoxia. Significant increases in the activities of the lung protective enzymes superoxide dismutase (129 to 160% of control), catalase (112 to 274% of control), and glutathione peroxidase (118 to 256% of control) were noted when activity was expressed on a DNA basis after 12 day exposures to the various patterns of hyperoxia. Lung changes noted after a 7-day recovery period in air included interstitial thickening (117% of control), persistance of the microscopic injury, and retarded alveolar development seen immediately after initial 6-day hyperoxic exposures. At the conclusion of a second wk of recovery in air, the lungs of hyperoxic exposed animals resembled controls in most respects, but a significantly altered compliance was exhibited by the lungs of animals initially exposed to 6 days of 0.4 or greater than 0.95 FiO2. The dose dependency of oxygen-induced lung injury is complex. Straightforward, stepwise dose-response adequately describes the evolution of microscopic injury and slowing of alveolar development in hyperoxia, but the dose dependency is not as clearly identified in the oxygen-induced retardation of lung growth including DNA content and in changes in antioxidant enzyme activities. Changes in lung compliance clearly do not follow expected dose response relationships.
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PMID:The development of the newborn rat lung in hyperoxia: a dose-response study of lung growth, maturation, and changes in antioxidant enzyme activities. 725 58

Isoxsuprine, a beta-sympathomimetic agent used clinically to delay premature parturition and to possibly accelerate fetal lung maturation, was administered to pregnant rats at 48 and 24 h prior to delivery. Newborn rats were placed in 96-98% O2 (or room air) to determine if the prenatal isoxsuprine treatment compromised their tolerance to prolonged hyperoxic exposure. (Exogenous catecholamines are known to exacerbate O2 toxicity in adult animals). Survival of the isoxsuprine-treated pups in O2 (52%) was no different than for control neonates exposed to hyperoxia for 7 days (57%) (P = 0.22). Body weight, lung weight, lung protein, and DNA content of the newborns were also not altered by the prenatal isoxsuprine treatment. Lung antioxidant enzyme activities for superoxide dismutase, catalase, and glutathione peroxidase were the same at birth in the isoxsuprine-treated and control rat pups, and the enzyme activities increased in response to hyperoxic exposure in each group to an equivalent degree. Thus, in utero treatment with isoxsuprine had no apparent adverse effect on newborn rats exposed to a prolonged O2 challenge.
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PMID:Effect of prenatal isoxsuprine on pulmonary oxygen toxicity in the newborn rat. 737 21

Surfactant liposomes, encapsulating CuZn-superoxide dismutase (SOD) and catalase, increase alveolar type II cell antioxidant activity and protect cells against oxidant stress. We examined whether intratracheal instillation of antioxidant-surfactant liposomes increases lung antioxidant activity in premature rabbits. Pregnant New Zealand White rabbits were delivered by cesarean section on day 28 or 29 of gestation or allowed to deliver spontaneously. After premature birth or at 2 days of age in the term rabbits, the pups from each litter were divided into four groups. One group received 0.1 ml/15 g birth wt of antioxidant-surfactant liposomes by intratracheal injection and was then exposed to hyperoxia (> 95% oxygen) for 24 h and killed. The second group received an equal amount of surfactant liposomes without antioxidant enzymes and was exposed to hyperoxia for 24 h. The third group received air placebo and was exposed to hyperoxia for 24 h, and the fourth group was killed after birth if premature or at 2 days of age if term. After the pups were killed, lung homogenates were investigated for total SOD and catalase activity and DNA content. Each treatment group consisted of 12-15 rabbit pups. Lung antioxidant enzyme activity increased with advancing maturity. Among the premature rabbits, total lung SOD and catalase activity were lowest in the pups killed before hyperoxia and the air placebo controls exposed to hyperoxia, intermediate in the pups treated with liposomes without antioxidant enzymes and hyperoxia, and highest in the pups that received antioxidant-surfactant liposomes and hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antioxidant-surfactant liposomes mitigate hyperoxic lung injury in premature rabbits. 749 79


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