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

"Oxidative stress" takes place in animal tissues when the balance between the cellular defense mechanisms (glutathione cycle, superoxide dismutase, catalase, vitamin E, etc.) and conditions capable of triggering oxidative reactions is altered. The oxidative reactions which occur under a variety of conditions were assessed by two non-invasive methods, low-level chemiluminescence and volatile hydrocarbon production. Oxidative stress induced by hyperoxia or organic hydroperoxides in isolated hepatocytes or the perfused liver, respectively, is accompanied by low-level chemiluminescence, the intensity of which is enhanced upon perturbation of the glutathione cycle system, i.e., glutathione depletion and/or selenium deficiency. Oxidative stress during redox cycling of paraquat, when infused into the perfused liver, is not accompanied by light emission, whereas menadione, a substance also capable of redox cycling, was found to elicit photoemission under similar conditions. The basal rates of ethane release by the perfused liver are enhanced during oxidative conditions such as metabolism of hydroperoxides, paraquat redox cycling, and ethanol oxidation. Alkane release during the latter involves the participation of alcohol dehydrogenase and further products of ethanol oxidation, i.e., acetaldehyde, as well as free radicals in some stage of the process. In vivo ethane release by animals with adjuvant arthritis was found higher than in controls, presumably due to a systemic response of liver to inflammation.
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PMID:Active oxygen metabolites and their action in the hepatocyte. Studies on chemiluminescence responses and alkane production. 696 Jun 50

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

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

Hyperoxia and paraquat ingestion are two clinical examples of lung injury thought to be mediated by oxidant mechanisms. An in vitro cytotoxicity assay using freshly explanted 51Cr-labeled lung tissue as the target was used to quantify the ability of hyperoxia and paraquat to directly injure lung parenchymal cells in an environment where indirect mechanisms such as recruitment of inflammatory cells were not possible. There are clear species differences in the susceptibility of lung parenchyma to direct injury by hyperoxia (95% O2) and paraquat (10 microM--10 mM) for 18 h at 37 degrees C, with human and rat lung being more sensitive than rabbit lung. Oxygen radical inhibitors, particularly catalase (1,100 U/ml) and alpha-tocopherol (10 micrograms/ml), reduced hyperoxia and paraquat-induced lung injury, although their ability to do so depended on the oxidant and the species. The simultaneous use of hyperoxia and paraquat accelerated the in vitro lung parenchymal cell injury in each species tested. These studies demonstrate that both oxygen and paraquat can directly injure the cells of the lower respiratory tract without enlisting the aid of additional blood-derived inflammatory cells. In addition, the 51Cr-labeled lung explant assay used for these studies allows for the quantitative assessment of direct lung cell injury and thus may prove useful as an in vitro model by which to investigate lung injury of other etiologies.
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PMID:Oxidant injury of lung parenchymal cells. 729 52

Bacterial endotoxin has a marked protective effect against pulmonary O2 toxicity in rats placed directly in atmospheres of greater than 95% O2. To determine whether endotoxin treatment during exposure to relatively low levels of hyperoxia would protect rats from the accelerated O2 toxicity that normally occurs when these rats are transferred to greater than 95% O2, we gave endotoxin or saline 1) during exposure to 40% O2 (5 days), or 2) during exposure to 40%-60%-85% O2 (2 days at each level). Saline-treated rats showed significantly decreased tolerance on transfer to greater than 95% O2 [LT50 = 47.5 h (exposure 1) and 48.5 h (exposure 2)] compared with normal nonpreexposed rats (LT50 = 66 h). In contrast, endotoxin-treated rats showed a marked tolerance on transfer to greater than 95% O2 [% of rats surviving 72 h = 14/16 (88%) endotoxin-treated vs. 2/16 (13%) saline-treated]. The endotoxin-treated rats, unlike the saline-treated rats, showed significant elevations in lung superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase levels after the O2 preexposure periods; this may account for their significantly improved tolerance when challenged with greater than 95% O2 exposure.
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PMID:Endotoxin reverses the decreased tolerance of rats to greater than 95% O2 after preexposure to lower O2. 732 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

The activities of the enzymes superoxide dismutase, catalase and glutathione peroxidase increase in the lungs of neonatal rats exposed to normobaric hyperoxia. The oxygen-mediated increase in activity of these enzymes, known from previous studies to be an inductive response, was studied in 10- and 25-day-old rats as a function of both oxygen concentration and length of time of exposure to greater than 95% oxygen. In the lungs of 10-day-old rats the increase in superoxide dismutase, catalase, and glutathione peroxidase occurs only at 80% ambient oxygen or greater. In 25-day-old rats a similar pattern of response occurs with pulmonary catalase and glutathione peroxidase. However, unlike the response in 10-day-old rats, pulmonary superoxide dismutase does not increase in oxygen-exposed 25-day-old rats. The time course of enzyme induction was different for 10-day-old rats compared with 25-day-old rats. Exposure of 10-day-old rats to 95+% oxygen resulted in a significant increase in activity of superoxide dismutase after only 4 h when compared with air-exposed control animals. Catalasee and glutathione peroxidase in the same age group increased significantly after 6 h and 12 h of exposure to oxygen, respectively. Maximal levels of superoxide dismutase, catalase and glutathione peroxidase were reached after 6, 12 and 24 h of exposure to hyperoxia, respectively. This level of activity was then maintained throughout the subsequent exposure time up to 96 h. The activity of pulmonary catalase and glutathione peroxidase in 25-day-old rats did not increase significantly after 6 h of exposure to hyperoxia. An apparent plateau of increased activity was reached after 24 h of exposure. As observed with the 3 enzymes in 10-day-old rats, maximal enzyme activities were maintained throughout the subsequent period of oxygen exposure up to 96 h.
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PMID:Adaptation to hyperoxia in the neonatal rat: kinetic parameters of the oxygen-mediated induction of lung superoxide dismutases, catalase and glutathione peroxidase. 742 31

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

Studies have implicated active oxygen species (AOS) in the pathogenesis of various lung diseases. Many chemical and physical agents in the environment are potent generators of AOS, including ozone, hyperoxia, mineral dusts, paraquat, etc. These agents produce AOS by different mechanisms, but frequently the lung is the primary target of toxicity, and exposure results in damage to lung tissue to varying degrees. The lung has developed defenses to AOS-mediated damage, which include antioxidant enzymes, the superoxide dismutases [copper-zinc (CuZnSOD) and manganese-containing (MnSOD)], catalase, and glutathione peroxidase (GPX). In this review, antioxidant defenses to environmental stresses in the lung as well as in isolated pulmonary cells following exposure to a number of different oxidants, are summarized. Each oxidant appears to induce a different pattern of antioxidant enzyme response in the lung, although some common trends, i.e., induction of MnSOD following oxidants inducing inflammation or pulmonary fibrosis, in responses to oxidants occur. Responses may vary between the different cell types in the lung as a function of cell-cycle or other factors. Increases in MnSOD mRNA or immunoreactive protein in response to certain oxidants may serve as a biomarker of AOS-mediated damage in the lung.
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PMID:Regulation of antioxidant enzymes in lung after oxidant injury. 752 4


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