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

1. Using a preterm guinea pig model we examined the impact of oxidative and nutritional stress on the vitamin E status of a number of immature tissues. 2. Liver, brain, lung, red blood cell and plasma alpha-tocopherol concentrations were measured in fed and fasted, preterm guinea pigs exposed to 21 or 95% oxygen for 48 hr. 3. Exposure to hyperoxia did not influence plasma, red blood cell, lung or brain vitamin E status of preterm pups. Liver alpha-tocopherol content was reduced 20% following 48 hr hyperoxic exposure (P < 0.05). 4. Food restriction (48 hr) alone reduced liver (41%) and red blood cell (32%) alpha-tocopherol concentrations in preterm animals while plasma, lung and brain vitamin E levels were unaffected. Combined with hyperoxic exposure, food restriction resulted in a (50%) fall in liver alpha-tocopherol concentration (P < 0.01). 5. The findings of this study suggest that the liver acts as a reservoir for vitamin E in the perinatal period, releasing increased quantities of this lipid soluble antioxidant for use by non-hepatic tissues during periods of hyperoxic and nutrient stress.
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PMID:Distribution of vitamin E between tissues during periods of hyperoxic and nutritional stress in the preterm guinea pig. 810 85

Normobaric hyperoxia has known deleterious effects on survival, presumably due to the generation of superoxide anion and hydrogen peroxide. To investigate the anatomical substrate of the effect of normobaric hyperoxia on the myocardial and striated muscles and the protective effect, if any, of alpha-tocopherol (vitamin E) on these tissues, we administered 95-99% O2 to adult male Wistar rats for 24, 48, 60 and 72 h. The animals were divided into four groups: 1) control I: six rats which breathed room air were used as controls for the ultrastructural studies; 2) control II: 10 rats which breathed 95-99% of O2 for up to 72 h were used as controls for arterial pressure, blood gases/pH, PvO2 and Hb measurements; 3) group A: hyperoxia: 24 rats divided into four subgroups according to the time of exposure to hyperoxia, A24, A48, A60, A72; and 4) group B: alpha-tocopherol/hyperoxia: 24 rats treated with alpha-tocopherol, 15 mg/kg/day, for 14 days before the beginning and throughout the period of hyperoxia, were divided into four subgroups (B24, B48, B60, B72) according to the time of exposure to hyperoxia. Our results showed that: 1) up to the 60th hour, arterial pressure (MAP) was satisfactory; PaO2 > 280 mmHg; PaCO2, pH and Hb were within normal limits; 2) ultrastructural studies of the myocardial apex, the diaphragm and the quadriceps femoris showed dilatation of the sarcoplasmic reticulum/T-tubuli system, swelling of mitochondria, and structural derangement of myofibrils, in particular in the z-bands. The findings were proportionally related to the time of exposure of hyperoxia. They were also more intensely shown on myocardial and diaphragmatic fibers in group A; 3) the survival time (mean +/- SD) was 63.8 +/- 2.5 h in group A and 68.9 +/- 3.8 h in group B. These results suggest that normobaric hyperoxia exerts a cytotoxic effect on the myocardial and striated muscle fibers and that the administration of alpha-tocopherol may delay or change the development of oxygen toxicity.
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PMID:Ultrastructural changes of the myocardial and striated muscle following a challenge of normobaric hyperoxia: the protective effects of alpha-tocopherol. 874 23

The objective of the present study was to demonstrate an antioxidant function for Zn in vivo by comparing the efficacy of Zn or Vitamin E without additional energy intake for protection of Zn-deficient (ZnDF) or energy-restricted (ER) rats from hyperoxia-induced lung damage. Zn (200 mumol ZnCl2/kg b.wt.) or Vitamin E (100 mg alpha-tocopherol/kg b.wt.) was injected IP before exposure to 85% oxygen or air for 5 d. During the exposure period, all injected ZnDF or ER rats were restricted to 5 g Zn-deficient or Zn-adequate diet/day, respectively, the amount of diet consumed by the untreated ZnDF or ER rats. We clearly demonstrated that injection of Zn without additional energy intake can protect ZnDF and ER rats from hyperoxia-induced lung damage assessed by the histopathological scoring system and magnetic resonance imaging (MRI). Vitamin E was not as effective as Zn in either ZnDF or ER rats for preventing hyperoxia-induced lung damage. Zn injection did not exert its antioxidant effect through increased lung CuZn-superoxide dismutase activity or metallothionein. This difference in the effectiveness of Vitamin E and Zn for hyperoxic protection in lung injury may be due to the specificity of antioxidant function, i.e., vitamin E inhibits oxidation of membrane lipids and Zn protects sulfhydryl groups of proteins.
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PMID:Comparison of Zn and vitamin E for protection against hyperoxia-induced lung damage. 898 Oct 47

Although the effect of hyperoxia on antioxidant enzymes is well known, the effect of subtoxic levels of hyperoxia on gamma-glutamyltransferase (gamma-GT), involved in the degradation and uptake of extracellular GSH for intracellular GSH synthesis, is unknown. The aim of the study was to investigate (1) the effects of in vitro hyperoxia on gamma-GT activity of type II cells and (2) the effects of the lazaroid U-74389G and N-acetylcysteine (NAC) on the hyperoxia-induced changes in gamma-GT and antioxidant enzyme activities. At 48 h after isolation, rat type II cells were exposed for 2 days to air, 60% O2 or 85% O2 with or without 30 microM U-74389G or 100 microM NAC. After the exposure, the cells were harvested and assayed for superoxide dismutase (SOD), glutathione peroxidase (GPx), gamma-GT activity, and GSH levels. In another series of experiments 85% O2-exposed cells, with or without U-74389G, were used for Northern blotting of gamma-GT mRNA. Exposure to 60% O2 decreased gamma-GT and GSH by -47 and -34%, respectively, while SOD and GPx activities remained unchanged. After 85% O2-exposure gamma-GT decreased by -55%, SOD and GPx increased by +55 and +87%, respectively, while GSH decreased by -35%. NAC treatment decreased gamma-GT activity by -42% in the air-exposed cells. After 60% O2, U-74389G led to significantly higher gamma-GT (+117%) and GSH (+26%) while NAC only led to higher GSH (+28%) compared to the oxygen-exposed cells not treated with NAC or U-74389G. After 85% O2 U-74389G increased gamma-GT, SOD, and GSH by +72, +58, and +68%, respectively, while NAC only increased SOD (+49%) and GSH (+26%) compared to the oxygen-exposed cells not treated with NAC or U-74389G. The 85% O2 exposure, with or without U-74389G, had no effect on gamma-GT mRNA levels. The results show that hyperoxia decreases rat type II cell gamma-GT activity in vitro. This effect was not related to an altered regulation at mRNA level and it was not associated with the hyperoxia-induced decrease in intracellular GSH, since restoration of the GSH levels by NAC did not restore gamma-GT activity. The lazaroid U-74389G with vitamin E-like properties effectively prevented the decrease in gamma-GT and GSH, so that direct inactivation of the membrane-bound gamma-GT by hyperoxia is the most likely mechanism.
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PMID:Decrease in gamma-glutamyltransferase activity in rat type II cells exposed in vitro to hyperoxia: effects of the 21-aminosteroid U-74389G. 920 59

Experimental and clinical studies have provided evidence for the involvement of oxygen free radicals in development of acute and chronic lung diseases. Hyperoxia is very often an indispensable therapeutic intervention which seems to impose oxidative stress on lung tissue. We measured the effect of hyperoxia (80% O2 for 20 h) (1) on the lipid composition of pulmonary surfactant treated in vitro, (2) on surfactant lipid synthesis and secretion of type II pneumocytes in primary culture, (3) on the lipid composition and on the SP-A content of rat lung lavages and (4) on the turnover of phospholipids, cholesterol, plasmalogens and vitamin E in type II pneumocytes, lamellar bodies and lavages of adult rat lungs. (1) Hyperoxia of lung lavages in vitro reduces the vitamin E content significantly but does not change the relative proportion of PUFA or the content of plasmalogens. (2) Hyperoxia does not affect the biosynthesis or secretion of surfactant lipids and plasmalogens by type pneumocytes in primary culture. (3) Hyperoxic treatment of rats increases the SP-A content and reduces the vitamin E content significantly but does not change the concentration of other lipid components of lung lavage. (4) The vitamin E turnover, measured in type II pneumocytes, lamellar bodies and lung lavages, is increased 2-fold in these fractions. In contrast, the turnover of surfactant cholesterol and surfactant lipids does not change. (5) Hyperoxia caused an increase of the vitamin E uptake by type II pneumocytes resulting in a vitamin E enrichment of lamellar bodies. From these results we conclude that type II pneumocytes are able to regulate the turnover of lipophilic constituents of the alveolar surfactant independently of each other. Hyperoxia caused type II pneumocytes to increase the vitamin E content of lamellar bodies. The lipid and SP-A content of alveolar fluid can be regulated independently each other.
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PMID:Effect of hyperoxia on the composition of the alveolar surfactant and the turnover of surfactant phospholipids, cholesterol, plasmalogens and vitamin E. 921 3

The effect of oxidative stress on the function of brain synapse, the difference in susceptibility of synapse to hyperoxia with age, and the changes in vitamin E status by stress and aging were investigated. Synaptic membrane permeability to sucrose was increased with age. When rats were subjected to hyperoxia, the membrane permeability on each age increased significantly. The susceptibility of synapse of 25 month old rats exposed to stress was about 2.5 times higher than unexposed old rats. The synaptic plasma membrane fluidity decreased significantly either in response to hyperoxia or during aging. The thiobarbituric acid reactive substances (TBARS) in the synaptic plasma membranes increased with age, and those in the membranes of oxygen-exposed rats were higher than in the unexposed rats. The cholesterol/phospholipids (C/P) ratio of the membranes increased significantly with age, and the values in the membranes of oxygen-exposed rats increased more significantly than in unexposed rats of each age. In a measurement of fatty acid content in the membranes, the content of docosahexaenoic acid (DHA, C22:6) decreased significantly during aging and by hyperoxia. These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the membrane, resulting in the deterioration of function of brain synapse, and that susceptibility of synapse to oxidative stress was significantly increased with age. Vitamin E content in the synaptic plasma membranes decreased with age. When rats were subjected to oxidative stress, the content was lower in each age than in normal rat membranes. An intraperitoneal administration of vitamin E prior to stress reduced these abnormalities. It is obvious that vitamin E contributes to the protection against nerve terminal dysfunction caused by oxidative stress.
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PMID:Aging and oxidative stress in neurodegeneration. 952 34

A rat clonal pheochromocytoma cell line (PC12) was cultured under normoxic (21% O2) and hyperoxic (50% O2) conditions. PC12 cells underwent apoptotic cell death when they were cultured in charcoal-stripped medium in a high-oxygen atmosphere. Vitamin E homologs, alpha-tocopherol (alphaT), beta-tocopherol (betaT), gamma-tocopherol (gammaT), and delta-tocopherol (deltaT), were added to the culture medium to study their biological activities. AlphaT was more effective than gammaT and deltaT in preventing hyperoxia-induced cell death. Addition of exogenous alphaT to charcoal-treated medium prevented lactate dehydrogenase (LDH) leakage from PC12 cells and also inhibited the apoptosis, which was accompanied by DNA fragmentation. Additional alphaT was rapidly concentrated in PC12 cells, suggesting that it exerts antioxidant effects. Our data show that PC12 cell death under high-oxygen conditions is due to apoptosis and that, among the vitamin E homologs, alphaT most effectively prevents hyperoxic apoptosis.
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PMID:alpha-Tocopherol protects PC12 cells from hyperoxia-induced apoptosis. 957 8

Previously it was reported that hyperoxia induced death of the human lung adenocarcinoma cell line (A549 cells) by necrosis, not by apoptosis. This study examined proliferation and death of untransformed human small airway epithelial (SAE) cells in normoxia or hyperoxia in comparison with A549 cells. We tested the hypothesis that SAE cells respond differently to hyperoxic injury than do A549 cells. We measured total cell number and viability, thymidine incorporation (SAE cells only), lactate dehydrogenase (LDH) release, and apoptotic changes as markers for cell proliferation and death. Protective effects of antioxidant vitamins also were examined in SAE cells. In normoxia, subconfluent SAE cells had less apoptosis and fewer detached cells, but higher thymidine incorporation than did near-confluent cells. Hyperoxia suppressed thymidine incorporation and augmented apoptosis in both subconfluent and near-confluent SAE cells. Hyperoxia decreased the total cell number only in subconfluence, whereas SAE cell viability declined with hyperoxia in near confluence, but not in subconfluence. For SAE cells, necrosis assessed by LDH release was minimal in all conditions and was not augmented by hyperoxia in SAE cells. In contrast, normoxic A549 cells proliferated more rapidly than did SAE cells with a large number of cells detached during the culture. A549 cells underwent necrotic cell death under confluent or in hyperoxic conditions, but had much less apoptotic cell death. In SAE cells, vitamin E partially prevented the decline of thymidine incorporation with hyperoxia in subconfluence and protected against apoptotic changes with hyperoxia in both subconfluent and near-confluent conditions. Vitamin C prevented apoptosis with hyperoxia only in near-confluent SAE cells. Thus, SAE cells maintained balanced apoptosis and cell proliferation that were altered by cell density and hyperoxia and demonstrated very little necrosis with hyperoxia. Although A549 cells underwent cell death mainly by necrosis, they also were influenced by cell density and hyperoxia. Cell density also determined specific antioxidant vitamin protection in SAE cells.
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PMID:The effects of hyperoxic injury and antioxidant vitamins on death and proliferation of human small airway epithelial cells. 973 Aug 70

We investigated, by measuring oxygen radical absorbance capacity (ORAC), whether hyperoxia causes alterations in antioxidant status and whether these alterations could be modulated by dietary antioxidants. Rats were fed for 8 wk a control diet or a control diet supplemented with vitamin E (500 IU/kg) or with aqueous extracts (ORAC: 1.36 mmol Trolox equivalents/kg) from blueberries or spinach and then were exposed to air or >99% O2 for 48 h. Although the constituents of the extracts were not extensively characterized, HPLC indicated that blueberry extract was particularly rich in anthocyanins, and the spinach extract did not contain any anthocyanins. The ORAC was determined in samples without proteins [serum treated with perchloric acid (PCA); ORACPCA] and with proteins (ORACtot). Hyperoxia induced a decrease in serum protein concentration, an increase in serum ORACPCA, decreases in lung ORACPCA and ORACtot, and an equilibration of proteins and ORACPCA between serum and pleural effusion. These alterations suggested a redistribution of antioxidants between tissues and an increase in capillary permeability during hyperoxia. Only the blueberry extract was effective in alleviating the hyperoxia-induced redistribution of antioxidants between tissues.
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PMID:Hyperoxia-induced changes in antioxidant capacity and the effect of dietary antioxidants. 1036 43

The generation of reactive oxygen species (ROS) is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drug or alcohol, exposure to UV or therapeutic radiation, and deficiency in antioxidant vitamins. Uncontrolled production of ROS often leads to damage of cellular macromolecules (DNA, protein, and lipids) and other small antioxidant molecules. A number of major cellular defense mechanisms exist to neutralize and combat the damaging effects of these reactive substances. The enzymic system functions by direct or sequential removal of ROS (superoxide dismutase, catalase, and glutathione peroxidase), thereby terminating their activities. Metal binding proteins, targeted to bind iron and copper ions, ensure that these Fenton metals are cryptic. Nonenzymic defense consists of scavenging molecules that are endogenously produced (GSH, ubiquinols, uric acid) or those derived from the diet (vitamins C and E, lipoic acid, selenium, riboflavin, zinc, and the carotenoids). These antioxidant nutrients occupy distinct cellular compartments and among them, there are active recycling. For example, oxidized vitamin E (tocopheroxy radical) has been shown to be regenerated by ascorbate, GSH, lipoic acid, or ubiquinols. GSH disulfides (GSSG) can be regenerated by GSSG reductase (a riboflavin-dependent protein), and enzymic pathways have been identified for the recycling of ascorbate radical and dehydroascorbate. The electrons that are used to fuel these recycling reactions (NADH and NADPH) are ultimately derived from the oxidation of foods. Sickle cell anemia, thalassemia, and glucose-6-phosphate-dehydrogenase deficiency are all hereditary disorders with higher potential for oxidative damage due to chronic redox imbalance in red cells that often results in clinical manifestation of mild to serve hemolysis in patients with these disorders. The release of hemoglobin during hemolysis and the subsequent therapeutic transfusion in some cases lead to systemic iron overloading that further potentiates the generation of ROS. Antioxidant status in anemia will be examined, and the potential application of antioxidant treatment as an adjunct therapy under these conditions will be discussed.
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PMID:Interaction of antioxidants and their implication in genetic anemia. 1060 86


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