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

We reported previously that Se-adequate neonatal rat pups born to Se-adequate dams were resistant to lung damage by hyperoxia. To assess whether early postnatal Se repletion could also protect developing pups reared under hyperoxia, female Sprague-Dawley rats (n = 20) were bred and fed a Se-deficient (0.04 microgram/g) diet during pregnancy. On d 1 postpartum, dams were divided into two groups and fed either a Se-deficient diet or a Se-repleted (0.5 microgram/g) diet. On d 4 postpartum, litters in each group were randomly assigned to either air or high oxygen (greater than 95% O2) environments. Histologic evaluation of lungs from d-8 pups indicated that Se repletion significantly reduced the incidence of lung lesions caused by hyperoxia. Selenium-repleted pups also had significantly greater lung volumes and internal surface areas. The 7-d period of Se repletion resulted in significantly elevated maternal milk Se concentrations compared with a Se-deficient group, which was reflected in the pups by elevated plasma and hepatic Se concentrations and Se-dependent glutathione peroxidase (SeGPx) activities. Pulmonary glutathione concentration and SeGPx activity in pups were affected by oxygen exposure only, not by Se nutrition. Therefore, early postnatal Se repletion can protect the developing lung from oxygen-induced injury, a protection that is not entirely due to the effects of Se on pulmonary SeGPx activity and glutathione concentration.
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PMID:Postnatal selenium repletion protects lungs of neonatal rats from hyperoxia. 151 25

Our study was designed to assess the role of selenium (Se) in development of neonatal lungs under conditions of normoxia and hyperoxia. Thirty-six female Sprague Dawley rats were bred and fed a Se-deficient (0.03 ppm Se) or a Se-adequate (0.5 ppm Se) diet during pregnancy and lactation. At d 2 postpartum, 24 litters were randomly assigned to either high oxygen (greater than 95%) or air and were cross-fostered for 4 d. Lung weight was significantly enhanced in Se-adequate pups and was not related to high oxygen or air exposure of either the pups or dams. Two types of histologic lesions were observed in the lungs of the pups: septal attenuation and interstitial inflammation. When reared in oxygen, all (17 of 17) Se-deficient pups had lesions. In contrast, only 60% (9 of 15) of Se-adequate pups were affected (p less than 0.01). Lung lesions also were more severe in Se-deficient pups. Se-deficient pups also displayed a significant degree of septal attenuation when reared in air. Se-dependent glutathione peroxidase activity in the pup lung was significantly elevated in response to hyperoxia and was unrelated to Se nutriture. No differences in activities of lung superoxide dismutase, catalase, and glutathione s-transferase were noted between Se-deficient and Se-adequate pups reared in air or high oxygen environments. These data indicate that Se has an important role in the development of neonatal lungs, a role that is even more pronounced during conditions of hyperoxia. The protective role of Se in developing lung tissue cannot be completely explained by enhanced glutathione peroxidase activity.
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PMID:The role of selenium nutrition in the development of neonatal rat lung. 189 47

Exposure of cultured pulmonary artery endothelial cells to 95% O2 resulted in the following sequence of events: decrease in [3H]thymidine incorporation after 24 h; increase of intracellular glutathione (GSH) and loss of cellular protein after 48 h; increase of spontaneous and decrease of provoked prostacyclin formation as well as increased release of cellular LDH after 72 h. This oxygen toxicity model was used to study the following 2 questions. (1) What is the relative importance of the GSH redox cycle compared to catalase as antioxidative defense against hyperoxia? Endothelial cells were grown in selenium-depleted medium to inhibit glutathione peroxidase activity. Endothelial GSH biosynthesis was inhibited by buthionine sulfoximine. Catalase activity was reduced by aminotriazole. Endothelial cells with an impaired GSH redox cycle were easily killed by hyperoxia within 24 h, while inhibition of catalase did not enhance the susceptibility of endothelial cells to hyperoxia. (2) Can endothelial GSH content be increased by exogenous sulfhydryl reagents and does this result in an increase of endothelial cells' resistance to hyperoxia? Exogenous GSH, N-acetylcysteine, cysteine, and L-2-oxothiazolidine-4-carboxylate (L-2-oxo) increased intracellular GSH. All sulfhydryl reagents (with the exception of L-2-oxo) protected endothelial cells from hyperoxia. Concentrations of exogenous GSH and N-acetylcysteine that did not increase intracellular GSH reduced hyperoxia-induced endothelial cell injury. Thus the capacity of the GSH redox cycle rather than intracellular GSH levels or catalase determines endothelial cells' resistance to hyperoxia.
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PMID:Glutathione redox cycle is an important defense system of endothelial cells against chronic hyperoxia. 192 73

Recent evidence supports the concept that Adriamycin cytotoxicity may be mediated by drug semiquinone free radical and oxyradical generation. We tested this hypothesis further by exposing drug-sensitive (WT) and 500-fold Adriamycin-resistant MCF-7 human breast tumor cells (ADRR) to exogenous superoxide- and hydrogen peroxide-generating systems and subsequently monitored cell proliferation as a measure of cytotoxicity. The ADRR tumor cells tolerated a 4-fold greater exposure than sensitive cells to superoxide generated by the xanthine/xanthine oxidase system. Likewise, exposure to hydrogen peroxide produced by the action of glucose oxidase on glucose revealed a 4-fold diminished susceptibility of the drug-resistant cells to this reduced form of oxygen. Similar results were obtained by the direct application of hydrogen peroxide to cells. For both cell lines, cytotoxicity was dependent upon the magnitude and the duration of reactive oxygen exposure. When WT and ADRR cells were cultured under hyperoxia (95% O2:5% CO2), in order to stimulate the intracellular production of oxyradicals, proliferation was inhibited to a greater extent in the drug-sensitive cell line. Additionally, hyperoxia potentiated the cytotoxicity of Adriamycin to both sensitive and drug-resistant cells, but the effect depended upon the concentration of the drug. Under hyperoxic conditions, Adriamycin caused oxygen radical-dependent cytotoxicity to the WT tumor cells at clinically relevant drug concentrations as low as 2 to 3 nM. With ADRR tumor cells, hyperoxia increased the cytotoxicity of Adriamycin at concentrations above 5 microM. Paradoxically, both the WT and the ADRR tumor cells were equally susceptible to the cytotoxic effects of gamma irradiation. It is known that the Adriamycin-resistant MCF-7 cells greatly overexpress glutathione peroxidase and glutathione transferase activities; however, other biochemical defenses against reactive drug intermediates and oxygen radicals have been reported to be similar in the two cell lines. We have reexamined those observations in this report. The resistance of ADRR breast tumor cells to Adriamycin appears to be associated with a developed tolerance to superoxide, most likely because of a twofold increase in superoxide dismutase activity, and a decreased susceptibility to hydrogen peroxide, most likely because of 12-fold augmented selenium-dependent glutathione peroxidase activity. Acting in concert, these two enzymes would decrease the formation of hydroxyl radical from reduced molecular oxygen intermediates.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differential oxygen radical susceptibility of adriamycin-sensitive and -resistant MCF-7 human breast tumor cells. 253 95

1. During the development of D. pictus larvae (Amphibia) in normoxia, selenium (Se) GSH-Px increased whereas non-Se GSH-Px did not change. 2. Acclimation to 60 or 100% O2 did not change Se GSH-Px or non-Se GSH-Px. 3. Hyperoxia did not change tissue peroxidation (TBA-RS) confirming the good capacity of D. pictus tadpoles for O2-adaptation. 4. Since hyperoxic induction of catalase (CAT) has been previously described in D. pictus tadpoles, it is concluded that CAT is more important than both GSH-Px for the establishment of O2-adaptation. 5. Increases of Se GSH-Px, SOD and CAT, are probably important for adaptation to the change from aquatic to aerial environment during metamorphosis in normoxia. 6. Chronic exposure to 100% O2 enormously reduced the lung size of D. pictus larvae.
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PMID:Hyperoxia decreases lung size of amphibian tadpoles without changing GSH-peroxidases or tissue peroxidation. 256 23

Exposure of rats to 100% O2 at high pressure (greater than 2.0 ATA) results in generalized convulsions and death within several hours. The tripeptide, glutathione, has been shown to protect rats exposed to hyperbaric hyperoxia with delayed onset of seizures and prolonged survival. To investigate the hypothesis that glutathione exerts its protective effects via the glutathione redox cycle, we injected selenium-deficient rats and their selenium-supplemented controls with either glutathione (1 mmol/kg) or an equivolume of saline before exposure to 100% O2 at 4 ATA. Selenium-deficient rats exhibit marked reduction in liver glutathione peroxidase activity (GSH-Px). Glutathione administration significantly delayed both the onset of seizures and time to death in the control animals. In selenium-deficient rats, however, glutathione administration was not protective, having no significant effects on time to seizure or time to death. We also measured changes in glutathione concentrations in lung, liver, and brain of these same groups of animals exposed either to hyperbaric hyperoxia or to room air. In control rats, lung and brain glutathione concentrations did not change with the hyperbaric exposure regardless of glutathione pretreatment status, but hepatic glutathione concentration declined significantly during the exposure when glutathione was not supplied. If these animals were pretreated with glutathione, the decline in hepatic glutathione concentrations did not occur. In selenium-deficient rats, the hyperbaric exposure did not result in changes in lung, brain, or liver glutathione concentrations either in the glutathione-pretreated or in the saline-pretreated animals. Exogenous GSH administration does not protect selenium-deficient rats from hyperbaric hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of selenium deficiency on glutathione-induced protection from hyperbaric hyperoxia in rat. 261 Feb 68

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

Rats treated with low doses of bacterial endotoxin have been shown to be protected from oxygen poisoning under normobaric conditions. Induction of lung activity of the antioxidant enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) has been reported to occur with endotoxin administration. GSH-Px is a selenoenzyme and selenium-deficient rats have decreased lung GSH-Px activity and enhanced lung toxicity during a hyperoxic exposure. To determine whether bacterial endotoxin administration can provide protection for animals with decreased antioxidant defenses, selenium-deficient and control rats received daily intraperitoneal injections of 250 micrograms/kg bacterial endotoxin or phosphate-buffered saline (PBS) during normobaric exposure to greater than 95% O2. Both groups of animals were protected from hyperoxia by bacterial endotoxin administration despite the extremely low lung GSH-Px activity in the selenium-deficient rats. GSH-Px, SOD, or CAT activities were not induced in the selenium-deficient rats by 48 hr (the time when the selenium-deficient rats treated with PBS began to die). In the selenium-deficient rat, mechanisms other than enzyme induction appear to be providing early protection from hyperoxia.
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PMID:Endotoxin protects selenium-deficient rats from hyperoxia. 669 Jun 38

Tolerance and adaptation to hyperoxia have been correlated with increases in antioxidant enzymes. This study evaluated whether selenium deficiency would prevent an increase in glutathione peroxidase (GSHPX), a selenium-containing enzyme, during oxygen exposure, and, thus, inhibit adaptation. Because the Torula yeast-based diet, which was used to produce selenium deficiency, was also deficient in cysteine and methionine, the effects of these deficiencies were also evaluated. When rats were exposed to 80% oxygen for 1 week, mortality was 80% for rats deficient in both selenium and the sulfur-containing amino acids, 40% for selenium-deficient rats, 35% for cysteine- and methionine-deficient rats, and 0% for rats fed either a standard laboratory diet or a selenium, cysteine-, and methionine-supplemented Torula yeast diet. However, only one of the six surviving rats with low selenium and none of the rats from any other dietary group died during a subsequent 96 hours of 98% oxygen, indicating adaptation to hyperoxia (LD50 for unadapted rats is 72 hours.) GSHPX activity (per gram of dry weight) was decreased 85% in lungs from unexposed rats fed the low selenium diets. After oxygen exposure, lung GSHPX activity was elevated in all dietary groups. Rats fed the high selenium diets had a 47% increase in enzyme activity, whereas rats with high selenium had a 214% increase. Although hyperoxia caused a relatively high percentage increase in the low Se rats, the resulting absolute GSHPX activity was only 34 to 70% of that of unexposed high selenium rats. The results indicate that both selenium and sulfur-containing amino acids contribute to antioxidant defense. However, although the stress of hyperoxic exposure produces an increase in glutathione peroxidase activity, the absolute lung GSHPX activity is better correlated with tolerance than with adaptation to hyperoxia.
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PMID:Roles of selenium and sulfur-containing amino acids in protection against oxygen toxicity. 687 43

"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


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