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

By culturing HeLa cells at stepwise increased oxygen tensions over a prolonged period of time (approximately 21 months) we selected a substrain capable of growing under 80% O2/19% N2/1% CO2, an oxygen level that is lethal to normal HeLa cells, adapted to 20% O2/79% N2/1% CO2. The 80% O2-adapted cells exhibited the following characteristics. At the ultrastructural level an abnormal mitochondrial morphology was observed: compared to normal cells, mitochondria of the hyperoxia-adapted cells exhibited a 3-fold larger mean profile area in sections and were slightly decreased in number; the relative mitochondrial volume was increased 2-fold, whereas the size of both cell types was the same. Mitochondrial matrix appeared less dense in the hyperoxia-adapted cells; no structural damage was detected. Compared to the 20% O2-adapted cells O2 consumption per cell was approximately 40% decreased in the 80% O2-adapted cells. Under hyperoxic conditions 20% O2-adapted and 80% O2-adapted cells exhibited very similar cyanide-resistant respiration rates (0.16 +/- 0.04 and 0.15 +/- 0.02 fmoles/cell/minute, respectively), suggesting that the increased O2 tolerance of the 80% O2-adapted cells was not due to a decreased cellular production of activated oxygen species at hyperoxia. Cellular levels of the enzymes directly involved in protection against activated oxygen species, i.e., superoxide dismutases, catalase, and glutathione peroxidase, were normal or slightly below normal in the 80% O2-adapted cells, implying that these enzymes were of no significance for the increased O2 tolerance. In addition, the specific activity of glucose-6-phosphate dehydrogenase, a key enzyme for cellular production of NADPH, was not related to the degree of O2 tolerance. Our results suggest that the increased O2 tolerance of the 80% O2-adapted cells is neither based on cellular properties controlling the formation or removal of intracellular activated oxygen species nor on the cellular capacity to repair or replace damaged cellular components. We speculate that the increased O2 tolerance is largely due to a genetically determined increased resistance of oxygen-sensitive cellular targets.
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PMID:Some characteristics of hyperoxia-adapted HeLa cells. A tissue culture model for cellular oxygen tolerance. 298 61

The activity of antioxidant enzymes were measured in alveolar type II cells isolated from control and 85% oxygen-exposed rats to determine if type II cells, an oxygen-resistant lung cell type had constitutively high enzyme activities and to measure the effect of hyperoxia on these antioxidant enzyme. Type II cells were isolated from lungs of control rats and rats exposed to 85% O2 for 7 days. In whole lungs of rats exposed to 85% oxygen there is an increase in activity (per lung or per mg lung DNA) in the antioxidant enzymes CuZn superoxide dismutase, Mn superoxide dismutase, catalase, glutathione peroxidase and glucose-6-phosphate dehydrogenase. Oxygen exposure significantly increased (p less than 0.05) all type II cell antioxidant enzyme activities when expressed per mg DNA. The protein content of oxygen exposed type II cells increased 25% from (63.9 +/- 4.8 micrograms/10(6) cells to 79.6 +/- 4.2 micrograms/10(6) cells, p less than 0.05). When type II cell enzyme activities were expressed in U/mg cell protein, only CuZn superoxide dismutase and Mn superoxide dismutase increased in activity following oxygen exposure (by 43% and 28% relative to air exposed lung type II cells, respectively, p less than 0.05). This suggested that most lung cell antioxidant enzymes increased in activity following oxidant stress in proportion to increased cell mass. CuZn and Mn superoxide dismutase increased activity to an extent greater than the increase in type II cell protein content after oxygen exposure. Alveolar macrophages lavaged from control and oxygen-exposed rats were also evaluated, and they had no significant change in CuZn and Mn superoxide dismutase activities. Type II cells accounted for 10% and 17% of alveolar cells in control and oxygen treated rats. By knowing the antioxidant enzyme activities in type II cells, the total enzyme activity of whole lung and the number of type II cells in control and oxygen exposed rats from morphometric data, we calculated the percent of whole lung enzyme activity accounted for by type II cells. Type II cells accounted for a high percentage of lung glucose-6-phosphate dehydrogenase (58% in control rats, 65% in oxygen exposed rats) but a low percentage of Mn superoxide dismutase (4% in control rats, 6% in oxygen exposed rats).
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PMID:Antioxidant enzyme activity in alveolar type II cells after exposure of rats to hyperoxia. 300 82

The present study was conducted on bone tissue responses to irradiation towards a treatment model of mandibular irradiation injury by comparing the results of experimental observations of irradiation effects on rabbit hind legs and rat mandibular bones (paper I, II and III) with clinical observations of irradiation effects on the human mandible (paper IV, V and VI). The main results of the study were as follows: Bone marrow haemorrhage, eosinophilia and incipient edema were encountered in the rabbit leg one day after a single irradiation dose. Edema and fibrosis were the salient features after five weeks, while both regenerative and fibrotic changes predominated eleven weeks after irradiation. The changes were the more extensive the greater the irradiation dose was. Empty lacunae as a sign of cell damage in cortical bone already appeared on the first day after irradiation; this effect reached its maximum when the dose was 20 Gy or more. Bone marrow and subcutaneous tissue pO2 and pCO2 were measured by means of implanted Silastic tonometers in irradiated and nonirradiated rabbit hind legs. Single dose irradiation was followed by a rapid, dose dependent decrease of marrow pO2. The corresponding effect on pCO2 was weaker and appeared later. The response to hyperoxia in the bone marrow became weaker when the irradiation dose increased. Less significant was the response of CO2 tension to hyperoxia. O2 and CO2 tensions were recovered after single dose irradiation both in subcutaneous tissue and in bone marrow, but the reduction was less in bone marrow. During the twelve weeks observation period clearly better recovery in tissue gas tensions was observed in subcutaneous tissue than in bone marrow. Nonirradiated periosteal grafts on irradiated bone cavities in the rabbit tibia induced more rapid and intense mature bone formation than irradiated periosteal grafts. The irradiated periosteum, even after a single dose of 20 Gy, had some osteogenetic capacity. The alkaline phosphatase content was lowered eight weeks after surgery in irradiated legs but clearly exceeded control values twelve weeks after surgery indicating new bone formation. Lysosomal enzyme DAP II contents were increased in all irradiated specimens as a sign of disturbed bone formation. The tissue concentrations of acid phosphatase, cytochrome oxidase, lactate dehydrogenase, isocitrate dehydrogenase, glucose-6-phosphate dehydrogenase and succinate dehydrogenase in the immediate postirradiation period showed a greater increase in activity in the cut lines of the irradiated rat mandibles than in those of the nonirradiated mandibles.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bone tissue response to irradiation and treatment model of mandibular irradiation injury. An experimental and clinical study. 309 Aug 54

The in vivo effects of hyperoxia were studied in lung colonies formed by B16-F10 melanoma cells in C57BL/6 mice. Several antioxidant defenses were found to change with in vivo exposure: glutathione reductase and glucose-6-phosphate dehydrogenase activities decreased as compared with levels in the cultured cells, glutathione peroxidase activity dramatically increased, and Mn-superoxide dismutase activity and levels of total glutathione were similar in vivo and in vitro. Exposure of tumor-bearing animals to 70%, O2 for 3 weeks did not alter the antioxidant defenses measured in the tumors. One hundred percent O2 exposure did not affect either initial arrest or subsequent retention of radiolabeled B16-F10 cells in the lung. Likewise, hyperoxia did not appear to alter cell division in B16-F10 cells growing in the lung. These results are consistent with our previous studies indicating that the B16-F10 cell line is resistant to levels of O2 in vivo that adversely affect other tumor cell lines.
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PMID:Effects of hyperoxia on B16-F10 cells in vivo. 318 29

Single, preexposure, parenteral injection with both recombinant tumor necrosis factor/cachectin (TNF/C) and interleukin-1 (IL-1) prolonged the survival of rats (144 +/- 9 h) in continuous hyperoxia (greater than 99% O2 at 1 atm) when compared with rats injected with boiled TNF/C and boiled IL-1 (61 +/- 2 h), TNF/C alone (61 +/- 2 h), IL-1 alone (62 +/- 2 h), or saline (64 +/- 3 h). After exposure to hyperoxia for 52 h, pleural effusion volume, pulmonary artery pressure, total pulmonary resistance, and lung morphologic damage were decreased in those rats given TNF/C and IL-1 as compared with saline-injected rats. In parallel, ratios of reduced (GSH) to oxidized (GSSG) glutathione were greater (P less than 0.05) in lungs of TNF/C + IL-1-injected rats (91 +/- 20) than of saline-injected rats (30 +/- 4) that had been exposed to hyperoxia for 52 h. No differences were found in superoxide dismutase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, or catalase activities in lungs of TNF/C + IL-1- or saline-treated, hyperoxia-exposed rats. Our results indicate that pretreatment with TNF/C and IL-1 favorably altered lung glutathione redox status, decreased lung injury, and enhanced survival of rats exposed to hyperoxia.
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PMID:Recombinant tumor necrosis factor/cachectin and interleukin 1 pretreatment decreases lung oxidized glutathione accumulation, lung injury, and mortality in rats exposed to hyperoxia. 349 53

Administration of monoamine oxidase type A inhibitor clorgyline to rats before hyperoxia prevented oxygen-induced increase in diene conjugate and Shiff's base brain and plasma levels in hyperoxia. This was due to antioxidative effect of clorgyline which resulted in stabilization of blood cellular membranes. Clorgyline had a normalizing effect on extraerythrocyte hemoglobin level, total peroxidase activity and glucose-6-phosphate dehydrogenase activity in the serum.
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PMID:[Effect of clorgyline on the intensity of lipid peroxidation and on erythrocyte membrane stability in hyperoxia]. 380 52

The hypothesis was tested that continuous hyperoxia would enhance the development of lung tumors in mice. In strain A/J mice treated with a single dose of urethan (1000 mg/kg) and exposed to 70% O2 for 16 wk, an average of 5 tumors per lung developed, whereas in animals kept in air, an average of 20 tumors per lung was found. When the animals were returned to air after oxygen exposure, it was found that a difference of 15 tumors per lung between the two groups persisted up to 1 yr later, indicating that O2 was tumoricidal. The shortest duration of O2 exposure to be effective was 4 wk, and delay of O2 exposure up to 12 wk after urethan still was effective in reducing the number of developing tumors. Histopathology showed that continued exposure to 70% O2 produced some hyperplasia of the bronchiolar epithelium and only very discrete changes in the pulmonary parenchyma. Analysis of cell proliferation patterns with a continuous [3H]thymidine labeling technique showed a persistent high cell labeling in the bronchiolar epithelium and a temporary increase in alveolar wall cell labeling. Chronic hyperoxia failed to alter the activities of pulmonary superoxide dismutase or glucose-6-phosphate dehydrogenase. Ornithine decarboxylase, on the other hand, was increased as long as the animals remained exposed to oxygen. It was concluded that hyperoxia kills developing tumor cells in mouse lung.
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PMID:Inhibition of mouse lung tumor development by hyperoxia. 394 76

Diethylmaleate (DEM) decreases glutathione (GSH) levels in various organs by enzymatic conjugation with reduced GSH catalyzed by GSH transferase. We have examined levels of GSH, glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PD) in lungs of 200-250-g rats after intraperitoneal injection of 0.5 or 1 g DEM/kg body wt. The GSH levels are severely depressed at 2 and 4 h but have essentially recovered by 12 and 24 h after either dose of DEM. The GR and G6PD activities in the 1 g/kg group are depressed at 4 h to a lesser extent than the GSH levels and also return to normal by 12 and 24 h. These enzymes are not affected in the 0.5 g/kg group. To determine whether these transient decreases in GSH and related enzymes affected O2 tolerance, we exposed rats injected with DEM to greater than 98% O2 and found that halftime (t1/2) for survival was decreased in rats receiving both 0.5 and 1 g DEM/kg body wt when compared with untreated or saline-injected controls (t1/2 control, 74 h; 0.5 g DEM, 59 h; 1 g DEM, 53 h). No deaths occurred in air controls at 1 mg/kg DEM for up to 5 days. DEM, in itself, caused no morphological alteration of the lung. Thus a decrease in lung GSH and related enzymes, occurring by 4 h and reversed by 12 h, has a significant effect on the subsequent progression of lung pathology and indicates that early biochemical events occurring in lungs exposed to hyperoxia may be very important in determining the degree of longer-term damage to rat lungs.
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PMID:Transient depletion of lung glutathione by diethylmaleate enhances oxygen toxicity. 398 Mar 59

We used a nutritional deprivation model to produce intrauterine growth-retarded (IGR) rat pups (birth weight = approximately 75% of normal). The IGR newborns evidenced a marked reduction in tolerance to greater than 95% O2 exposure: 10-day survival = 10/47 (21%) versus 18/36 (50%) for control pups, and LT50 = 7.2 days versus 10 days for controls (p less than 0.01). Various lung parameters at birth and during O2 exposure were examined to try to define why prenatal undernutrition should compromise the survival of IGR rats in hyperoxia. We found decreased lung glutathione peroxidase and glucose-6-phosphate dehydrogenase activity (with normal superoxide dismutase and catalase levels) in the IGRs at birth; decreased lung disaturated phosphatidylcholine content (even more markedly decreased in 1-day premature pups); and decreased lung surface area/body weight. These factors and other features of newborn IGRs reported in the literature may help to explain how prenatal undernutrition compromises postnatal tolerance to prolonged high-O2 exposure.
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PMID:Intrauterine growth-retarded rat pups show increased susceptibility to pulmonary O2 toxicity. 398 89

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


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