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

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

Because high partial pressures of oxygen (O2) can cause peroxidative cleavage of membrane lipids, it is plausible to hypothesize that hyperoxia alters the physical state and composition of lipids in the membranes of pulmonary endothelial cells and that manipulation of the lipid profile may modify endothelial cell tolerance to hyperoxic injury. To test this, porcine pulmonary artery endothelial cells were exposed to 95% O2 at 1 atmosphere absolute (ATA) in the presence or absence of cis vaccenic acid (CVA), a monounsaturated fatty acid (C18:1#11). Plasma membrane fluidity was assessed by fluorescence spectroscopy, plasma membrane lipid composition was quantitated using thin layer and gas chromatography, and cytotoxicity was monitored by measuring release of lactate dehydrogenase (LDH). Hyperoxia caused peroxidation of membrane lipids and decreased fluidity in three distinct lipid domains within the plasma membrane. Incubation with CVA was associated with a reduction in the degree of unsaturation of the constituent fatty acids within all plasma membrane lipid subclasses except monoglycerides. CVA-treated cells were also more resistant to hyperoxic injury as judged by LDH release. These results support the hypothesis that cells with membranes in which the fatty acyl chains are more resistant to the disordering effects of high O2 tensions may be more resistant to O2 toxicity.
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PMID:Interaction between oxygen and cell membranes: modification of membrane lipids to enhance pulmonary artery endothelial cell tolerance to hypoxia. 320 30

We compared the effects of 95% O2 (hyperoxia) alone, endotoxin (20 ng/ml) alone, and 95% O2 plus endotoxin on the release of lactate dehydrogenase (LDH), uptake of 5-hydroxytryptamine (5-HT), and antioxidant enzyme activities in porcine pulmonary arterial and aortic endothelial cells in monolayer culture. Hyperoxia increased LDH release and decreased 5-HT in both endothelial cell types. Hyperoxia also caused a decrease in catalase (CAT) activity and an increase in total superoxide dismutase (SOD) and glutathione reductase (GSH-Red) activities in both cell types. Endotoxin alone had no effect on LDH release, 5-HT uptake, or antioxidant enzyme activities. However, endotoxin prevented the hyperoxic increase in LDH release and the hyperoxic decrease in 5-HT uptake. Endotoxin plus 95% O2 had no consistent effect on the antioxidant enzyme profile in pulmonary artery or aortic endothelial cells. These results indicate that (1) hyperoxia injures both pulmonary artery and aortic endothelial cells in culture and causes changes in the antioxidant enzyme profile that are similar in the two cell types; (2) hyperoxia-induced decreases in CAT activity and increases in SOD activity may be responsible for increased sensitivity of endothelial cells to O2 toxicity; and (3) endotoxin protects against hyperoxic injury to endothelial cells in vitro, but increases in antioxidant enzyme activities are not the mechanism for this protection.
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PMID:Effect of oxygen and endotoxin on lactate dehydrogenase release, 5-hydroxytryptamine uptake, and antioxidant enzyme activities in endothelial cells. 388 60

Paraquat (PQ) is a herbicide known to generate O2 radicals and to injure lung epithelial cells, leading eventually to pulmonary fibrosis. To test for the possible existence of a direct cytotoxic action of PQ on endothelial cells, we have studied, for up to 5 days, the action of 10(-6) to 10(-4) M PQ on primary cultures of pig aortic endothelial cells and compared these effects to those obtained with exposure to 95% O2-5% CO2. The decrease in DNA and protein content of Petri dishes and the increase in lactate dehydrogenase release were found to depend on PQ concentration and the duration of exposure to PQ. The toxic effects of hyperoxia were intermediate, ranging between those obtained with 10(-5) and 10(-4) M PQ. Hyperoxia and 10(-4) M PQ produced a similar marked inhibition of DNA synthesis after a 1-day period of exposure. Combined exposure to both PQ and hyperoxia resulted in changes comparable to those obtained with hyperoxia alone (decrease in protein and DNA content) or PQ alone (lactate dehydrogenase release). Additive effects were seen only for the inhibition of DNA synthesis. The selenomethionine-related increase in glutathione peroxidase activity had a protective effect against hyperoxia-induced lactate dehydrogenase release but not against PQ induced cytolysis. Finally, shorter exposures to O2 and PQ revealed the existence of a trend toward recovery only for cells exposed to hyperoxia. The prolonged toxic action of PQ could not be related to PQ accumulation and storage by endothelial cells. These studies indicate that PQ can exert a direct, dose-dependent, and prolonged cytotoxic effect on cultured endothelial cells.
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PMID:Direct toxic effects of paraquat and oxygen on cultured endothelial cells. 396 1

Macrophages synthesize many secretory products in vitro but the stimuli for their production and their pathophysiologic significance in vivo are largely unknown. In the present investigation, we found that hyperoxia damaged rabbit alveolar macrophages (AM) in vitro as manifested by decreased cell numbers, increased lactate dehydrogenase (LDH) release, and the development of ultrastructural abnormalities that resembled those seen in AM in situ or lavaged from lungs of rabbits exposed to hyperoxia in vivo. Hyperoxia also stimulated cultured rabbit AM to release chemotaxins for polymorphonuclear leukocytes (PMN) that were similar in molecular weight to chemotaxins obtained from lung lavages of rabbits exposed to hyperoxia in vivo. Our results suggest that alveolar macrophage secretory products may play a physiologically relevant role in recruitment of PMN to the lungs in pulmonary oxygen toxicity.
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PMID:Macrophage effector function in pulmonary oxygen toxicity: hyperoxia damages and stimulates alveolar macrophages to make and release chemotaxins for polymorphonuclear leukocytes. 658 27

Increased intracellular production of oxygen radicals is a major etiology of cell damage from many quinoid antibiotics, environmental toxicants, and hyperoxia. Enhancing the intracellular content of protective enzymes can provide a means of limiting biological damage caused by free radicals. Liposomal entrapment and intracellular delivery of superoxide dismutase to cultured porcine aortic endothelial cells increased the specific activity of cellular superoxide dismutase 6 to 12-fold. This augmented superoxide dismutase activity persisted in cultured endothelial cell monolayers and rendered these cells resistant to oxygen-induced injury. Culture of confluent endothelial cells in hyperoxia increased 51Cr and lactate dehydrogenase release in an oxygen concentration-dependent manner. Superoxide dismutase-augmented endothelial cells were resistant to oxygen damage compared to untreated controls, in a superoxide dismutase concentration-dependent manner. Free superoxide dismutase in the absence or presence of liposomes containing no enzyme had no effect on cellular enzyme activity and did not protect from oxygen damage. Liposomes made from saturated fatty acid-containing phospholipids had a small but significant protective effect on oxygen-induced cell damage. These liposomes probably increased endothelial cell membrane saturated lipid content and thereby decreased peroxidative damage when the cells were exposed to hyperoxia. Conversely, preincubation of cells with arachidonic acid increased cell arachidonic acid content, sensitivity to hyperoxia, and hyperoxia-induced production of thiobarbituric acid material. These data suggest that intracellular delivery of superoxide dismutase prevents oxygen-induced cell damage and that superoxide is an important mediator of cellular oxygen toxicity.
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PMID:Liposome-mediated augmentation of superoxide dismutase in endothelial cells prevents oxygen injury. 668 7

To determine what biochemical indexes might be useful in measuring the endothelial response to hyperoxia in vitro we exposed endothelial cell monolayers (ECM) from pig aortas to either hyperoxic (95% O2:5% CO2, 1 atm) or control conditions (95% air:5% CO2) and made the following measurements: (a) DNA and protein contents remaining in the ECM; (b) lactate dehydrogenase (LDH) activity in the medium; (c) the net uptake of rubidium (Rb+), adenine, and adenosine; and (d) cellular ATP and medium lactate. Twelve hours of hyperoxic exposure did not cause significant changes. After 24 or 48 h of hyperoxia, DNA and protein contents were decreased; LDH activity and the protein-to-DNA ratio were increased; adenosine uptake was decreased per ECM but was unchanged when corrected for culture DNA and protein contents. Adenine uptake was unaltered as were cellular ATP content and medium lactate concentration. The net Rb+ uptake-to-DNA ratio was increased after 24 h but not after 48 h of hyperoxia. The extent of the DNA and LDH changes indicated that the cellular disturbance caused by hyperoxia was progressive from 12 to 48 h. Presence of superoxide dismutase (250 U/ml) prevented both the increase of LDH activity and the decrease of protein after 48 h but did not affect the decrease of DNA. These results suggest that the cells remaining in the ECM after hyperoxia have normal biochemical function and may represent a subpopulation of cells more resistant to oxygen toxicity than the damaged cells.
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PMID:Effects of hyperoxia on biochemical indexes of pig aortic endothelial function. 688 2

The hypothesis that severe lung damage generated by acid aspiration or a 50-hour exposure to 100% oxygen aggravates ethanol-induced hemorrhagic mucosal lesions in the stomach was examined in the rat. Animals were either given intratracheally with pyrogen-free saline or HCl (pH 1.75) or exposed for 50 h to 100% oxygen before the intragastric application of 1 ml of 50 or 75% ethanol. All rats receiving 50% ethanol were also given 3% monastral blue, 3 min before ethanol administration as a vascular tracer. Lung acid damage and inflammation as assessed by bronchopulmonary lavage were severe. We observed a significant increase in extracellular lactate dehydrogenase beta-glucosaminidase, albumin and the number of polymorphonuclear leukocytes in the lavage fluid. The number of resident macrophages decreased significantly. Blood gas analysis was not influenced. Hemorrhagic gastric mucosal lesions after 50 or 75% ethanol increased from 4.4 or 8.2% to 9.8 or 13.1% after HCl and from 6.7 or 18.2% to 10.6 or 21.6% of the glandular stomach following oxygen exposure. The area of mucosal vascular damage caused by 50% ethanol as revealed by monastral blue labelling was 3.3 and 2.6 times larger in rats with lung damage induced by HCl or hyperoxia, respectively. Thus, severe lung damage predisposes to microvascular damage and aggravates chemically induced hemorrhagic mucosal lesions.
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PMID:Lung damage aggravates gastric mucosal lesions induced by ethanol in the rat. 765 45

Exposure to hyperoxia causes alveolar macrophage (AM) injury. The present study investigates the roles of intracellular antioxidant enzymes and of glutathione in the protection of AMs against hyperoxia in a biphasic cell culture system in aerobiosis. The effect of normoxia or hyperoxia on the integrity of AMs was related to indices of cell injury (ATP cell content and lactate dehydrogenase release into culture medium) and cell mass (protein content of AMs). Antioxidant activities were measured in guinea-pig AMs exposed to 95% O2 or to normoxia (control cells) for 3 days. A 3-day AM culture in normoxia showed a significant decrease in protein and catalase, whereas ATP cell content, superoxide dismutase (SOD) (both Cu,Zn-SOD and Mn-SOD) and glutathione peroxidase (GPx) activities significantly increased. The content of reduced glutathione (GSH) did not change. Using the ATP content in AMs expressed as a cell injury index (CII), AM injury increased with increasing O2 exposure time (1 day: 13 +/- 4.4%; 2 days: 34 +/- 3.8%; 3 days: 40 +/- 4.1%; 4 days: 55 +/- 7.3%; 6 days: 87.5 +/- 5.4%). Exposure to 95% O2 for 3 days was associated with a significant decrease in ATP cell content, protein, catalase and GSH to the total glutathione ratio, whereas SOD, GSH and total glutathione did not change significantly. The GPx activities increased significantly. There was no significant correlation between the AM CII and SOD or GPx content. In contrast, a significant correlation was observed between hyperoxia-induced AM CII and catalase content (r = 0.71) and glutathione content (r = 0.71).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between oxygen-induced alveolar macrophage injury and cell antioxidant defence. 774 27

Leukemia inhibitory factor (LIF) and tumor necrosis factor (TNF) have been shown to protect animals from radiation, hyperoxia, and endotoxic shock. TNF is also known to induce the expression of manganese superoxide dismutase (MnSOD) in vitro and in vivo. We therefore examined the effects of these cytokines on reperfusion injury in the isolated rabbit heart model. Rabbits were injected intravenously with 10 micrograms of either human TNF-alpha or lymphotoxin (TNF-beta), or murine TNF-alpha or murine LIF dissolved in saline. Control animals were injected with an equal volume of saline. After 24 h, hearts were isolated and perfused. Following an equilibration period, the hearts were subjected to 1 h ischemia and 1 h of reperfusion. All treated groups showed significant increases in percent recovery of developed tension (% preischemic) when compared to saline-treated control hearts. In addition there were significant decreases in lactate dehydrogenase release (LDH), accumulation of thiobarbituric acid reactive substances (TBARS), and accumulation of carbonyl proteins. These results correlate with increases in myocardial MnSOD activity. Thus, the protection from myocardial reperfusion injury seen in the pretreated group may be due to a mechanism that involves the induction of MnSOD.
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PMID:Leukemia inhibitory factor and tumor necrosis factor induce manganese superoxide dismutase and protect rabbit hearts from reperfusion injury. 776 Mar 46


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