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

The increase of cytochrome P-450 by 34% and its catalytic activity with substrate amidopyrine by 57% as compared with control has been shown under hypoxia (0.029 MPa, 1 h). Hyperoxia (0.2 MPa, 1 h) increases the metabolism of amidopyrine by 148%, benzo[a]pyrene by 158% and aniline by 114% and consecutive affection of hypoxia and hyperoxia--by 247, 45 and 138% correspondingly at fixed cytochrome P-450 amount in both series. The amount of diene conjugates and Schiff's bases under hypoxia increases by 40 and 69% correspondingly, the activity of SOD and catalase decreases by 25 and 23%. The activity of hyperoxia raises the diene conjugate content by 19% at all this SOD activity increases by 95%. Consecutive affection of hypoxia and hyperoxia increases the level of diene conjugates and Schiff's bases by 26 and 23% correspondingly, without changing SOD and catalase activity. The relative microsomal viscosity of lipid layer and zones of enzyme-lipid contacts decreased by 20 and 24% under hypoxia, but under hyperoxia and consecutive affection and hypoxia and hyperoxia it increases by 29-28% and 56-40% correspondingly.
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PMID:[The effect of hypoxia and of subsequent baro-oxygenation on the function of the microsomal oxidation system in the rat liver]. 130 2

Influence of hypoxia (0.029 MPa, I h) followed by hyperoxia (0.2 MPa, I h) on microsomal oxidation and lipoperoxidation was studied in rat liver and lungs. Distinct increase of cytochrome P-450 catalytic activity with amidopyrine and benzo-a-pyrene as substrates of the I type was found after hypoxia, subsequent hyperoxia resulted in significant increase of amidopyrine and benzo-a-pyrene metabolism in liver and lung tissues and of aniline metabolism in liver tissue. Both hypoxia and hyperoxia led to increase in content of diene conjugates and Schiff bases in liver and lungs, while the increase of diene conjugates in liver and both diene conjugates and Schiff bases in lungs were observed under hyperoxic conditions.
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PMID:[Cytochrome P-450 activity and lipid peroxidation in rat liver and lung microsomes during hypoxia and followed by pressure oxygenation]. 175 89

Induction by phenobarbital and 3-methylcholanthrene of enzymes metabolizing xenobiotics in rat exposed 55 hrs to hyperoxia, is maintained. The level of microsomal pulmonary and hepatic cytochrome P-450 has even increased. In rat protected against a hyperoxia 6 days, stimulation of UDP-glucuronosyltransferase does not decrease and malondialdehydes level does not change. These results assume the probable role of enzymatic induction in the tolerance to hyperoxia induced in rast by treatment with phenobarbital and 3- methylcholanthrene.
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PMID:[Enzymatic induction with phenobarbital and 3-methylcholanthrene in rats exposed to normobaric oxygen]. 210 74

Age-related changes in pulmonary formation of arachidonic acid (AA) metabolites are thought to play an important role in regulating cardiopulmonary function. This study addresses the potential role of reduced glutathione (GSH) in modulating cyclooxygenase product formation in the developing lung. Prostaglandin H2 (PGH2) metabolism was studied in microsomal fractions isolated from the lungs of unventilated fetal, neonatal and adult goats. GSH-dependent PGH2 to PGE2 isomerase activity in microsomal fractions from the perinatal (fetal and neonatal) goat lung was not saturable with respect to GSH and can respond to changes in GSH concentration over the range of 0.01 to 30 mM, which encompasses the full range the intracellular GSH levels reported in the literature. However, in fractions from the adult, a lower rate of PGE2 formation is observed at higher GSH concentrations. In addition, the tissue levels of GSH exhibited developmental stage-related differences with fetal being higher than neonatal or adult. The present observations may have physiologic relevance, in that decreases in pulmonary GSH levels after birth may contribute to decreases in plasma PGE2 levels by decreasing pulmonary PGE2 synthesis, thereby contributing to closure of the ductus arteriosus; conversely, increased GSH levels associated with hyperoxia may contribute to persistence of ductal patency. Formation of 6-keto-PGF1 alpha and of TXB2 (the stable metabolites of prostacyclin and TXA2) was decreased when PGE2 formation was increased by GSH activation of PGE2 isomerase in fractions isolated from all three developmental stages. A similar pattern of product formation was observed when AA was employed as substrate. These data suggest the possibility that changes in GSH concentration may modulate eicosanoid formation in cells that contain GSH-dependent PGE2 isomerase, as well as either or both prostacyclin or thromboxane synthase(s).
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PMID:Concentration-activity profile of the modulation of cyclooxygenase product formation by reduced glutathione in microsomal fractions from the goat lung. 211 78

We compared the superoxide anion generating capacity of subcellular fractions from the lungs of neonatal and adult rats. Microsomal and mitochondrial fractions from adult rats produced approximately three times more superoxide (nanomoles per minute per milligram protein) than fractions from neonatal rats in the presence of 100% O2. Subcellular superoxide anion generating capacity was also examined in adult and neonatal rats exposed to greater than 95% fractional concentration of O2 in inspired gas. The O2- produced by mitochondrial and microsomal fractions of adult and neonatal rats increased above control levels for the first 24 h and declined below control values after 48 h of exposure in adults, whereas the elevated O2- production was sustained in microsomal fractions of neonates through 60 h. During the course of hyperoxic exposure, the largest difference in the superoxide generating capacity between adult and neonate was observed after 8-24 h of hyperoxia. The microsomal and mitochondrial fractions from adult rats produced three to seven times more O2- compared with neonatal rats. Cu,Zn superoxide dismutase (SOD) increased during the course of hyperoxia only in neonates at 8, 24, and 48 h of exposure. No change was observed in the activity of Mn SOD. The ratio of SOD activity (units per lung) to subcellular superoxide generating capacity (nanomoles per minute per lung) was calculated for the normal adults and neonates. The ratio for adult rats averaged 23 and 17 for mitochondrial and microsomal fractions, respectively, and 51 for neonatal rats for both subcellular fractions under normoxic conditions. These results suggest that O2- tolerance of neonates may be explained by the favorable balance between antioxidant defenses and subcellular superoxide generating capacity. The role of increased activity of Cu,Zn SOD as an accompanying or a causative phenomenon in O2 tolerance of neonates could not be determined from these experiments.
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PMID:Oxygen tolerance in neonatal rats: role of subcellular superoxide generation. 255 83

The lung is especially sensitive to a variety of vastly different agents and conditions including hyperoxia, certain drugs and xenobiotics, particulate debris, and ischemia/reperfusion. There is a growing body of experimental data to suggest that most, if not all, of these agents or conditions mediate pulmonary injury by forming reactive O2 metabolites such as O2-., H2O2.OH, HOCl, and RNHCl. The presence mechanisms by which these different agents converge to produce free radical-mediated pulmonary injury is not entirely clear. The lung does contain several metabolic pathways that will produce large amounts of reactive O2 metabolites. For example, hyperoxia-induced pulmonary injury may be mediated by oxidants produced by both mitochondrial and microsomal electron transport. Certain drugs and xenobiotics may be metabolized by nonspecific flavoproteins found in the mitochondrial electron transport chain and associated with microsomal mixed function oxidase system to yield a variety of free radicals and oxidants. Inhalation of particulate debris will activate resident phagocytic leukocytes to produce large quantities of cytotoxic oxidants. Ischemia and reperfusion appear to produce substantial amounts of xanthine oxidase-derived oxy-radicals that recruit and activate inflammatory phagocytes to produce cytotoxic HOCl and N-chlorinated oxidants. Finally, inappropriate metabolism of arachidonate by prostaglandin synthetase in the presence of NADH (NADPH) produces a burst of O2-. The fact that the lung contains so many different metabolic avenues for oxidant and free radical production suggests that this particular organ may be the most sensitive to oxidative insult.
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PMID:Metabolic sources of reactive oxygen metabolites during oxidant stress and ischemia with reperfusion. 265 Sep 65

Peroxidation of lung membrane lipids in vitro produces very specific changes in lung membrane fatty acid content with some fatty acids being affected more than others. We performed a series of experiments to determine the changes occurring in fatty acid composition in lung microsomes and mitochondria during an in vivo hyperoxic exposure. Hyperoxia did produce specific changes in the relative content of fatty acids present in lung microsomes and mitochondria of both vitamin E-supplemented and vitamin E-deficient rats. Changes were noted to occur in saturated and polyunsaturated fatty acids. The total amount of lung lipids extractable in the microsomal fractions decreased after hyperoxia in both the vitamin E-supplemented and the vitamin E-deficient animals with no changes occurring in extraction of lung mitochondrial total lipids. Decreases in lung mitochondrial fatty acids caused by hyperoxia occurred in the same fatty acids in both the vitamin E-supplemented and the vitamin E-deficient animals with few polyunsaturated fatty acids (PUFA) being affected. Decreases in lung microsomal fatty acids occurring during hyperoxia were different in the vitamin E-supplemented animals from those in the vitamin E-deficient animals with many more PUFA decreasing in the vitamin E-deficient group. The greatest number of PUFA found to decrease after hyperoxia when comparing all the different groups occurred in the microsomal fraction of the vitamin E-deficient rats. These data suggest that vitamin E-deficient animals have increased peroxidation of lung microsomal PUFA or a decrease in production of lung microsomal PUFA in vivo during a hyperoxic exposure.
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PMID:Effects of hyperoxia and vitamin E on the fatty acid composition of rat lung microsomes and mitochondria. 276 78

Rats were pretreated with various inducers of cytochrome P-450 before being exposed to pure normobaric oxygen (O2) in order to determine whether the inducers interfere with toxicity. The pulmonary and liver inducers beta-naphthoflavone (beta NF) and 3-methylcholanthrene (3MC) increased the survival rate and decreased the amount of pleural and lung fluid accumulation in adult rats exposed to oxygen. Phenobarbital (PB), which is essentially active in the hepatic microsomal cytochrome P-450, was less effective in counteracting oxygen toxicity. After 7 days of exposure to oxygen, none of the untreated rats survived, whereas 40, 73, and 90% survival was observed in rats treated with PB, 3MC, and beta NF, respectively. After 60 h of O2 exposure, significantly less pleural and lung fluid accumulation was observed in beta NF- and 3MC-treated rats than in untreated or PB-treated rats (p less than 0.001). Both beta NF and 3MC prevented the increase of lung peroxidation (assessed by measuring of malondialdehyde) and that of hydrogen peroxide production by lung microsomes induced by O2 exposure. These protective effects are associated with a large increase in the components of the pulmonary cytochrome P-450 system and its peroxidase activity and with an increased response to hyperoxia by lung antioxidant enzyme activities. In contrast, in control rats, the activities of the antioxidant enzymes were not increased, and both the quantity and the peroxidase activity of cytochrome P-450 were significantly decreased by O2 exposure. We conclude that in the rat, pretreatment by inducers of pulmonary cytochrome P-450 results in marked protection against O2 toxicity and an increase of antioxidant enzyme response to hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection of rat from oxygen toxicity by inducers of cytochrome P-450 system. 283 Aug 13

The effects of normobaric hyperoxia on both microsomal membrane fluidity and mechanism of phospholipid synthesis in rabbit liver and kidney have been studied. Hyperoxia induces in both organs an impairment of de novo synthesis of glycerolipids which could be due to an inactivation of acyltransferase activities involved in the initial formation of phosphatidic acid. The ability to replace phospholipid fatty acids by reacylation mechanism decreases slightly in the hyperoxic kidney, while it does not change in the hyperoxic liver. Concerning the effect of high arterial pO2 on microsomal membrane fluidity, the hyperoxic liver shows a more fluid environment within the membrane core of microsomes; however, no difference was shown in that of microsomal membrane core of hyperoxic kidney. An insight into the lipid composition of microsomes indicates that liver microsomal membranes have lower cholesterol content and higher unsaturation degree of phospholipid fatty acids, whereas hyperoxic kidney microsomes become more saturated and did not show any difference in their cholesterol content. In both hyperoxic liver and kidney microsomes, phospholipid content decreases in agreement with the depression of phosphatidic acid biosynthesis. These results are discussed in relation to the values of microsomal membrane microviscosity obtained.
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PMID:Lipid alterations in liver and kidney induced by normobaric hyperoxia: correlations with changes in microsomal membrane fluidity. 288 41

The effects of oxidative stress caused by hyperoxia or administration of the redox active compound diquat were studied in isolated hepatocytes, and the relative contribution of lipid peroxidation, glutathione (GSH) depletion, and NADPH oxidation to the cytotoxicity of active oxygen species was investigated. The redox cycling of diquat occurred primarily in the microsomal fraction since diquat was found not to penetrate into the mitochondria. Depletion of intracellular GSH by pretreatment of the animals with diethyl maleate promoted lipid peroxidation and sensitized the cells to oxidative stress. Diquat toxicity was also greatly enhanced when glutathione reductase was inhibited by pretreatment of the cells with 1,3-bis(2-chloroethyl)-1-nitrosourea. Despite extensive lipid peroxidation, loss of cell viability was not observed, with either hyperoxia or diquat, until the GSH level had fallen below approximately 6 nmol/10(6) cells. The iron chelator desferrioxamine provided complete protection against both diquat-induced lipid peroxidation and loss of cell viability. In contrast, the antioxidant alpha-tocopherol inhibited lipid peroxidation but provided only partial protection from toxicity. The hydroxyl radical scavenger alpha-keto-gamma-methiol butyric acid, finally, also provided partial protection against diquat toxicity but had no effect on lipid peroxidation. The results indicate that there is a critical GSH level above which cell death due to oxidative stress is not observed. As long as the glutathione peroxidase - glutathione reductase system is unaffected, even relatively low amounts of GSH can protect the cells by supporting glutathione peroxidase-mediated metabolism of H2O2 and lipid hydroperoxides.
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PMID:Effects of oxidative stress caused by hyperoxia and diquat. A study in isolated hepatocytes. 350 39


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