Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The synthesis of Cu,Zn SOD by rat lung increases spontaneously in the fetus in late gestation and during exposure of neonatal and adult rats to greater than 95% O2. To explore the regulation of these increases, we measured rat lung Cu,Zn SOD synthesis and activity. We also cloned and sequenced a rat lung Cu,Zn SOD cDNA that was used to measure Cu,Zn SOD mRNA concentration. We found that (a) under normal gestational and postgestational conditions the synthesis of this enzyme was regulated pretranslationally; (b) the increased synthesis that occurs under hyperoxia (greater than 95% O2), was pretranslationally mediated in otherwise unmanipulated neonatal rats but translationally controlled in hyperoxic adult rats; and (c) in lungs of rats made tolerant to greater than 95% O2 by allowing 24 h rest in air after an initial 48 h in greater than 95% O2, the increased Cu,Zn SOD synthesis that occurred during the second period of hyperoxia was regulated pretranslationally. We conclude Cu,Zn SOD gene expression in the lung is developmentally regulated under normal conditions and in response to an oxidant challenge. Tolerance, whether endogenous or induced, appears to require the accumulation of increased amounts of Cu,Zn SOD mRNA.
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PMID:Rat lung Cu,Zn superoxide dismutase. Isolation and sequence of a full-length cDNA and studies of enzyme induction. 270 31

The importance of respiratory chain activity in the induction of manganese superoxide dismutase biosynthesis was examined in the yeast Saccharomyces cerevisiae by immunological measurement of the level of manganese superoxide dismutase and comparison with copper/zinc superoxide dismutase and two subunits of respiratory chain proteins, cytochrome c1 and core 2, under conditions of growth in which respiratory chain activity was varied. Oxygen consumption by the yeast was also monitored during growth. These comparative studies indicated that under normoxic conditions, glucose repression of the respiratory chain subunits resulted in a parallel repression of the level of manganese superoxide dismutase protein. The increase in the protein levels of manganese superoxide dismutase and core 2 protein under derepressing growth conditions reflected an increase in the level of the mRNA for each protein; thus regulation is, at least in part, at the level of transcription. The following observations support the conclusion that under normoxic conditions manganese superoxide dismutase biosynthesis is primarily regulated by the same means as the respiratory chain components; that is, by glucose (catabolite) repression rather than by oxygen metabolites. 1) When yeast cells were transferred from repressing to derepressing growth conditions in normoxia, manganese superoxide dismutase biosynthesis increased at a rate parallel to that of core 2, and occurred approximately 5 h in advance of increased oxygen consumption by the yeast. 2) When an important site of mitochondrial superoxide radical generation, the cytochrome bc1 complex, was inactivated by deletion of the gene coding for one of its subunits, the level of manganese superoxide dismutase protein was not changed in the mutant compared with the parental strain. However, regulation of manganese superoxide dismutase can be separated from regulation of the respiratory chain proteins in certain instances. During the transition from the logarithmic growth phase to the stationary phase in non-fermentable carbon sources, the level of manganese superoxide dismutase decreased by approximately 50%, whereas the levels of cytochrome c1 and core 2 remained unchanged. Furthermore, yeast grown in hyperoxia of 70-80% oxygen utilizing either repressing or depressing carbon sources, contained significantly higher levels of manganese superoxide dismutase and copper/zinc superoxide dismutase compared to yeast grown in normoxia, whereas the levels of respiratory chain proteins were not affected by hyperoxia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of manganese superoxide dismutase in Saccharomyces cerevisiae. The role of respiratory chain activity. 283 36

The failure of adult rats to survive prolonged exposure to greater than 95% O2 is generally ascribed to the inability of their lungs to increase antioxidant enzyme synthesis in response to the oxidant challenge. We studied the synthesis rate of the antioxidant enzyme CuZn superoxide dismutase (CuZn SOD) in lungs of adult and neonatal rats exposed to conditions that alter the lung's oxidant-to-antioxidant balance. Lung CuZn SOD synthesis in the adult was significantly increased after 24 h of hyperoxia but fell to control levels after further exposure, whereas in neonatal lungs an increased rate of synthesis of CuZn SOD was found only after 72 h of hyperoxia. The adult lung responded to two in vitro oxidant stresses, [diethyldithiocarbamate exposure and heat (42 degrees C)] with increases in CuZn SOD synthesis twice the magnitude of those in the neonatal lung. These data indicate that the adult lung is at least as capable as the neonatal lung of increasing its synthesis of CuZn SOD in response to an oxidative stress. However, the inability of the adult lung to maintain an increased rate of CuZn SOD synthesis during in vivo hyperoxia may contribute to the poor tolerance of the adult lung to greater than 95% O2.
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PMID:Differences in CuZn superoxide dismutase induction in lungs of neonatal and adult rats. 303 15

The effect of increased intracellular oxygen activation on cellular antioxidant defenses in CHO and HeLa cells was studied. In both cell types, hyperoxic exposure (up to 4 days, 600-700 mm Hg O2) and in CHO cells menadione (up to 3 days, 15 microM) failed to affect the enzymatic antioxidant defenses Mn-containing superoxide dismutase (Mn-SOD), CuZn-SOD, catalase and glutathione peroxidase. The markedly increased antioxidant enzyme activities observed in a recently obtained oxygen-tolerant CHO variant persisted under normoxia. These data suggest that the synthesis of antioxidant enzymes is constitutive. Glutathione levels of HeLa cells did not respond to hyperoxia whereas in CHO cells hyperoxia and menadione exposure resulted in a 2- and 7-fold increase in glutathione contents, respectively. However, considering the large variations in glutathione contents observed under normal culture conditions, it is uncertain whether this increase is to be considered as a true adaptive response.
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PMID:Effect of normobaric hyperoxia on antioxidant defenses of HeLa and CHO cells. 334 21

Studies about the proposed antioxidant physiological role of the catalase (CAT) enzyme in relation to different environmental oxygen tensions are reported for the first time in amphibian larvae of Discoglossus pictus and Rana ridibunda perezi during their development. The CAT levels of whole tadpoles increased constantly in both species during the larval period, reaching a maximum during the metamorphic climax. All through development, CAT activity levels were always greater in D. pictus than in R. ridibunda perezi. This correlates well with the already reported higher SOD activity and hyperoxia resistance of the D. pictus species when compared to R. ridibunda perezi. Long-term acclimation to different levels of hyperoxia (40, 60, and 100% O2) showed dose-related increases in the CAT activity of D. pictus tadpoles. These increases did not take place when the animals were subjected to acute hyperoxia (24 h). The increase in CAT activity observed after 15 days of acclimation to acute hyperoxia (710 mm Hg: 100% O2) was reversed after 15 additional days of postacclimation to normal air (149 mm Hg O2). When recently metamorphosed frogs were acclimated to acute hyperoxia, significant increases in CAT activity were observed after 15 days, but not after 7 days. The results are interpreted as supporting a protective role for the CAT enzyme in amphibian larvae and froglets against oxygen toxicity.
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PMID:Different levels of hyperoxia reversibly induce catalase activity in amphibian tadpoles. 366 17

The administration of very low doses of bacterial endotoxin protects rats during exposure to hyperoxia and is associated with the induction of lung antioxidant enzyme activities. Copper-deficient rats have increased susceptibility to O2 toxicity, which may be related to their decreased lung superoxide dismutase activity (SOD) or decreased plasma ceruloplasmin concentrations. To determine whether endotoxin can protect against hyperoxia in this susceptible model, we exposed copper-deficient and control rats to a fractional inspiratory concentration of O2 greater than 0.95 for 96 h after pretreatment with 500 micrograms/kg of bacterial endotoxin or phosphate-buffered saline (PBS). Mortality in the copper-deficient and control rats given PBS and exposed to O2 for 96 h was 100%. Copper-deficient rats died significantly earlier during the exposure than controls. No mortality occurred in either group treated with endotoxin and hyperoxia despite the decreased activity of copper-dependent enzymes in the copper-deficient rats. Copper-deficient rats treated with endotoxin and exposed to hyperoxia did increase lung Cu-Zn-SOD activity, but activity remained below levels found in air-exposed controls. Mn-SOD activity was found to be induced above air-exposed controls in the copper-deficient rats treated with endotoxin and exposed to hyperoxia. Hyperoxic exposure resulted in a marked increase in plasma ceruloplasmin concentrations in the control rats, but no increases in ceruloplasmin occurred in the copper-deficient animals. Endotoxin protects copper-deficient rats from hyperoxia despite their decreased lung Cu-Zn-SOD activity, and decreased plasma ceruloplasmin.
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PMID:Effects of bacterial endotoxin on protecting copper-deficient rats from hyperoxia. 375 84

L-Arginine is the substrate for synthesis of nitric oxide (NO.) by NO synthase which physiologically produces vasodilation. The reaction of NO. or its metabolites with O2 or its metabolites, however, can produce toxic reactive species which may cause cellular injury. We hypothesized that excessive NO. production in isolated perfused rabbit lungs at elevated PO2 could support the production of toxic nitrogen metabolites. In isolated perfused rabbit lungs ventilated with 95% O2, 1.0 mM L-arginine caused significant pulmonary hypertension and edema. These effects of L-arginine were attenuated by the NO. synthase inhibitor, L-NAME (0.5 mM), not affected by SOD pretreatment (100 u/ml) and reversed by pretreatment with catalase (200 u/ml), suggesting a mechanism involving H2O2. This mechanism was supported by producing L-arginine mediated injury in normoxic lungs in the presence of a H2O2 generating system. This injury also was attenuated by L-NAME. On the basis of these results, we conclude that H2O2 interacts with NO. or one of its oxidized metabolites to contribute to acute lung injury during hyperoxia. Such a mechanism may involve peroxynitrite anion, although direct proof of its formation is lacking under these conditions.
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PMID:L-arginine enhances injury in the isolated rabbit lung during hyperoxia. 754 44

The significance of manganese superoxide dismutase (MnSOD) induction in cells and tissues during oxidant stress is still poorly understood. In this study, transformed human bronchial epithelial cells (BEAS 2B) were treated with interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), or with combination of these cytokines (10 ng/ml concentrations) for 48 or 72 h and exposed to selected oxidants. TNF-alpha and IFN-gamma + TNF-alpha combination resulted in a marked increase of MnSOD protein and MnSOD activity. When cells pretreated with the cytokines were exposed to hyperoxia (95% O2, 72 h), menadione (5-50 microM, 4 h), or H2O2 (0.5 and 5 mM, 4 h), in all cases IFN-gamma and TNF-alpha enhanced oxidant-related cell injury. The effect was most significant with cells pretreated with a combination of IFN-gamma and TNF-alpha. Antioxidant enzymes such as total SOD, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase did not change significantly during the cytokine treatment. Catalase activity was not changed by IFN-gamma or TNF-alpha but it decreased significantly (34%) in IFN-gamma + TNF-alpha-treated cells. Free radical generation was not changed by these cytokines in acute (30 min) experimental conditions or after 48-h treatment. These results suggest that cytokine-induced MnSOD does not protect bronchial epithelial cells against endogenously or exogenously generated oxidants in vitro. In fact, cells that contained the highest MnSOD activity were the most sensitive to subsequent oxidant damage.
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PMID:Mitochondrial superoxide dismutase induction does not protect epithelial cells during oxidant exposure in vitro. 784 Feb 31

We have analyzed the magnitude and uniformity of the expression of manganese superoxide dismutase (Mn SOD) protein in alveolar type II cells of rats exposed to hyperoxia using quantitative colloidal gold immunocytochemistry and morphometric techniques. Sprague-Dawley rats were exposed continuously to normal air or to 85% oxygen for 7 and 14 days. The lungs were fixed by intratracheal instillation of a paraformaldehyde-glutaraldehyde fixative. Lung samples were dehydrated in ethanol and embedded in LR-White. Thin sections for electron microscopy were labeled with anti-rat Mn SOD rabbit antiserum followed by protein-A gold. The labeling density (gold particles/micron 2) over subcellular compartments was determined, and relative organelle volumes were measured using a random point overlay. The results confirm that alveolar type II cells are a locus of Mn SOD response in the lungs of hyperoxic rats and contribute to this response through a combination of changes: an increase of Mn SOD concentration in the mitochondrial matrix, an increase of mitochondrial volume per cell, and type II cell hyperplasia.
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PMID:Quantitative immunocytochemical analysis of Mn SOD in alveolar type II cells of the hyperoxic rat. 794 50


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