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

The content of N-acetyl-l-asparaginic acid, CoA, CoASAc and the N-acetylaspartate amunohydrolase activity was determined in cerebral areas of rats at the normal level and at different stages of oxygen poisoning. At the preconvulsive stage of the oxygen poisoning the content of N-acetyl-l-asparaginic acid decreases in cerebral hemispheres by 54, in the midbrain and diencephalon by 23, in the medulla oblongata--by 27, and in the cerebellum by 21%. The N-acetylaspartate aminohydrolase activity, vice versa, increases by 58, 62, 57 and 60%, respectively. The content of CoA and CoASAc is unchanged. At the convulsive stage of hyperoxia the content of N-acetyl-l-asparaginic acid in the cerebral hemispheres and cerebellum is unchanged in the midbrain and diencephalon increases by 21% and in the medulla oblongata-by 15%. The n-acetylaspartate aminohydrolase activity in he cerebral hemispheres, midbrain, diencephalon and medulla oblongata is unchanged, in the cerebellum it increases by 100%. The CoA content in the brain decreases by 20%, CoASAc-by 16%.
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PMID:[Effect of hyperbaric oxygenation on N-acetyl-L-asparaginic acid metabolism in different cerebral areas]. 725 21

This study examined the effects of hyperoxic training on specific cardiorespiratory and metabolic responses. A group of 19 male subjects trained for 5 weeks on a cycle ergometer at 70 percent of hyperoxic or normoxic maximal heart rate, the hyperoxic group (HG) breathing 70 percent O2, the normoxic group (NG) breathing 21 percent O2. The subjects were tested pre- and post-training under both hyperoxia and normoxia. Measurements included cardiac output (Q(c)), stroke volume (SV), heart rate (HR), pulmonary ventilation (V(E)), oxygen consumption (VO(2)), partial pressure of oxygen (PO(2)), partial pressure of inspired carbon dioxide (PCO(2)), blood lactate concentration [La], and fiber type composition. The V(E) was significantly lower at submaximal work rates (P <0.05) and maximal V(E) increased after training in both groups for both test conditions; hyperoxic V(E) was lower than normoxic V(E) (P <0.05). The maximal V0(2) increased significantly (P <0.05) in both groups for both tests and was 11 percent - 12 percent higher during hyperoxia. Post-training maximal heart rate (HR(max)) was significantly decreased (P <0.05) at the same absolute work rate regardless of the training group or test type. The SV was increased at each work rate and Q c was unchanged. The maximal Q(c) increased significantly (P <0.05) for both groups and types of test: for normoxia: NG 27.3-30.41*min(-1) and HG 30.3-32.31*min(-1) and for hyperoxia: NG 24.7-25.6 and HG 27.9-31.21*min(-1). Although working at the same intensity relative to HR(max), HG showed significantly lower [La] following a single training session, yet maximal values were unchanged after training. Both groups showed a significant increase in the percentage of type IIA fibers post-training but HG retained a larger percentage of IIB fibers. Mitochondrial enzymes; citrate kinase, 3-hydroxyacyl CoA dehydrogenase, and cytochrome c-oxidase were increased in the normoxic trained subjects (P <0.05). In summary, training induced adaptive responses in maximal aerobic power, HR, SV, Q(c), [La], and muscle fiber type composition, independent of inspired PO(2). Intramuscular data suggested there may be some differences between hyperoxic and normoxic training and these were substantiated by mitochondrial enzyme and lactate findings. Our data would suggest that transport mechanisms may limit the ability to increase aerobic power.
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PMID:Cardiorespiratory and metabolic adaptations to hyperoxic training. 886 67

Patients with poorly functioning lungs often require treatment with high concentrations of supplemental oxygen, which, although often necessary to sustain life, can cause lung injury. The mechanisms responsible for hyperoxic lung injury have been investigated intensely and most probably involve oxidant stress responses, but the details are not well understood. In the present studies, we exposed adult male C57/Bl6 mice to >95% O2 for up to 72 h and obtained lung and liver samples for assessment of lung injury, measurements of tissue concentrations of coenzyme A (CoASH) and the corresponding mixed disulfide with glutathione (CoASSG), as possible biomarkers of intramitochondrial thiol redox status. Subcellular fractions were prepared from both tissues for determination of glutathione reductase (GR) activities. Lung injury in the hyperoxic mice was demonstrated by increases in lung weight to body weight ratios at 48 h and by increases in bronchoalveolar lavage protein concentrations at 72 h. Lung CoASH concentrations declined in the hyperoxic mice, but CoASSG concentrations were not increased nor were CoASH/CoASSG ratios decreased, as would be expected for an oxidant shift in mitochondrial thiol-disulfide status. Interestingly, CoASSG concentrations increased (from 6.72+/-0.54 to 14.10+/-1.10 nmol/g of liver in air-breathing controls and 72 h of hyperoxia, respectively, P<0.05), and CoASH/CoASSG ratios decreased in the livers of mice exposed to hyperoxia. Some apparent effects of duration of hyperoxia on GR activities in lung or liver cytosolic, mitochondrial, or nuclear fractions were observed, but the changes were not consistent or progressive. Yields of isolated hepatic nuclear protein were decreased in the hyperoxic mice within 24 h of exposure, and by 72 h of hyperoxia, protein recoveries in purified nuclear fractions had declined from 41.8 to 14.8 mg of protein/g animal body weight. Concentrations of 10-formyltetrahydrofolate dehydrogenase were diminished in hepatic mitochondria of hyperoxic mice. A second protein in hepatic mitochondria of approximately 25 kDa showed apparent decreases in thiol content, as determined by fluorescence intensities of monobromobimane derivatives separated by SDS-PAGE. The mechanisms responsible for the observed effects and the possible implications for the adverse effects of hyperoxic therapies are not known and need to be investigated.
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PMID:Mitochondrial thiol status in the liver is altered by exposure to hyperoxia. 1164 Oct 46

Coenzyme A (CoASH) is compartmentalized preferentially in the mitochondria, and CoASH and its mixed disulfide with glutathione (CoASSG) undergo thiol/disulfide exchange reactions with glutathione (GSH) and glutathione disulfide (GSSG) in vitro. We measured CoASH and CoASSG in freeze-clamped lung tissues from Fischer-344 and Sprague-Dawley rats maintained in room air or exposed to >95% O(2) for 48 h to test the hypothesis that oxidant stresses on lung thiol status would be observed in the CoASH/CoASSG redox couple, suggesting oxidant stress responses in the mitochondria. Lung tissue concentrations of CoASSG in the Fischer-344 rats declined from 0.89 +/- 0.15 to 0.51 +/- 0.13 nmol/g of lung after 48 h of hyperoxia. CoASH levels declined from 6.40 +/- 0.84 to 3.0 +/- 0.65 nmol/g of lung, and acetyl CoA levels also were lower in the lungs of animals exposed to hyperoxia. CoASH/CoASSG ratios were lower in animals exposed to hyperoxia, satisfying our previously defined criteria for an oxidant stress on this thiol/disulfide redox couple, but absolute CoASSG levels were not increased, as would be expected for oxidant stresses driven simply by increases in reactive oxygen species or other oxidants. Pulmonary edema was observed in the hyperoxic rats and accounted for some of the declines in CoASH concentrations, but CoASH contents per total lung also declined. Lung mitochondrial succinate dehydrogenase activities were not diminished in rats exposed to hyperoxia, indicating that the decreases in CoASH concentrations are not attributable to general destruction of lung mitochondria. Lung GSSG contents were greater in the hyperoxia animals, but GSH/GSSG ratios, which are dominated by extramitochondrial pools, did not decrease in these animals. The mechanisms responsible for, and the possible pathophysiologic consequences of, the decreases in lung CoASH concentrations are not evident from the data available at the present time, but the loss of more than half the tissue contents of CoASH is likely to generate additional metabolic effects that could have significant pathophysiologic consequences.
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PMID:CoASH and CoASSG levels in lungs of hyperoxic rats as potential biomarkers of intramitochondrial oxidant stresses. 1186 41

Exposure of rats and mice to hyperoxia decreases lung coenzyme A (CoASH) contents, with a decrease of 50% observed in adult male Fischer-344 rats exposed to >95% O(2) for 48 h. Decreases in lung CoASH levels are not accompanied by increases in contents of the mixed glutathione disulfide of CoA, as might be expected of a primary oxidative stress on CoASH status. Animals exposed to hyperoxia exhibit decreased food intake, and the present studies were to test the hypothesis that fasting would decrease lung CoASH contents, thereby suggesting a mechanism for the effects of hyperoxia. Adult male Fischer-344 rats were examined after 0, 24, or 48 h of fasting (n = 5, 6, and 6, respectively). Fasting for 24 or 48 h did not affect lung CoASH levels or lung weights, despite 6 and 12% losses in body weight. Lung glutathione concentrations (nanomoles per gram of tissue) and contents (nanomoles per whole organ) and glutathione disulfide contents were 10 to 20% lower in rats fasted for 48 h than in fed rats. Liver weights and glutathione and glutathione disulfide contents and concentrations were 30 to 70% lower in rats fasted for 24 or 48 h than in fed rats. Hepatic CoASH concentrations increased during fasting, but hepatic contents of CoASH remained remarkably constant. Liver protein contents (milligrams of protein per whole organ) decreased after 24 and 48 h of fasting, but protein concentrations (milligrams of protein per gram of tissue) were higher in rats fasted 48 h than in fed rats. Overall, glutathione, glutathione disulfide, and protein contents in liver and skeletal muscle decreased with fasting, but significant changes in CoASH contents were not observed. Diminished food intake in animals does not explain the effects of hyperoxia on lung CoASH contents. CoASH and derived thioesters participate in many cellular functions, and if depletion of lung CoASH during hyperoxia proves to be relevant to mechanisms of lung injury, support of mechanisms needed to sustain CoA levels could be helpful in prematurely born infants and in adults.
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PMID:Effects of fasting on tissue contents of coenzyme A and related intermediates in rats. 1219 81

Treatments with supplemental oxygen in premature infants can impair lung development, leading to bronchopulmonary dysplasia (BPD). Although a stage-specific alteration of lung lipidome occurs during postnatal lung development, whether neonatal hyperoxia, a known mediator of BPD in rodent models, changes lipid profiles in mouse lungs is still to be elucidated. To answer this question, newborn mice were exposed to hyperoxia for 3 days and allowed to recover in normoxia until postnatal day (pnd) 7 and pnd14, time-points spanning the peak stage of alveologenesis. A total of 2263 lung lipid species were detected by liquid chromatography-mass spectrometry, covering 5 lipid categories and 18 lipid subclasses. The most commonly identified lipid species were glycerophospholipids, followed by sphingolipids and glycerolipids. In normoxic conditions, certain glycerophospholipid and glycerolipid species augmented at pnd14 compared to pnd7. At pnd7, hyperoxia generally increased glycerophospholipid, sphingolipid, and glycerolipid species. Hyperoxia increased NADPH, acetyl CoA, and citrate acid but reduced carnitine and acyl carnitine. Hyperoxia increased oxidized glutathione but reduced catalase. These changes were not apparent at pnd14. Hyperoxia reduced docosahexaenoic acid and arachidonic acid at pnd14 but not at pnd7. Altogether, the lung lipidome changes throughout alveolarization. Neonatal hyperoxia alters the lung lipidome, which may contribute to alveolar simplification and dysregulated vascular development.
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PMID:Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice. 3282 9