Elevated Partial Pressure Of Oxygen Research Articles

Mécanismes pathogéniques de la cataracte chez le vitrectomisé

Cataract is the most common complication after vitrectomy. At first posterior subcapsular, it evolves into a nuclear type. A better understanding of the pathophysiologic mechanisms could help to develop strategies to prevent this complication. The main causative factors are oxidative stress, as evidenced by the persistence of an elevated partial pressure of oxygen in the lens after vitrectomy and the ionic changes in the lens. Mechanical factors may also be implicated: direct contact by gas tamponade or by silicone oil leads to desiccation cataract. The key of prevention of the formation of these cataracts is based on the reduction of oxidative stress.

Acute and potentially persistent effects of scuba diving on the blood transcriptome of experienced divers

During scuba diving, the circulatory system is stressed by an elevated partial pressure of oxygen while the diver is submerged and by decompression-induced gas bubbles on ascent to the surface. This diving-induced stress may trigger decompression illness, but the majority of dives are asymptomatic. In this study we have mapped divers' blood transcriptomes with the aim of identifying genes, biological pathways, and cell types perturbed by the physiological stress in asymptomatic scuba diving. Ten experienced divers abstained from diving for >2 wk before performing a 3-day series of daily dives to 18 m depth for 47 min while breathing compressed air. Blood for microarray analysis was collected before and immediately after the first and last dives, and 10 matched nondivers provided controls for predive stationary transcriptomes. MetaCore GeneGo analysis of the predive samples identified stationary upregulation of genes associated with apoptosis, inflammation, and innate immune responses in the divers, most significantly involving genes in the TNFR1 pathway of caspase-dependent apoptosis, HSP60/HSP70 signaling via TLR4, and NF-κB-mediated transcription. Diving caused pronounced shifts in transcription patterns characteristic of specific leukocytes, with downregulation of genes expressed by CD8+ T lymphocytes and NK cells and upregulation of genes expressed by neutrophils, monocytes, and macrophages. Antioxidant genes were upregulated. Similar transient responses were observed after the first and last dive. The results indicate that sublethal oxidative stress elicits the myeloid innate immune system in scuba diving and that extensive diving may cause persistent change in pathways controlling apoptosis, inflammation, and innate immune responses.

Methemoglobinemia from curing salt

A previously healthy 52-year-old Asian woman presented to the emergency department after a syncopal episode. She appeared grey and cyanotic. At 65% fraction of inspired oxygen, pulse oximetry showed an oxygen saturation level of 86%. Her arterial blood gas had an elevated partial pressure of oxygen

Combustible Matter Conversion in an Oxy-fuel Circulating Fluidized-Bed (CFB) Environment

Studies on combustible matter conversion during oxy-fuel combustion in a circulating fluidized-bed (CFB) environment are presented. A CFB facility has been modified to be ready for operation in an oxy-fuel mode, which means an elevated partial pressure of oxygen in a gaseous atmosphere of O2/CO2. The maximum thermal load of the unit is estimated at 0.1 MW, and the main dimensions of combustion chamber are as follows: a height of 5 m and an inner diameter of 0.1 m. Polish bituminous coal was burnt. The paper is focused on carbon and combustible sulfur behavior in a combustion chamber that runs under oxy-fuel CFB conditions. The analysis is based on sampling of in-furnace flue gases and calculations of carbon and sulfur conversion ratios. The effect of both oxygen fraction in O2/CO2 mixtures and excess oxygen was studied. An increased concentration of CO2 visibly inhibits fuel conversion and does not affect SO2 formation. A higher excess oxygen accelerates burnout of combustible matter; however, the value of 1.15 seems to be sufficient with respect to efficient combustion. The described investigations are the first part of the core work scheduled in the project “Advanced Technologies for Energy Generation: Oxy-combustion Technology for PC and FBC Boilers with CO2 Capture”.

Seed storage at elevated partial pressure of oxygen, a fast method for analysing seed ageing under dry conditions.

Background and AimsDespite differences in physiology between dry and relative moist seeds, seed ageing tests most often use a temperature and seed moisture level that are higher than during dry storage used in commercial practice and gene banks. This study aimed to test whether seed ageing under dry conditions can be accelerated by storing under high-pressure oxygen.MethodsDry barley (Hordeum vulgare), cabbage (Brassica oleracea), lettuce (Lactuca sativa) and soybean (Glycine max) seeds were stored between 2 and 7 weeks in steel tanks under 18 MPa partial pressure of oxygen. Storage under high-pressure nitrogen gas or under ambient air pressure served as controls. The method was compared with storage at 45 °C after equilibration at 85 % relative humidity and long-term storage at the laboratory bench. Germination behaviour, seedling morphology and tocopherol levels were assessed.Key ResultsThe ageing of the dry seeds was indeed accelerated by storing under high-pressure oxygen. The morphological ageing symptoms of the stored seeds resembled those observed after ageing under long-term dry storage conditions. Barley appeared more tolerant of this storage treatment compared with lettuce and soybean. Less-mature harvested cabbage seeds were more sensitive, as was the case for primed compared with non-primed lettuce seeds. Under high-pressure oxygen storage the tocopherol levels of dry seeds decreased, in a linear way with the decline in seed germination, but remained unchanged in seeds deteriorated during storage at 45 °C after equilibration at 85 % RH.ConclusionsSeed storage under high-pressure oxygen offers a novel and relatively fast method to study the physiology and biochemistry of seed ageing at different seed moisture levels and temperatures, including those that are representative of the dry storage conditions as used in gene banks and commercial practice.

Sulfonic Acid‐Catalyzed Autoxidative Carbon‐Carbon Coupling Reaction under Elevated Partial Pressure of Oxygen

AbstractAn aerobic organocatalytic oxidative CC bond formation reaction of benzylic CH bonds with various C‐nucleophiles is described. The coupling reaction proceeds by simply stirring the substrates under elevated partial pressure of oxygen in the presence of a sulfonic acid catalyst at room temperature. Elevation of the pressure enables the reaction of a broad scope of nucleophile substrates otherwise showing poor reactivity at ambient pressure. The benzylic CH bonds of xanthene, acridanes, isochromane and related heterocycles could be functionalized with nucleophiles including ketones, 1,3‐dicarbonyl compounds and aldehydes. Electron‐rich arenes could be utilized as nucleophiles at elevated temperatures. The reactions are believed to proceed via autoxidation of the benzylic CH bonds to the hydroperoxides and subsequent nucleophilic substitution catalyzed by sulfonic acids.

Oxy-fuel circulating fluidized bed combustion in a small pilot-scale test rig

Coal combustion under the elevated partial pressure of oxygen in a circulating fluidized bed environment was investigated. The fuel used was bituminous coal. The concentration of oxygen in the air was increased to 35% per volume. Excess oxygen ranged from 1.1 to 1.3 and the temperature ranged from ca. 1073 K to 1273 K. A 0.1 MW th CFB combustor was adapted for oxy-combustion. The conversion ratios respectively studied were: carbon, sulfur and nitrogen to CO, SO 2 and NO X. An increase of nitrogen and sulfur conversion ratios and a strong decrease of incomplete combustion losses were found under the oxygen-enriched conditions. Moreover, a strong increase in temperature was noticed during oxy-combustion.

Effects of hyperbaric oxygen on uric acid and arachidonic acid: a metabolomic study in rats and humans

Hyperoxia is routinely used to prevent or treat hypoxemia and acute respiratory failure, and sustain aerobic life in military and commercial operations. However, breathing oxygen acutely at high pressures and for long durations is toxic. The present study aimed to investigate effects of hyperbaric oxygen (HBO) exposure on plasma metabolite profiles. We applied a liquid chromatography-mass spectrometry based metabolomic approach to analyze metabolites from plasma of both rats and humans under HBO conditions to explore the possible effects of HBO on the body. Uric acid (UA) and arachidonic acid concentrations were changed significantly in both rat and human plasma, and some precursor metabolites of UA in the UA pathway were also changed. For acute and chronic HBO exposures on plasma UA after exogenous UA injection, the results indicated exogenous administration of UA significantly increased plasma UA and ascorbic acid levels. However, these returned to normal levels 48 h after HBO exposure. These findings suggest HBO exposure can combat the harmful effects of increased UA from exposure to elevated partial pressure of oxygen. Furthermore, exogenous administration of UA not only does not disturb its metabolism, but also increases its anti-oxidative capacity (increase ascorbic acid). These findings suggest that the use of antioxidants might be necessary under HBO exposure, especially under extreme HBO exposure.

Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: an oxidative stress response.

The purpose of this investigation was to determine the impact of elevated partial pressures of O(2) on the steady state concentration of nitric oxide ((*)NO) in the cerebral cortex. Rodents with implanted O(2)- and (*)NO-specific microelectrodes were exposed to O(2) at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA) for up to 45 min. Elevations in (*)NO concentration occurred with all partial pressures above that of ambient air. In rats exposed to 2.8 ATA O(2) the increase was 692 +/- 73 nM (S.E., n = 5) over control. Changes were not associated with alterations in concentrations of nitric oxide synthase (NOS) enzymes. Based on studies with knock-out mice lacking genes for neuronal NOS (nNOS) or endothelial NOS (eNOS), nNOS activity contributed over 90% to total (*)NO elevation due to hyperoxia. Immunoprecipitation studies indicated that hyperoxia doubles the amount of nNOS associated with the molecular chaperone, heat shock protein 90 (Hsp90). Both (*)NO elevations and the association between nNOS and Hsp90 were inhibited in rats infused with superoxide dismutase. Elevations of (*)NO were also inhibited by treatment with the relatively specific nNOS inhibitor, 7 nitroindazole, by the ansamycin antibiotics herbimycin and geldanamycin, by the antioxidant N-acetylcysteine, by the calcium channel blocker nimodipine, and by the N-methyl-D-aspartate inhibitor, MK 801. Hyperoxia did not alter eNOS association with Hsp90, nor did it modify nNOS or eNOS associations with calmodulin, the magnitude of eNOS tyrosine phosphorylation, or nNOS phosphorylation via calmodulin kinase. Cerebral cortex blood flow, measured by laser Doppler flow probe, increased during hyperoxia and may be causally related to elevations of steady state (*)NO concentration. We conclude that hyperoxia causes an increase in (*)NO synthesis as part of a response to oxidative stress. Mechanisms for nNOS activation include augmentation in the association with Hsp90 and intracellular entry of calcium.

Effect of supplemental oxygen on blood plasma organic acids within embryos from selected lines of turkeys

The hypothesis was tested that increased oxygen tensions during the plateau stage of oxygen consumption (25 and 26 d of incubation) would cause different metabolic responses from embryos selected for increased egg production or growth. Embryos were exposed to 171 or 152 mm Hg partial pressure of oxygen from 25 to 28 d of incubation, a time when the oxygen conductance properties of the eggshell are exceeded by the embryonic tissue demands for oxygen. Carbohydrate and lipid metabolism were observed by measuring plasma organic acids in embryos from selected lines and randombred controls. (E was selected for increased egg production; RBC1 is the randombred line from which it was selected. F was selected for increased BW; RBC2 is the randombred line from which it was selected.) During the plateau stage in oxygen consumption, RBC2 embryos responded to added oxygen by utilizing fat rather than carbohydrate, whereas F embryos responded by using less fat as well as less carbohydrate from the liver and kidney. The response of F embryos to added oxygen is the opposite that might be expected for aerobic metabolism. The reason that selection for growth has resulted in such a metabolism is unknown. The E embryos displayed depressed lactate and beta-hydroxybutyrate levels, but plasma urates were elevated compared with RBC1, suggesting that the selection for egg production has also resulted in a unique metabolism. The embryonic processes described in the current study suggest that selected embryos are unable to respond to elevated partial pressure of oxygen by adjusting energy metabolism, which may result in increased embryonic mortality during this stage.

Elevation of manganese superoxide dismutase gene expression by thioredoxin.

Manganese superoxide dismutase (MnSOD) is a mitochondrial enzyme that dismutates potentially toxic superoxide radical into hydrogen peroxide and dioxygen. This enzyme is critical for protection against cellular injury due to elevated partial pressures of oxygen. Thioredoxin (TRX) is a potent protein disulfide reductase found in most organisms that participates in many thiol-dependent cellular reductive processes and plays an important role in antioxidant defense, signal transduction, and regulation of cell growth and proliferation. Here we describe induction of manganese superoxide dismutase by thioredoxin. MnSOD mRNA and activity were increased dramatically by low concentrations of TRX (28 microM). Elevation of MnSOD mRNA by TRX was inhibited by actinomycin D, but not cycloheximide, occurring both in cell lines and primary human lung microvascular endothelial cells. mRNAs for other antioxidant enzymes including copper-zinc superoxide dismutase and catalase were not elevated, demonstrating specificity of induction of MnSOD by TRX. Thiol oxidation by diamide or alkylation by chlorodinitrobenzene inhibited MnSOD induction, further indicating a requirement for reduced TRX. Because both oxidized and reduced thioredoxin (28 microM) induced MnSOD mRNA, the intracellular redox status of externally added Escherichia coli oxidized TRX was determined. About 45% of internalized E. coli TRX was reduced, with 8% in fully reduced form and about 37% in partially reduced form. However, when TRX reductase and nicotinamide adenine dinucleotide (NADPH) were added to the extracellular medium with TRX, more than 80% of E. coli TRX was found to be in a fully reduced state in human adenocarcinoma (A549) cells. Although lower concentrations of oxidized TRX (7 microM) did not induce MnSOD mRNA, this concentration of TRX, when reduced by NADPH and TRX reductase, increased MnSOD mRNA six-fold. In additional studies, MCF-7 cells stably transfected with the human TRX gene had elevated expression of MnSOD mRNA relative to vector-transfected controls. Thus, both endogenously produced and exogenously added TRX elevate MnSOD gene expression. These findings suggest a novel mechanism involving reduced TRX in regulation of MnSOD.

In Situ TEM Investigation of Processes Catalyzed by Pd-Ni Alloy Particles on Carbon Substrates in the Presence and Absence of Oxygen

Processes catalyzed by small Pd-Ni alloy particles (10-20 nm in diameter) vapour-deposited on thin carbon films were investigated by in situ experiments in a transmission electron microscope. During exposure to elevated partial pressures of oxygen, and in the regime of high concentrations of Pd, the carbon support was oxidized at the edges of the particles at temperatures from 770 to 870 K, as was apparent by holes developing in the substrate. The activity was highest for pure Pd, and decreased strongly with increasing content of Ni. At concentration values of Ni from 5 to 10 at.%, segregation of Ni and oxidation to NiO was found, while the remaining Pd particle continued to be active in oxidizing the carbon. For further increasing concentrations of Ni, the tendency of NiO segregation decreased, and at about 25%, the particles appeared to be rather stable and no carbon oxidation could be detected any longer. Instead, a weak activity of graphitization of the carbon support was observed, which increased strongly with further increasing concentration of Ni. This was most pronounced for pure Ni, and was apparent in the transmission electron microscopy image by the formation of graphite shells around the particles, and of graphitized areas in the surrounding substrate area by dispersing Ni. At 870 K, this behaviour was found to be similar to the well known case without the presence of oxygen, whereas at somewhat lower temperatures the Ni was oxidized. The dependence on composition of the oxidation or graphitization of the carbon substrate is interpreted as being caused by competitive processes: dissociative adsorption of oxygen on alloys rich in Pd, segregation and oxidation of Ni at the surface of alloys with low concentrations of Ni, and dissolution and diffusion of carbon from the substrate in alloys with medium to high concentrations of Ni, leading to the formation of segregated graphite on the surface of the particles, as well as to graphitization of the substrate.

A Critical Role for Thiol, But Not ATP, Depletion in 95% O2-Mediated Injury of Preterm Pneumocytes in Vitro

Prolonged exposure to elevated partial pressures of oxygen results in lung cell toxicity, both in vivo and in vitro, due to the excess production and target molecule reactions of reactive oxygen species. Events primarily responsible for cell death vary with the type of oxidant injury and with cell type. Because of the susceptibility of the premature lung to oxygen toxicity, and the critical barrier function of the epithelium, we have investigated the role of two potentially lethal consequences of O2 exposure in premature distal lung epithelial cells in vitro. A 48-h exposure of distal fetal rat lung epithelial cells to 95% O2 caused cytotoxicity, which was associated with DNA injury and depletion of both cellular protein and nonprotein reduced sulfhydryls. The observed DNA injury preceded other markers of cell injury and was not sufficient to either activate the chromosomal enzyme poly(ADP-ribose) polymerase or cause secondary ATP depletion. Buthionine sulfoxamine-induced depletion of nonprotein reduced sulfhydryls increased the sensitivity of cells to subsequent O2-mediated cytotoxicity. Addition of the glutathione precursor N-acetylcysteine to the culture medium maintained cellular protein and nonprotein reduced sulfhydryl concentrations and prevented O2-mediated cytotoxicity. We conclude that loss of protein and nonprotein reduced sulfhydryls, but not DNA injury, is causally related to the toxic effects of elevated O2 on premature distal lung epithelial cells.

Hyperoxia and Lung Metabolism

N umerous studies have been conducted on the pathologic changes that occur in the lung due to exposure to hyperbaric oxygen. These studies indicate that the entire lung, from the epithelium of the upper respiratory tract down to the pulmonary capillary endothelium, can be damaged by prolonged exposure to elevated partial pressures of oxygen.' Reports of 2-4 lung tissue changes due to oxygen toxicity include interstitial and intracellular edema, thickening of the oxygen blood barrier, and swelling of mitochondria in the alveolar epithelium. Indirect mechanisms as well as the direct effects of oxygen can be responsible for the damage observed in lung tissue. In vitro studies have shown that many enzymes are inhibited by exposure to hyperbaric oxygen in the absence of hormonal and neurogenic factor^.^ Penrode reported in studies in which only one lung was exposed to the effects of elevated oxygen tensions that damage occurred in the absence of extrapulmonary factors. Studies on biochemical damage that occurs in the lung due to pulmonary oxygen toxicity are not numerous and little is known about biochemical changes that occur in the lungs of intact animals during exposure to subconvulsive levels of hyperbaric oxygen. After 15 to 30 minutes of breathing oxygen at 5.0 atmospheres absolute pressure ( ATA) , dehydrogenase activity and sulfhydryl content of lung tissue are significantly decreased.7 Other investigatorsR have reported that cats exposed to 100 percent oxygen showed a marked impairment of tracheal mucus flow, which could be reversed by administering epinephrine and adenosine tiphosphate ( ATP) . The authors0 interpreted the effect of oxygen on mucus flow as an interference by oxygen on carbohydrate metabolism. Proposals as to the mechanism of pulmonary oxygen toxicity include enzyme inhibition, free radical formation, and peroxidation. Previous pa;hologic and biochemical studies have shown that significant damage occurs in the lung due to oxygen toxicity. We found biochemical changes occurring in the lung of rats exposed to 1.0 ATA 160 percent 0, from zero to seven days. Pathologic changes in the lung were monitored, simultaneously. Succinic dehydrogenase activity, basal and ADP-stimulated respiration rates, and ATP concentrations were measured.