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Oxygen toxicity as result of increased lipid peroxidation - lysosomal enzymes in rats exposed to 100 percent oxygen, and stability of rat liver and brain lysosomes
Pressure chamber experiments for studying changes in motor, cadiovascular, respiratory, and central nervous systems during oxygen toxicity
Pathological characteristics and mechanism of pulmonary involvement in high pressure oxygen toxicity in guinea pigs and dogs
Prolonged exposure to hyperbaric hyperoxia can lead to pulmonary oxygen toxicity (PO 2 tox). PO 2 tox is a mission limiting factor for special operations forces divers using closed-circuit rebreathing apparatus and a potential side effect for patients undergoing hyperbaric oxygen (HBO) treatment. In this study, we aim to determine if there is a specific breath profile of compounds in exhaled breath condensate (EBC) that is indicative of the early stages of pulmonary hyperoxic stress/PO 2 tox. Using a double-blind, randomized 'sham' controlled, cross-over design 14 U.S. Navy trained diver volunteers breathed two different gas mixtures at an ambient pressure of 2 ATA (33 fsw, 10 msw) for 6.5 h. One test gas consisted of 100% O 2 (HBO) and the other was a gas mixture containing 30.6% O 2 with the balance N 2 (Nitrox). The high O 2 stress dive (HBO) and low O 2 stress dive (Nitrox) were separated by at least seven days and were conducted dry and at rest inside a hyperbaric chamber. EBC samples were taken immediately before and after each dive and subsequently underwent a targeted and untargeted metabolomics analysis using liquid chromatography coupled to mass spectrometry (LC-MS). Following the HBO dive, 10 out of 14 subjects reported symptoms of the early stages of PO 2 tox and one subject terminated the dive early due to severe symptoms of PO 2 tox. No symptoms of PO 2 tox were reported following the nitrox dive. A partial least-squares discriminant analysis of the normalized (relative to pre-dive) untargeted data gave good classification abilities between the HBO and nitrox EBC with an AUC of 0.99 (±2%) and sensitivity and specificity of 0.93 (±10%) and 0.94 (±10%), respectively. Furthermore, the resulting classifications identified specific biomarkers that included human metabolites and lipids and their derivatives from different metabolic pathways that may explain metabolomic changes resulting from prolonged HBO exposure.
Physiological effects on four men exposed for 14 days to increased oxygen tension at 5 psia, showing symptoms of oxygen toxicity that could be tolerated
Of the many roles ascribed to glutathione (GSH) the one most clearly established is its role in the protection of higher eucaryotes against oxygen toxicity through destruction of thiol-reactive oxygen byproducts. If this is the primary function of GSH then GSH metabolism should have evolved during or after the evolution of oxygenic photosynthesis. That many bacteria do not produce GSH is consistent with this view. In the present study we have examined the low-molecular-weight thiol composition of a variety of phototrophic microorganisms to ascertain how evolution of GSH production is related to evolution of oxygenic photosynthesis. Cells were extracted in the presence of monobromobimane (mBBr) to convert thiols to fluorescent derivatives, which were analyzed by high-pressure liquid chromatography. Significant levels of GSH were not found in the green bacteria (Chlorobium thiosulfatophilum and Chloroflexus aurantiacus). Substantial levels of GSH were present in the purple bacteria (Chromatium vinosum, Rhodospirillum rubrum, Rhodobacter sphaeroides, and Rhodocyclus gelatinosa), the cyanobacteria [Anacystis nidulans, Microcoleus chthonoplastes S.G., Nostoc muscorum, Oscillatoria amphigranulata, Oscillatoria limnetica, Oscillatoria sp. (Stinky Spring, Utah), Oscillatoria terebriformis, Plectonema boryanum, and Synechococcus lividus], and eucaryotic algae (Chlorella pyrenoidsa, Chlorella vulgaris, Euglena gracilis, Scenedesmus obliquus, and Chlamydomonas reinhardtii). Other thiols measured included cysteine, gamma-glutamylcysteine, thiosulfate, coenzyme A, and sulfide; several unidentified thiols were also detected. Many of the organisms examined also exhibited a marked ability to reduce mBBr to syn-(methyl,methyl)bimane, an ability that was quenched by treatment with 2-pyridyl disulfide or 5,5'-bisdithio-(2-nitrobenzoic acid) prior to reaction with mBBr. These observations indicate the presence of a reducing system capable of electron transfer to mBBr and reduction of reactive disulfides. The distribution of GSH in phototrophic eubacteria indicates that GSH synthesis evolved at or around the time that oxygenic photosynthesis evolved.
Pilot plant makes oxygen difluoride highly-energetic, space-storable oxidizer not made commercially. Designed to handle reactants, product, and byproduct, most of which highly reactive, corrosive, and toxic. Oxygen difluoride evolves continuously from reactor containing potassium hydroxide in water at 10 degree C. Collection tanks alternated; one filled while other drained to storage cylinder. Excess OF2 and F2 dissipated in combustion of charcoal in burn barrel. Toxic byproduct, potassium fluoride, reacted with calcium hydroxide to form nontoxic calcium fluoride and to regenerate potassium hydroxide. Equipment processes toxic, difficult-to-make substance efficiently and safely.
Toxic effect of high partial oxygen pressure noted in constriction of peripheral visual field
The detailed examination is reported of the theory that narcosis results from expansion of the cell membrane under high partial pressures. The research is partially based on the hypothesis that, like oxygen toxicity, the mechanism of metabolic effects of rare gases may be similar at both low and high pressures and are simply more observable at high pressures. Using adult female goats, the parameters measured include oxygen consumption, CO2 production, respiration rate, heart rate, rectal and skin temperatures and the analysis of electroencephalograms and evoked response. Additionally, the specific activity is measured of plasma glucose subsequent to injection of glucose-UL-C-14, intravenous infusion, specific activity of expired CO2, unesterified fatty acid levels and whole blood lactate-to-pyruvate ratios. Also studied were the effects of acetylsalicylic acid, vitamin E and cationic detergents (which alleviate narcosis) upon metabolic changes induced by high pressure narcosis.
Bioenergetics protocol for evaluating effects of environment on biological systems, including metabolic effects of diluent gases and oxygen toxicity
Dietary antioxidant vitamin level effects on fine structure of proximal convoluted tubules in rats, studying changes due to oxygen toxicity
The pathogenesis of oxygen toxicity in the lung of rats was studied by electron microscopy. The following long-term effects were established: (1) a progressive destruction of the blood-air barrier beginning with the endothelial cell layer; (2) a profuse edema in the interstitial spaces in the pleural space in the alveoli and in the cytoplasm and organelles; (3) a continuing increase in the quantity and complexity of the alveolar exudate; (4) gradual hemolysis of red blood cells; and (5) eventual subsiding of the interstitial edema in surviving rats with a concomitant development of emphysema.
The experimental studies on the mitochondria of insect and mammalian cells are examined with a view to an analysis of intrinsic mitochondrial senescence, and its relation to the age-related changes in other cell organelles. The fine structural and biochemical data support the concept that the mitochondria of fixed postmitotic cells may be the site of intrinsic aging because of the attack by free radicals and lipid peroxides originating in the organelles as a by-product of oxygen reduction during respiration. Although the cells have numerous mechanisms for counteracting lipid peroxidation injury, there is a slippage in the antioxidant protection. Intrinsic mitochondrial aging could thus be considered as a specific manifestation of oxygen toxicity. It is proposed that free radical injury renders an increasing number of the mitochondria unable to divide, probably because of damage to the lipids of the inner membrane and to mitochondrial DNA.
Biological thiols are essential elements in most aspects of cell function but undergo rapid oxidation to disulfides in the presence of oxygen. The evolution of systems to protect against such oxygen toxicity was essential to the emergence of aerobic life. The protection system used by eukaryotes is based upon glutathione (GSH) and GSH-dependent enzymes but many bacteria lack GSH and apparently use other mechanisms. The objective of this research is to elaborate the thiol protective mechanisms employed by prokaryotes of widely divergent evolutionary origin and to understand why GSH became the central thiol employed in essentially all higher organisms. Thiol-selective fluorescent labeling and HPLC analysis has been used to determine key monothiol components.
The present studies have shown that GSH metabolism arose in the purple bacteria and cyanobacteria where it functions to protect against oxygen toxicity. Evidence was obtained indicating that GSH metabolism was incorporated into eucaryotes via the endosymbiosis giving rise to mitochrondria and chloroplasts. Aerobic bacteria lacking GSH utilize other thiols for apparently similar functions, the thiol being coenzyme A in Gram positive bacteria and chi-glutamylcysteine in the halobacteria. The thiol biochemistry of prokaryotes is thus seen to be much more highly diversified than that of eucaryotes and much remains to be learned about this subject.
Topics discussed in this volume include space motion sickness, cardiovascular adaptation, fluid shifts, extravehicular activity, general physiology, perception, vestibular response modifications, vestibular physiology, and pharmacology. Papers are presented on the clinical characterization and etiology of space motion sickness, ultrasound techniques in space medicine, fluid shifts in weightlessness, Space Shuttle inflight and postflight fluid shifts measured by leg volume changes, and the probability of oxygen toxicity in an 8-psi space suit. Consideration is also given to the metabolic and hormonal status of crewmembers in short-term space flights, adaptive changes in perception of body orientation and mental image rotation in microgravity, the effects of a visual-vestibular stimulus on the vestibulo-ocular reflex, rotation tests in the weightless phase of parabolic flight, and the mechanisms of antimotion sickness drugs.
This slide presentation reviews some of the problems and solutions that personnel have experienced during sessions in the Neutral Bu0yancy Lab (NBL). It reviews the standard dive that occurs at the NBL, Boyles and Henry's laws as they relate to the effects of diving. It then reviews in depth some of the major adverse physiologic events that happen during a diving session: Ear and Sinus Barotrauma, Decompression Sickness, (DCS), Pulmonary Barotrauma (i.e., Arterial Gas Embolism (AGE). Mediastinal Emphysema, Subcutaneous Emphysema, and Pneumothorax) Oxygen Toxicity and Hypothermia. It includes information about the pulmonary function in NBL divers. Also included is recommendations about flying after diving.
Reduction of flammable and toxic materials for use in oxygen rich manned spacecraft cabin atmospheres