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Chemical Compound Review

Dioxygen     molecular oxygen

Synonyms: Hyperoxia, Oxygenium, dioxygene, Sauerstoff, oxygen, ...
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Disease relevance of oxygen

  • SOD-null mutants have been prepared to reveal the biological effects of O2-. SodA, sodB E. coli exhibit dioxygen-dependent auxotrophies and enhanced mutagenesis, reflecting O2(-)-sensitive biosynthetic pathways and DNA damage [1].
  • In yeast and bacteria, regulatory operons coordinate expression of genes responsible for adaptive responses to hypoxia and hyperoxia [2].
  • Pulmonary oxygen toxicity. Early reversible changes in human alveolar structures induced by hyperoxia [3].
  • Thus, although some of the effects of exposure to 17 hours of more than 95 per cent oxygen are reversible, hyperoxia for even this short period lowers the structural or functional barriers that normally prevent alveolar-capillary "leak" and induces processes that can culminate in fibrosis of the alveolar wall [3].
  • Hyperoxia causes angiopoietin 2-mediated acute lung injury and necrotic cell death [4].
  • Hyperoxia-induced lung injury was decreased in db/db compared with wild-type mice [5].
  • Cathepsin S deficiency improves alveolarization, and attenuates macrophage influx and fibroproliferative changes in hyperoxia-induced neonatal mouse lung injury [6].

Psychiatry related information on oxygen

  • The O2 levels returned to baseline during intermittent wakefulness [7].
  • In five goats provided with chronic sagittal sinus fistulae, arteriovenous oxygen difference was measured in separate studies and found to be significantly lower during REM sleep compared with W; brain O2 consumption was similar in magnitude in the REM and W states [8].
  • A striking aspect of the reaction time course is that rapid O2-binding and trapping chemistry is followed by a progressive slowing down of succeeding steps in the process, which allows the various transient species to build up to concentrations sufficient for their detection by our time-resolved techniques [9].
  • It is suggested that the univalent reduction of oxygen in normal metabolism to O2- and subsequent production of more harmful radicals is the source of the DNA defects that, in cases where the defense mechanisms fail, lead to spontaneous cancer in the individual [10].
  • Oxygen affinity of hemoglobin regulates O2 consumption, metabolism, and physical activity [11].

High impact information on oxygen

  • In this site, the liver and probably the peripheral circulation, effector cells bind to the surface of parasitized erythrocytes and are activated to release superoxide (O2-) [12].
  • Antibodies on the surface of schizont-infected cells could facilitate binding of effector cells and trigger O2- release, thereby acting synergistically with cell-mediated immunity [12].
  • New evidence suggests that at least two members of the family of hypoxia-inducible factor (HIF) prolyl hydroxylases that regulate HIF stability in response to oxygen (O2) availability are also targeted for proteosome-dependent degradation by the E3 ubiquitin ligases Siah1a and Siah2 [13].
  • The skeletal muscle calcium release channel: coupled O2 sensor and NO signaling functions [14].
  • Recognition of an avirulent pathogen stimulates an oxidative burst generating O2- and H2O2, and these reactive oxygen intermediates (ROIs) cue the induction of defense genes and cell death in the development of a restricted lesion [15].

Chemical compound and disease context of oxygen

  • Maternal hyperoxia greatly reduces the incidence of phenytoin-induced cleft lip and palate in A/J mice [16].
  • Greatly diminished O2- production was seen with particles prepared from cells obtained from three patients with chronic granulomatous disease, with 2.5 mM NADPH as electron donor [17].
  • Previous work has shown that the Pseudomonas-derived protease, pseudomonas elastase (PAE), can modify transferrin to form iron complexes capable of catalyzing the formation of hydroxyl radical (.OH) from neutrophil (PMN)-derived superoxide (.O2-) and hydrogen peroxide (H2O2) [18].
  • Since xanthine oxidase is known to generate .O2- in reperfused ischemic tissue and in certain inflammatory disorders, we attempted to assess its role in porphyrin photosensitization [19].
  • In contrast, neither hemorrhagic hypotension (50 mmHg) nor hypoxia (6-8% O2) increased pancreatic NE output (delta = +80 +/- 110 and -20 +/- 60 pg/min, respectively, P less than 0.01 vs. neuroglucopenia) despite both producing increases of arterial plasma NE and epinephrine similar to glucopenia [20].

Biological context of oxygen

  • The crystal structure of the complex with the dioxygen analogue, NO and ACV bound to the active-site iron supports this hypothesis [21].
  • Inhibition of SOD causes accumulation of cellular O2- and leads to free-radical-mediated damage to mitochondrial membranes, the release of cytochrome c from mitochondria and apoptosis of the cancer cells [22].
  • Regulation of mammalian O2 homeostasis by hypoxia-inducible factor 1 [23].
  • We suggest that anoxygenic photosynthesis is a relatively recent phenomenon in the Black Sea initiated by shallowing of the chemocline over the past decade and development of an anoxic layer devoid of O2 and H2S [24].
  • Here, I report the effects of proton-motive force and membrane potential on two equilibria involving intermediates of the bimetallic centre at different levels of O2 reduction [25].

Anatomical context of oxygen

  • Here we show that COS-7 cells transfected with four NADPH oxidase components, but lacking H+ channels, produce O2- in the presence of Zn2+ concentrations that inhibit O2- production in neutrophils and eosinophils [26].
  • The Na+ pump derives its energy from ATP, splitting it into ADP and Pi, and it has reasonably been proposed that the changes in concentrations of ATP, ADP and Pi lead to a stimulation of the O2 consumption by the mitochondria and hence to a restoration of the stock of ATP [27].
  • Intraocular injection of VEGF at the onset of experimental hyperoxia prevents apoptotic death of endothelial cells and rescues the retinal vasculature [28].
  • The identification of an oxygen-sensing mechanism (namely the presence of an O2-sensitive potassium channel coupled to an O2 sensor protein) in the cells of pulmonary neuroepithelial bodies indicates that they are transducers of the hypoxia stimulus and hence may function as airway chemoreceptors in the regulation of respiration [29].
  • During hyperoxia Ang2 expression is induced in lung epithelial cells, while hyperoxia-induced oxidant injury, cell death, inflammation, permeability alterations and mortality are ameliorated in Ang2(-/-) and siRNA-treated mice [4].

Associations of oxygen with other chemical compounds


Gene context of oxygen

  • The implication of a reactive oxygen species, probably .O2-, as a mediator of Ras-induced cell cycle progression independent of MAPK and JNK suggests a possible mechanism for the effects of antioxidants against Ras-induced cellular transformation [34].
  • An absolute requirement for dioxygen as a cosubstrate and iron as cofactor suggests that HIF-PH functions directly as a cellular oxygen sensor [35].
  • Thus, H-RasV12-induced transformation can lead to the production of .O2- through one or more pathways involving a flavoprotein and Rac1 [34].
  • These data indicate that OS-9 is an essential component of a multiprotein complex that regulates HIF-1alpha levels in an O2-dependent manner [36].
  • However, retinal VEGF expression in hyperoxia-treated homozygous null mice did not decrease and remained at control levels [37].

Analytical, diagnostic and therapeutic context of oxygen

  • To study the early changes in the lower respiratory tract in persons exposed to periods of hyperoxia usually considered safe, we evaluated 14 normal subjects by bronchoalveolar lavage before and immediately after 16.7 +/- 1.1 hours of breathing more than 95 per cent oxygen [3].
  • Hyperoxia for an average of 17 hours did not change the total number or type of lung inflammatory and immune effector cells recovered by lavage (P greater than 0.05, all comparisons) [3].
  • Based on the structure, we propose a mechanism for penicillin formation that involves ligation of ACV to the iron centre, creating a vacant iron coordination site into which dioxygen can bind [21].
  • Protection against lethal hyperoxia by tracheal insufflation of erythrocytes: role of red cell glutathione [38].
  • Redox titrations with molecular oxygen (O2) and cobaltocene were carried out, and O2 was found to bind irreversibly in a 1:1 ratio to the model compound [39].


  1. Superoxide radical and superoxide dismutases. Fridovich, I. Annu. Rev. Biochem. (1995) [Pubmed]
  2. Oxygen sensing and molecular adaptation to hypoxia. Bunn, H.F., Poyton, R.O. Physiol. Rev. (1996) [Pubmed]
  3. Pulmonary oxygen toxicity. Early reversible changes in human alveolar structures induced by hyperoxia. Davis, W.B., Rennard, S.I., Bitterman, P.B., Crystal, R.G. N. Engl. J. Med. (1983) [Pubmed]
  4. Hyperoxia causes angiopoietin 2-mediated acute lung injury and necrotic cell death. Bhandari, V., Choo-Wing, R., Lee, C.G., Zhu, Z., Nedrelow, J.H., Chupp, G.L., Zhang, X., Matthay, M.A., Ware, L.B., Homer, R.J., Lee, P.J., Geick, A., de Fougerolles, A.R., Elias, J.A. Nat. Med. (2006) [Pubmed]
  5. Leptin resistance protects mice from hyperoxia-induced acute lung injury. Bellmeyer, A., Martino, J.M., Chandel, N.S., Scott Budinger, G.R., Dean, D.A., Mutlu, G.M. Am. J. Respir. Crit. Care Med. (2007) [Pubmed]
  6. Cathepsin S deficiency confers protection from neonatal hyperoxia-induced lung injury. Hirakawa, H., Pierce, R.A., Bingol-Karakoc, G., Karaaslan, C., Weng, M., Shi, G.P., Saad, A., Weber, E., Mariani, T.J., Starcher, B., Shapiro, S.D., Cataltepe, S. Am. J. Respir. Crit. Care Med. (2007) [Pubmed]
  7. Nocturnal oxygen desaturation in patients with sickle cell anemia. Scharf, M.B., Lobel, J.S., Caldwell, E., Cameron, B.F., Kramer, M., De Marchis, J., Paine, C. JAMA (1983) [Pubmed]
  8. Correlation between ventilation and brain blood flow during sleep. Santiago, T.V., Guerra, E., Neubauer, J.A., Edelman, N.H. J. Clin. Invest. (1984) [Pubmed]
  9. Resolution of the reaction sequence during the reduction of O2 by cytochrome oxidase. Varotsis, C., Zhang, Y., Appelman, E.H., Babcock, G.T. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  10. Spontaneous cancer and its possible relationship to oxygen metabolism. Totter, J.R. Proc. Natl. Acad. Sci. U.S.A. (1980) [Pubmed]
  11. Oxygen affinity of hemoglobin regulates O2 consumption, metabolism, and physical activity. Shirasawa, T., Izumizaki, M., Suzuki, Y., Ishihara, A., Shimizu, T., Tamaki, M., Huang, F., Koizumi, K., Iwase, M., Sakai, H., Tsuchida, E., Ueshima, K., Inoue, H., Koseki, H., Senda, T., Kuriyama, T., Homma, I. J. Biol. Chem. (2003) [Pubmed]
  12. The role of cell-mediated immune responses in resistance to malaria, with special reference to oxidant stress. Allison, A.C., Eugui, E.M. Annu. Rev. Immunol. (1983) [Pubmed]
  13. Siah proteins, HIF prolyl hydroxylases, and the physiological response to hypoxia. Simon, M.C. Cell (2004) [Pubmed]
  14. The skeletal muscle calcium release channel: coupled O2 sensor and NO signaling functions. Eu, J.P., Sun, J., Xu, L., Stamler, J.S., Meissner, G. Cell (2000) [Pubmed]
  15. Reactive oxygen intermediates mediate a systemic signal network in the establishment of plant immunity. Alvarez, M.E., Pennell, R.I., Meijer, P.J., Ishikawa, A., Dixon, R.A., Lamb, C. Cell (1998) [Pubmed]
  16. Maternal hyperoxia greatly reduces the incidence of phenytoin-induced cleft lip and palate in A/J mice. Millicovsky, G., Johnston, M.C. Science (1981) [Pubmed]
  17. The particulate superoxide-forming system from human neutrophils. Properties of the system and further evidence supporting its participation in the respiratory burst. Babior, B.M., Curnutte, J.T., McMurrich, B.J. J. Clin. Invest. (1976) [Pubmed]
  18. Protease-cleaved iron-transferrin augments oxidant-mediated endothelial cell injury via hydroxyl radical formation. Miller, R.A., Britigan, B.E. J. Clin. Invest. (1995) [Pubmed]
  19. A novel mechanism for the generation of superoxide anions in hematoporphyrin derivative-mediated cutaneous photosensitization. Activation of the xanthine oxidase pathway. Athar, M., Elmets, C.A., Bickers, D.R., Mukhtar, H. J. Clin. Invest. (1989) [Pubmed]
  20. Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system. Havel, P.J., Veith, R.C., Dunning, B.E., Taborsky, G.J. J. Clin. Invest. (1988) [Pubmed]
  21. Structure of isopenicillin N synthase complexed with substrate and the mechanism of penicillin formation. Roach, P.L., Clifton, I.J., Hensgens, C.M., Shibata, N., Schofield, C.J., Hajdu, J., Baldwin, J.E. Nature (1997) [Pubmed]
  22. Superoxide dismutase as a target for the selective killing of cancer cells. Huang, P., Feng, L., Oldham, E.A., Keating, M.J., Plunkett, W. Nature (2000) [Pubmed]
  23. Regulation of mammalian O2 homeostasis by hypoxia-inducible factor 1. Semenza, G.L. Annu. Rev. Cell Dev. Biol. (1999) [Pubmed]
  24. Evidence for anoxygenic photosynthesis from the distribution of bacteriochlorophylls in the Black Sea. Repeta, D.J., Simpson, D.J., Jorgensen, B.B., Jannasch, H.W. Nature (1989) [Pubmed]
  25. Identification of the electron transfers in cytochrome oxidase that are coupled to proton-pumping. Wikström, M. Nature (1989) [Pubmed]
  26. The voltage dependence of NADPH oxidase reveals why phagocytes need proton channels. DeCoursey, T.E., Morgan, D., Cherny, V.V. Nature (2003) [Pubmed]
  27. Oxygen uptake occurs faster than sodium pumping in bee retina after a light flash. Tsacopoulos, M., Orkand, R.K., Coles, J.A., Levy, S., Poitry, S. Nature (1983) [Pubmed]
  28. Vascular endothelial growth factor acts as a survival factor for newly formed retinal vessels and has implications for retinopathy of prematurity. Alon, T., Hemo, I., Itin, A., Pe'er, J., Stone, J., Keshet, E. Nat. Med. (1995) [Pubmed]
  29. Oxygen sensing in airway chemoreceptors. Youngson, C., Nurse, C., Yeger, H., Cutz, E. Nature (1993) [Pubmed]
  30. Electron currents generated by the human phagocyte NADPH oxidase. Schrenzel, J., Serrander, L., Bánfi, B., Nüsse, O., Fouyouzi, R., Lew, D.P., Demaurex, N., Krause, K.H. Nature (1998) [Pubmed]
  31. NMDA-dependent superoxide production and neurotoxicity. Lafon-Cazal, M., Pietri, S., Culcasi, M., Bockaert, J. Nature (1993) [Pubmed]
  32. Elevation of oxygen release by nitroglycerin without an increase in blood flow in the hepatic microcirculation. Kosaka, H., Seiyama, A. Nat. Med. (1997) [Pubmed]
  33. Structure of a cephalosporin synthase. Valegård, K., van Scheltinga, A.C., Lloyd, M.D., Hara, T., Ramaswamy, S., Perrakis, A., Thompson, A., Lee, H.J., Baldwin, J.E., Schofield, C.J., Hajdu, J., Andersson, I. Nature (1998) [Pubmed]
  34. Mitogenic signaling mediated by oxidants in Ras-transformed fibroblasts. Irani, K., Xia, Y., Zweier, J.L., Sollott, S.J., Der, C.J., Fearon, E.R., Sundaresan, M., Finkel, T., Goldschmidt-Clermont, P.J. Science (1997) [Pubmed]
  35. Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation. Jaakkola, P., Mole, D.R., Tian, Y.M., Wilson, M.I., Gielbert, J., Gaskell, S.J., Kriegsheim Av, n.u.l.l., Hebestreit, H.F., Mukherji, M., Schofield, C.J., Maxwell, P.H., Pugh, C.W., Ratcliffe, P.J. Science (2001) [Pubmed]
  36. OS-9 interacts with hypoxia-inducible factor 1alpha and prolyl hydroxylases to promote oxygen-dependent degradation of HIF-1alpha. Baek, J.H., Mahon, P.C., Oh, J., Kelly, B., Krishnamachary, B., Pearson, M., Chan, D.A., Giaccia, A.J., Semenza, G.L. Mol. Cell (2005) [Pubmed]
  37. c-abl is required for the development of hyperoxia-induced retinopathy. Nunes, I., Higgins, R.D., Zanetta, L., Shamamian, P., Goff, S.P. J. Exp. Med. (2001) [Pubmed]
  38. Protection against lethal hyperoxia by tracheal insufflation of erythrocytes: role of red cell glutathione. van Asbeck, B.S., Hoidal, J., Vercellotti, G.M., Schwartz, B.A., Moldow, C.F., Jacob, H.S. Science (1985) [Pubmed]
  39. A functional model related to cytochrome c oxidase and its electrocatalytic four-electron reduction of O2. Collman, J.P., Fu, L., Herrmann, P.C., Zhang, X. Science (1997) [Pubmed]
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