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1. Dioxygen
2. Oxygen 16
3. Oxygen-16
1. 7782-44-7
2. O
3. Molecular Oxygen
4. Oxygen Molecule
5. Dioxygen
6. Pure Oxygen
7. Oxygenium
8. Liquid Oxygen
9. Hyperoxia
10. Sauerstoff
11. Oxygen-16
12. Oxygen (liquid)
13. Oxygen, Liquified
14. Oxygenium Medicinale
15. Oxygene
16. Ccris 1228
17. Hsdb 5054
18. O2
19. Un1072
20. Un1073
21. Rns60 Component Oxygen
22. Ins No.948
23. Peroxide Ion
24. E-948
25. Rns-60 Component Oxygen
26. Chebi:15379
27. Ins-948
28. S88tt14065
29. Lox
30. E948
31. Oxygene [french]
32. Oxigeno [spanish]
33. Oxy
34. Compressed Oxygen
35. Oxygen [usp]
36. Einecs 231-956-9
37. Dioxidanediyl
38. Dioxygene
39. Disauerstoff
40. Oxygen Monoxide
41. Peroxy Radical
42. Singlet Dioxygen
43. Triplet Dioxygen
44. Unii-s88tt14065
45. Oxygen Usp
46. Oxygen, Compressed
47. Oxygen 93 Percent
48. Singlet Molecular Oxygen
49. Triplet Molecular Oxygen
50. Oxygen (8ci,9ci)
51. Oxygen [vandf]
52. Oxygen [hsdb]
53. Oxygen [inci]
54. Oxygen [jan]
55. Oxygen (jp17/usp)
56. Oxygen [who-dd]
57. Oxygen [who-ip]
58. Oxygen [mi]
59. Dioxygen(2.) (triplet)
60. Oxygen [mart.]
61. Oxygen, >=99.6%
62. Oxygen [green Book]
63. Oxygen, Compressed [un1072] [nonflammable Gas]
64. Oxygen [ep Monograph]
65. Oxygen [usp Monograph]
66. [oo]
67. Oxygen, >=99.998%
68. Chembl1234886
69. Dtxsid2037681
70. Chebi:26689
71. Chebi:27140
72. Oxygenium [who-ip Latin]
73. Oxygen, Refrigerated Liquid (cryogenic Liquid) [un1073] [nonflammable Gas]
74. Db09140
75. Un 1072
76. Un 1073
77. Oxygen, Messer(r) Cangas, 99.999%
78. Ds-014940
79. (1)o2
80. E 948
81. C00007
82. D00003
83. O2(2.)
84. Oxygen, Refrigerated Liquid (cryogenic Liquid)
85. Oxygen, Compressed [un1072] [nonflammable Gas]
86. (o2)(..)
87. (o2)(2.)
88. Q5203615
89. Aquanal(tm)-plus Oxygen (o2) 1-12 Mg/l, Refill Pack For 37428
90. Aquanal(tm)-plus Oxygen (o2) 1-12 Mg/l, Test Set With Color Comparator
91. 4-chloro-3-(chloro-difluoro-methyl)-4,4-difluoro-1-thiophen-2-yl-but-2-en-2-one
92. Oxygen, Refrigerated Liquid (cryogenic Liquid) [un1073] [nonflammable Gas]
| Molecular Weight | 31.999 g/mol |
|---|---|
| Molecular Formula | O2 |
| XLogP3 | -1.1 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 0 |
| Exact Mass | 31.989829239 g/mol |
| Monoisotopic Mass | 31.989829239 g/mol |
| Topological Polar Surface Area | 34.1 Ų |
| Heavy Atom Count | 2 |
| Formal Charge | 0 |
| Complexity | 0 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Supplemental oxygen is indicated when normal oxygenation is impaired because of pulmonarry injury, which may result from aspiration (chemical pneumonitis) or inhalation of toxic gases. The PO2 shoud be maintained at 70-80 mm Hg or higher if possible.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 490
Supplemental oxyugen usually is given empirically to patients with altered mental status or suspected hypoxemia.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 490
Oxygen (100%) is indicated for patients with carbon monoxide poisoning, to increase the conversion of carboxyhemoglobin and carboxymyoblobin to hemoglobin and myoglobin, and to increase oxygen saturation of the plasma and subsequent delivery to tissues.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 490
Hyperbaric oxygen (HBO) (100%) oxygen delivered to the patient in a pressurized chamber at 2-3 atm of pressure) may be beneficial for patients with severe carbon monoxide (CO) poisoning. It can hasten the reversal of CO binding to hemoglobin and intracellular myoglobin, can provide oxygen independent of hemoglobin, and may have protective actions in reducing postischemic brain damage.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 490
For more Therapeutic Uses (Complete) data for OXYGEN (16 total), please visit the HSDB record page.
In paraquat poisoning, oxygen may contribute to lung injury. In fact, slightly hypoxic environments (10-12% oxygen) have been advocated to reduce the risk of pulmonary fibrosis from paraquat.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 491
Relative contraindications to hyperbaric oxygen therapy include a history of recent middle ear or thoracic surgery, untreated pneumothorax, seizure disorder, and severe sinusitis.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 491
Prolonged high concentrations of oxygen are associated with pulmonary alveolar tissue damage. In general, the fraction of inspired oxygen (FIO2) shoud not be maintained at greater than 80% for more than 24 hours.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 491
Oxygen therapy may increase the risk of retrolental fibroplasia in neonates.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 491
For more Drug Warnings (Complete) data for OXYGEN (28 total), please visit the HSDB record page.
Oxygen therapy in clinical settings is used across diverse specialties, including various types of anoxia, hypoxia or dyspnea and any other disease states and conditions that reduce the efficiency of gas exchange and oxygen consumption such as respiratory illnesses, trauma, poisonings and drug overdoses. Oxygen therapy tries to achieve hyperoxia to reduce the extent of hypoxia-induced tissue damage and malfunction.
For oxygen supplementation and as a carrier gas during inhalation anaesthesia.
For oxygen supplementation during recovery.
Oxygen therapy improves effective cellular oxygenation, even at a low rate of tissue perfusion. Oxygen molecules adjust hypoxic ventilatory drive by acting on chemoreceptors on carotid bodies that sequentially relay sensory information to the higher processing centers in brainstem. It also attenuates hypoxia-induced mitochondrial depolarization that generates reactive oxygen species and/or apoptosis. Studies investigating on hyperbaric oxygen therapy has shown that oxygen supplementation can induce neural stem cell proliferation in neonatal rats thus promoting neurological regeneration after injuries. CD34+, CD45-dim leukocytes are also potential targets for hyperbaric oxygen therapy benefit as their mobilization was increased in vitro which could facilitate the acceleration of recovery at peripheral sites.
QV03AN01
V - Various
V03 - All other therapeutic products
V03A - All other therapeutic products
V03AN - Medical gases
V03AN01 - Oxygen
Route of Elimination
Exhalation
During inhalation of normal air the arterial blood leaves lungs about 95% saturated with oxygen, and with a subject standing at rest, the venous blood returns to lungs about 60 to 70% saturated. During 1 min approx 360 cc of oxygen are used up. After forced deep inspiration normal lung vol is about 5 to 5.5 L, 1 L which is O2 ...
Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 914
Arterial blood carries O2 in 2 forms. Most is normally bound to hemoglobin ... A smaller amt is free in soln. The amount of O2 carried ... depends on partial pressure of oxygen. When fully saturated with O2, each g of hemoglobin binds 1.3 vol % of O2. At 37 C, 0.003 vol % O2 is dissolved in blood/torr of partial pressure of O2.
Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980., p. 325
Fetal hemoglobin has more affinity for oxygen than maternal hemoglobin under similar conditions of pH & temp. If incompletely oxygen-saturated fetal & maternal blood are allowed to equilibrate across a membrane, partial pressure of O2 will be identical on both sides of membrane, but O2 content of fetal blood ... /will be/ higher ...
LaDu, B.N., H.G. Mandel, and E.L. Way. Fundamentals of Drug Metabolism and Disposition. Baltimore: Williams and Wilkins, 1971., p. 94
Oxygen enters the body primarily through the lungs, but may also be taken up by mucous membranes of the GI tract, the middle ear, and the paranasal sinuses. It diffuses from the alveoli into the pulmonary capillaries, dissolves in the blood plasma, enters the red blood cells, and binds to hemoglobin. The red cells transport bound O2 to tissues throughout the body via the circulatory system. In tissues where the partial pressure of O2 is lower than that of the blood, the O2 diffuses out of the red cells, through the capillaries and plasma, and into the cells. As the O2 plasma concentration diminishes, it is replaced by that contained in the red cells. The red blood cells are then circulated back to the lungs in a continuous recycling process ...
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:656
... Most O2 combines with carbon and hydrogen atoms from glucose molecules to form cellular energy, known as adenosine triphosphate or ATP, along with carbon dioxide (CO2) and water. The remaining O2 is combined with various compounds to synthesize cellular structures or elimination products. The CO2 generated in the cells then diffuses back to the red blood cells and returns to the lungs, where it is exhaled. The metabolic water combines with ingested water and the excess is eliminated by excretion through the kidneys or by evaporation from the lungs and skin.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:656
In the course of O2 metabolism, several toxic substances are generated, including superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH-), lipid peroxides, and others. Without the availability of several enzymes that destroy these toxic intermediary compounds, cell death quickly occurs. The protective enzymes include superoxide dismutases (SODs), catalase (CAT), and glutathione peroxidase (GP). Glutathione reductase (GR) participates by re-forming glutathione, which is preferentially oxidized, thereby sparing sulfhydryl-bearing proteins and cell wall constituents. Other contributors to the control of oxidant toxicity include vitamin C (ascorbic acid), vitamin E (alpha-tocopherol), vitamin A, and selenium, a cofactor for GP.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:661
Oxygen (O2) is reduced by both enzymatic and nonenzymatic processes to the superoxide radical (O2-). This radical species of oxygen is postulated to be formed in vivo in animals through activity of some iron-sulfur oxidation-reduction enzymes and certain flavoproteins ...
Doull, J., C.D. Klaassen, and M. D. Amdur (eds.). Casarett and Doull's Toxicology. 2nd ed. New York: Macmillan Publishing Co., 1980., p. 65
The partial reduction of molecular oxygen in biological systems produces the cytotoxic intermediates superoxide, hydrogen peroxide, and hydroxyl radical. The superoxide radical is now recognized to play significant roles in a number of pathophysiologic states including oxygen toxicity, radiation damage, phagocyte-mediated inflammation, and postischemic injury.
McCord JM; The Superoxide Free Radical; Its Biochemistry and Pathophysiology; Surgery 94 (3): 412-4 (1983)
Oxygen toxicity is mediated through increased production of partially reduced oxygen products such as superoxide anion, perhydroperoxy and hydroxyl radicals, peroxynitrite and possibly singlet molecular oxygen.
Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 6th ed. New York, NY: McGraw-Hill, 2001., p. 529
Approximately 122.24 seconds
Oxygen therapy increases the arterial pressure of oxygen and is effective in improving gas exchange and oxygen delivery to tissues, provided that there are functional alveolar units. Oxygen plays a critical role as an electron acceptor during oxidative phosphorylation in the electron transport chain through activation of cytochrome c oxidase (terminal enzyme of the electron transport chain). This process achieves successful aerobic respiration in organisms to generate ATP molecules as an energy source in many tissues. Oxygen supplementation acts to restore normal cellular activity at the mitochondrial level and reduce metabolic acidosis. There is also evidence that oxygen may interact with O2-sensitive voltage-gated potassium channels in glomus cells and cause hyperpolarization of mitochondrial membrane.
The exact mechanism whereby hypoxic pulmonary vasoconstriction is elicited is still unsettled. A possible role for toxic oxygen metabolites was evaluated, employing a set-up of blood-perfused isolated rat lungs. Hypoxic pulmonary vasoconstriction reflected as pulmonary arterial pressor responses, was evoked by alternately challenging the airways with a hypoxic- and a normoxic gas mixture, resulting in gradually increasing responses until a maximum was obtained. In a sequence of responses (mean +/- s.e. mean) increasing from 2.5 +/ - 0.2 kPa to 3.2 +/ - 0.1 kPa, administration to the perfusate of the inhibitor of xanthine oxidase, allopurinol reduced the subsequent response to 2.5 +/- 0.2 kPa (P < 0.001). By contrast, allopurinol did not affect vasoconstriction induced by serotonin or bradykinin. In control experiments responses continued to increase after administration of hypoxanthine (substrate of xanthine oxidase). Neither pretreatment with daily injections of the antioxidant vitamin E for 3 days in advance, nor addition to the perfusate of the scavenger enzymes superoxide dismutase and catalase, or dimethylsulfoxide had any impact on hypoxic pulmonary vasoconstriction; the subsequent responses rose at the same rate and in the same way as before. Thus, the present study has shown that allopurinol inhibition of xanthine oxidase depresses hypoxic pulmonary vasoconstriction. This could be due either to reduced production of toxic oxygen metabolites or to accumulation of purine metabolites. The absence of inhibitory effects of quenchers of toxic oxygen metabolites refutes a role for these metabolites in the elicitation of hypoxic pulmonary vasoconstriction. More likely, allopurinol inhibits hypoxic pulmonary vasoconstriction by interfering with the purine metabolism.
PMID:2389653 Kjaeve J et al; Acta Anaesthesiol Scand 34 (5): 384-8 (1990)
Exposure to hyperoxia results in endothelial necrosis followed by type II cell proliferation. This suggests that type II cells are resistant to hyperoxia. Oxygen-induced lung injury may result from an overproduction of oxygen metabolites normally scavenged by antioxidants such as superoxide dismutase, glutathione peroxidase, catalase and reduced glutathione. Therefore, resistance of type II cells to hyperoxia may be linked to high antioxidant activities. To test this hypothesis /the authors/ compared in vitro the effects of a 24 hr exposure period to 95% O2 on cultured type II cells, lung fibroblasts and alveolar macrophages isolated from rats. We show that type II cells, when compared with other cell types, are highly sensitive to hyperoxia as shown by increased lactate dehydrogenase release, decreased deoxyribose nucleic acid and protein content of Petri dishes and decreased thymidine incorporation into DNA. Synthesis of dipalmitoylphosphatidylcholine was also significantly reduced. Antioxidant enzyme activities as well as glutathione content were not higher in type II cells than in other cell types. However, hyperoxia results in a decreased superoxide dismutase activity and glutathione content in type II cells which was not observed in fibroblasts. /It was concluded/ that adaptative changes in superoxide dismutase and glutathione metabolism could be important defense mechanisms in cells exposed to hyperoxia.
PMID:1756840 Housset B et al; Eur Respir J 4 (9): 1066-75 (1991)
Oxygen, essential for mammalian life, is paradoxically harmful. If O2 is given at high enough concentrations for long enough times, the body's protective mechanisms are overwhelmed, leading to cellular injury and, with continued exposure, even death. In the course of O2 metabolism, several toxic substances are generated, including superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH-), lipid peroxides, and others. Without the availability of several enzymes that destroy these toxic intermediary compounds, cell death quickly occurs. The protective enzymes include superoxide dismutases (SODs), catalase (CAT), and glutathione peroxidase (GP). Glutathione reductase (GR) participates by re-forming glutathione, which is preferentially oxidized, thereby sparing sulfhydryl-bearing proteins and cell wall constituents. Other contributors to the control of oxidant toxicity include vitamin C (ascorbic acid), vitamin E (alpha-tocopherol), vitamin A, and selenium, a cofactor for GP. Normally, a balance exists between the production of toxic oxidants and their destruction by antioxidant mechanisms. Some individuals may lack the ability to produce sufficient antioxidants and suffer a slow progressive tissue deterioration as a result.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:662
Protein accumulation in the BAL fluid results from damage to the pavement-like cells that line the alveolar sacs, known as type I cells, which cover 95% of the alveolar surface. Type I cells are generally incapable of dividing, but when damaged, can be replaced by the type II alveolar cells interspersed among them. Type II cells are less susceptible to toxic injury, can proliferate rapidly, and can be transformed into type I cells. Toxic injuries that affect only type I cells can be repaired by this proliferative process. To the extent that type II cells are also injured, the effects are more severe and may lead to permanent changes. Other types of cells in the lung are also affected, especially the capillary endothelial cells, leading to leakage of blood plasma into the interstitial tissue between the alveoli, and ultimately into the alveoli. Blood cells in the capillaries may also form a clot or may leak into alveolar spaces (hemorrhage). Other cells in the interstitium, such as fibroblasts, are damaged. An inflammatory response, with infiltration of white blood cells, proliferation of fibroblasts, and subsequent fibrosis may follow.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:663
For more Mechanism of Action (Complete) data for OXYGEN (11 total), please visit the HSDB record page.
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