Common NameO2
DescriptionOxygen is the third most abundant element in the universe after hydrogen and helium and the most abundant element by mass in the Earth's crust. Diatomic oxygen gas constitutes 20.9% of the volume of air. All major classes of structural molecules in living organisms, such as proteins, carbohydrates, and fats, contain oxygen, as do the major inorganic compounds that comprise animal shells, teeth, and bone. Oxygen in the form of O2 is produced from water by cyanobacteria, algae and plants during photosynthesis and is used in cellular respiration for all living organisms. Green algae and cyanobacteria in marine environments provide about 70% of the free oxygen produced on earth and the rest is produced by terrestrial plants. Oxygen is used in mitochondria to help generate adenosine triphosphate (ATP) during oxidative phosphorylation. For animals, a constant supply of oxygen is indispensable for cardiac viability and function. To meet this demand, an adult human, at rest, inhales 1.8 to 2.4 grams of oxygen per minute. This amounts to more than 6 billion tonnes of oxygen inhaled by humanity per year. At a resting pulse rate, the heart consumes approximately 8-15 ml O2/min/100 g tissue. This is significantly more than that consumed by the brain (approximately 3 ml O2/min/100 g tissue) and can increase to more than 70 ml O2/min/100 g myocardial tissue during vigorous exercise. As a general rule, mammalian heart muscle cannot produce enough energy under anaerobic conditions to maintain essential cellular processes; thus, a constant supply of oxygen is indispensable to sustain cardiac function and viability. However, the role of oxygen and oxygen-associated processes in living systems is complex, and they and can be either beneficial or contribute to cardiac dysfunction and death (through reactive oxygen species). Reactive oxygen species (ROS) are a family of oxygen-derived free radicals that are produced in mammalian cells under normal and pathologic conditions. Many ROS, such as the superoxide anion (O2-)and hydrogen peroxide (H2O2), act within blood vessels, altering mechanisms mediating mechanical signal transduction and autoregulation of cerebral blood flow. Reactive oxygen species are believed to be involved in cellular signaling in blood vessels in both normal and pathologic states. The major pathway for the production of ROS is by way of the one-electron reduction of molecular oxygen to form an oxygen radical, the superoxide anion (O2-). Within the vasculature there are several enzymatic sources of O2-, including xanthine oxidase, the mitochondrial electron transport chain, and nitric oxide (NO) synthases. Studies in recent years, however, suggest that the major contributor to O2- levels in vascular cells is the membrane-bound enzyme NADPH-oxidase. Produced O2- can react with other radicals, such as NO, or spontaneously dismutate to produce hydrogen peroxide (H2O2). In cells, the latter reaction is an important pathway for normal O2- breakdown and is usually catalyzed by the enzyme superoxide dismutase (SOD). Once formed, H2O2 can undergo various reactions, both enzymatic and nonenzymatic. The antioxidant enzymes catalase and glutathione peroxidase act to limit ROS accumulation within cells by breaking down H2O2 to H2O. Metabolism of H2O2 can also produce other, more damaging ROS. For example, the endogenous enzyme myeloperoxidase uses H2O2 as a substrate to form the highly reactive compound hypochlorous acid. Alternatively, H2O2 can undergo Fenton or Haber-Weiss chemistry, reacting with Fe2+/Fe3+ ions to form toxic hydroxyl radicals (-.OH). (PMID: 17027622 , 15765131 ).
Structure
Molecular FormulaO2
Average Mass31.99880
Monoisotopic Mass31.98983
IUPAC Nameoxidanone
Traditional NameOxygen
CAS Registry Number7782-44-7
SMILESO=O
InChI IdentifierInChI=1S/O2/c1-2
InChI KeyMYMOFIZGZYHOMD-UHFFFAOYSA-N
CHEBI IDCHEBI:15379
HMDB IDHMDB0001377
Pathways
NameSMPDB/PathBank
Oxidative phosphorylation
Tyrosine metabolism
Glycine, serine and threonine metabolism
Arginine and proline metabolism
beta-Alanine metabolism
Lysine degradation
Sulfur metabolism
Purine metabolism
Tyrosine metabolism
Primary bile acid biosynthesis
Tryptophan metabolism
Valine, leucine and isoleucine degradation
Inositol phosphate metabolism
Nicotinate and nicotinamide metabolism
Phenylalanine and Tyrosine Metabolism
Cysteine Metabolism
Vitamin B6 Metabolism
Taurine and Hypotaurine Metabolism
Steroid Biosynthesis
Porphyrin Metabolism
Caffeine Metabolism
Oxidation of Branched Chain Fatty Acids
Methionine Metabolism
D-Arginine and D-Ornithine Metabolism
Histidine metabolism
Ubiquinone Biosynthesis
Aspartate Metabolism
Androgen and Estrogen Metabolism
Riboflavin Metabolism
Retinol Metabolism
Arachidonic Acid Metabolism
Piroxicam Action Pathway
Ibandronate Action Pathway
Simvastatin Action Pathway
Acetylsalicylic Acid Action Pathway
Etodolac Action Pathway
Ketoprofen Action Pathway
Ibuprofen Action Pathway
Rofecoxib Action Pathway
Pravastatin Action Pathway
Rosuvastatin Action Pathway
Diclofenac Action Pathway
Sulindac Action Pathway
Alendronate Action Pathway
Celecoxib Action Pathway
Ketorolac Action Pathway
Lovastatin Action Pathway
Suprofen Action Pathway
Bromfenac Action Pathway
Indomethacin Action Pathway
Meloxicam Action Pathway
Zoledronate Action Pathway
Mefenamic Acid Action Pathway
Cerivastatin Action Pathway
Risedronate Action Pathway
Oxaprozin Action Pathway
Nabumetone Action Pathway
Valdecoxib Action Pathway
Pamidronate Action Pathway
Fluvastatin Action Pathway
Naproxen Action Pathway
Steroidogenesis
Atorvastatin Action Pathway
2-Methyl-3-Hydroxybutryl CoA Dehydrogenase Deficiency
3-Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency
3-Methylglutaconic Aciduria Type I
3-Methylglutaconic Aciduria Type III
3-Methylglutaconic Aciduria Type IV
Adenosine Deaminase Deficiency
Adenylosuccinate Lyase Deficiency
AICA-Ribosiduria
Alkaptonuria
Aromatic L-Aminoacid Decarboxylase Deficiency
Beta-Ketothiolase Deficiency
Canavan Disease
Cystathionine Beta-Synthase Deficiency
Dihydropyrimidine Dehydrogenase Deficiency (DHPD)
Glutaric Aciduria Type I
Guanidinoacetate Methyltransferase Deficiency (GAMT Deficiency)
Hawkinsinuria
Histidinemia
Hypoacetylaspartia
Maple Syrup Urine Disease
Methylmalonic Aciduria
Molybdenum Cofactor Deficiency
Phenylketonuria
Prolidase Deficiency (PD)
Prolinemia Type II
Hypercholesterolemia
Purine Nucleoside Phosphorylase Deficiency
S-Adenosylhomocysteine (SAH) Hydrolase Deficiency
Tyrosinemia Type I
Xanthine Dehydrogenase Deficiency (Xanthinuria)
Methionine Adenosyltransferase Deficiency
Glycine N-methyltransferase Deficiency
Non Ketotic Hyperglycinemia
Propionic Acidemia
3-Methylcrotonyl Coa Carboxylase Deficiency Type I
Isovaleric Aciduria
Saccharopinuria/Hyperlysinemia II
Dimethylglycine Dehydrogenase Deficiency
Sarcosinemia
Clopidogrel Action Pathway
Diflunisal Action Pathway
Congenital Bile Acid Synthesis Defect Type II
Cerebrotendinous Xanthomatosis (CTX)
Zellweger Syndrome
Familial Hypercholanemia (FHCA)
Congenital Bile Acid Synthesis Defect Type III
Lysosomal Acid Lipase Deficiency (Wolman Disease)
Phenytoin (Antiarrhythmic) Action Pathway
Lidocaine (Antiarrhythmic) Action Pathway
Vitamin A Deficiency
Methylenetetrahydrofolate Reductase Deficiency (MTHFRD)
Hypermethioninemia
Hereditary Coproporphyria (HCP)
Acute Intermittent Porphyria
Congenital Erythropoietic Porphyria (CEP) or Gunther Disease
Porphyria Variegata (PV)
GABA-Transaminase Deficiency
Leukotriene C4 Synthesis Deficiency
17-Beta Hydroxysteroid Dehydrogenase III Deficiency
Hyperprolinemia Type II
Hyperprolinemia Type I
Arginine: Glycine Amidinotransferase Deficiency (AGAT Deficiency)
Ornithine Aminotransferase Deficiency (OAT Deficiency)
Lesch-Nyhan Syndrome (LNS)
Gout or Kelley-Seegmiller Syndrome
Tyrosinemia Type 2 (or Richner-Hanhart syndrome)
Tyrosinemia Type 3 (TYRO3)
Congenital Lipoid Adrenal Hyperplasia (CLAH) or Lipoid CAH
Adrenal Hyperplasia Type 5 or Congenital Adrenal Hyperplasia due to 17 Alpha-hydroxylase Deficiency
Adrenal Hyperplasia Type 3 or Congenital Adrenal Hyperplasia due to 21-hydroxylase Deficiency
Methylmalonate Semialdehyde Dehydrogenase Deficiency
Desmosterolosis
CHILD Syndrome
Chondrodysplasia Punctata II, X Linked Dominant (CDPX2)
Smith-Lemli-Opitz Syndrome (SLOS)
Lidocaine (Local Anaesthetic) Action Pathway
Codeine Action Pathway
Methadone Action Pathway
Imipramine Action Pathway
Desipramine Action Pathway
Citalopram Action Pathway
Fluoxetine Action Pathway
Azathioprine Action Pathway
Mercaptopurine Action Pathway
Disulfiram Action Pathway
Thioguanine Action Pathway
Nicotine Action Pathway
Etoposide Action Pathway
Teniposide Action Pathway
Cyclophosphamide Action Pathway
Ifosfamide Action Pathway
Ethanol Degradation
Phytanic Acid Peroxisomal Oxidation
Refsum Disease
Vitamin K Metabolism
Carnitine Synthesis
Degradation of Superoxides
Tamoxifen Action Pathway
Plasmalogen Synthesis
Dimethylglycine Dehydrogenase Deficiency
Hyperglycinemia, non-ketotic
Ureidopropionase Deficiency
Carnosinuria, carnosinemia
Tyrosinemia, transient, of the newborn
Tyrosine hydroxylase deficiency
Dopamine beta-hydroxylase deficiency
Beta-mercaptolactate-cysteine disulfiduria
Hypophosphatasia
Creatine deficiency, guanidinoacetate methyltransferase deficiency
Hyperornithinemia with gyrate atrophy (HOGA)
Hyperornithinemia-hyperammonemia-homocitrullinuria [HHH-syndrome]
L-arginine:glycine amidinotransferase deficiency
Cholesteryl ester storage disease
Hyper-IgD syndrome
Mevalonic aciduria
Wolman disease
Xanthinuria type I
Xanthinuria type II
3-hydroxyisobutyric acid dehydrogenase deficiency
3-hydroxyisobutyric aciduria
Isobutyryl-coa dehydrogenase deficiency
Isovaleric acidemia
Hyperlysinemia I, Familial
Hyperlysinemia II or Saccharopinuria
Sulfite oxidase deficiency
Monoamine oxidase-a deficiency (MAO-A)
Adenine phosphoribosyltransferase deficiency (APRT)
Mitochondrial DNA depletion syndrome
Myoadenylate deaminase deficiency
Aromatase deficiency
17-alpha-hydroxylase deficiency (CYP17)
Homocystinuria-megaloblastic anemia due to defect in cobalamin metabolism, cblG complementation type
Pyridoxine dependency with seizures
11-beta-hydroxylase deficiency (CYP11B1)
21-hydroxylase deficiency (CYP21)
Corticosterone methyl oxidase I deficiency (CMO I)
Corticosterone methyl oxidase II deficiency - CMO II
Ibuprofen Metabolism Pathway
Etoposide Metabolism Pathway
Teniposide Metabolism Pathway
Cyclophosphamide Metabolism Pathway
Ifosfamide Metabolism Pathway
Tamoxifen Metabolism Pathway
Clopidogrel Metabolism Pathway
Lidocaine (Local Anaesthetic) Metabolism Pathway
Codeine Metabolism Pathway
Methadone Metabolism Pathway
Imipramine Metabolism Pathway
Desipramine Metabolism Pathway
Citalopram Metabolism Pathway
Nicotine Metabolism Pathway
Felbamate Metabolism Pathway
Carbamazepine Metabolism Pathway
Valproic Acid Metabolism Pathway
Venlafaxine Metabolism Pathway
Tramadol Metabolism Pathway
Levomethadyl Acetate Metabolism Pathway
Clomipramine Metabolism Pathway
Doxepin Metabolism Pathway
Nevirapine Metabolism Pathway
Celecoxib Metabolism Pathway
Fluoxetine Metabolism Pathway
Sorafenib Metabolism Pathway
Lamivudine Metabolism Pathway
Artemether Metabolism Pathway
Mycophenolic Acid Metabolism Pathway
Rosiglitazone Metabolism Pathway
Antipyrine Action Pathway
Antrafenine Action Pathway
Carprofen Action Pathway
Etoricoxib Action Pathway
Fenoprofen Action Pathway
Flurbiprofen Action Pathway
Magnesium salicylate Action Pathway
Lumiracoxib Action Pathway
Lornoxicam Action Pathway
Phenylbutazone Action Pathway
Nepafenac Action Pathway
Trisalicylate-choline Action Pathway
Tolmetin Action Pathway
Tiaprofenic Acid Action Pathway
Tenoxicam Action Pathway
Salsalate Action Pathway
Salicylate-sodium Action Pathway
Salicylic Acid Action Pathway
Acetaminophen Action Pathway
Apparent mineralocorticoid excess syndrome
3-Beta-Hydroxysteroid Dehydrogenase Deficiency
2-aminoadipic 2-oxoadipic aciduria
27-Hydroxylase Deficiency
3-Phosphoglycerate dehydrogenase deficiency
Cystinosis, ocular nonnephropathic
The Oncogenic Action of Succinate
The Oncogenic Action of Fumarate
Glutaminolysis and Cancer
Androstenedione Metabolism
Estrone Metabolism
StateNot Available
Water SolubilityNot Available
logP-0.28
logSNot Available
pKa (Strongest Acidic)Not Available
pKa (Strongest Basic)Not Available
Hydrogen Acceptor Count2
Hydrogen Donor Count0
Polar Surface Area34.14 Ų
Rotatable Bond Count0
Physiological Charge0
Formal Charge0
Refractivity2.89 m³·mol⁻¹
Polarizability1.53

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