Common NameH2o2
DescriptionHydrogen peroxide (H2O2) is a very pale blue liquid that appears colourless in a dilute solution. H2O2 is slightly more viscous than water and is a weak acid. H2O2 is unstable and slowly decomposes in the presence of light. It has strong oxidizing properties and is, therefore, a powerful bleaching agent that is mostly used for bleaching paper. H2O2 has also found use as a disinfectant and as an oxidizer. H2O2 in the form of carbamide peroxide is widely used for tooth whitening (bleaching), both in professionally- and in self-administered products. H2O2 is a well-documented component of living cells and is a normal metabolite of oxygen in the aerobic metabolism of cells and tissues. A total of 31 human cellular H2O2 generating enzymes has been identified so far (PMID: 25843657 ). H2O2 plays important roles in host defence and oxidative biosynthetic reactions. At high levels (>100 nM) H2O2 is toxic to most cells due to its ability to non-specifically oxidize proteins, membranes and DNA, leading to general cellular damage and dysfunction. However, at low levels (<10 nM), H2O2 functions as a signalling agent, particularly in higher organisms. In plants, H2O2 plays a role in signalling to cause cell shape changes such as stomatal closure and root growth. As a messenger molecule in vertebrates, H2O2 diffuses through cells and tissues to initiate cell shape changes, to drive vascular remodelling, and to activate cell proliferation and recruitment of immune cells. H2O2 also plays a role in redox sensing, signalling, and redox regulation (PMID: 28110218 ). This is normally done through molecular redox “switches” such as thiol-containing proteins. The production and decomposition of H2O2 are tightly regulated (PMID: 17434122 ). In humans, H2O2 can be generated in response to various stimuli, including cytokines and growth factors. H2O2 is degraded by several enzymes including catalase and superoxide dismutase (SOD), both of which play important roles in keeping the amount of H2O2 in the body below toxic levels. H2O2 also appears to play a role in vitiligo. Vitiligo is a skin pigment disorder leading to patchy skin colour, especially among dark-skinned individuals. Patients with vitiligo have low catalase levels in their skin, leading to higher levels of H2O2. High levels of H2O2 damage the epidermal melanocytes, leading to a loss of pigment (PMID: 10393521 ). Accumulating evidence suggests that hydrogen peroxide H2O2 plays an important role in cancer development. Experimental data have shown that cancer cells produce high amounts of H2O2. An increase in the cellular levels of H2O2 has been linked to several key alterations in cancer, including DNA changes, cell proliferation, apoptosis resistance, metastasis, angiogenesis and hypoxia-inducible factor 1 (HIF-1) activation (PMID: 17150302 , 17335854 , 16677071 , 16607324 , 16514169 ). H2O2 is found in most cells, tissues, and biofluids. H2O2 levels in the urine can be significantly increased with the consumption of coffee and other polyphenolic-containing beverages (wine, tea) (PMID: 12419961 ). In particular, roasted coffee has high levels of 1,2,4-benzenetriol which can, on its own, lead to the production of H2O2. Normal levels of urinary H2O2 in non-coffee drinkers or fasted subjects are between 0.5-3 uM/mM creatinine whereas, for those who drink coffee, the levels are between 3-10 uM/mM creatinine (PMID: 12419961 ). It is thought that H2O2 in urine could act as an antibacterial agent and that H2O2 is involved in the regulation of glomerular function (PMID: 10766414 ).
Structure
Molecular FormulaH2O2
Average Mass34.01470
Monoisotopic Mass34.00548
IUPAC Nameperoxol
Traditional NameHydrogen peroxide
CAS Registry Number7722-84-1
SMILESOO
InChI IdentifierInChI=1S/H2O2/c1-2/h1-2H
InChI KeyMHAJPDPJQMAIIY-UHFFFAOYSA-N
CHEBI IDCHEBI:16240
HMDB IDHMDB0003125
Pathways
NameSMPDB/PathBank
Glycine, serine and threonine metabolism
Glutathione metabolism
beta-Alanine metabolism
Lysine degradation
Sulfur metabolism
Purine metabolism
Tyrosine metabolism
Tryptophan metabolism
Valine, leucine and isoleucine degradation
Nicotinate and nicotinamide metabolism
Arginine and proline metabolism
Phenylalanine and Tyrosine Metabolism
Vitamin B6 Metabolism
Porphyrin Metabolism
Caffeine Metabolism
Methionine Metabolism
D-Arginine and D-Ornithine Metabolism
Histidine metabolism
Aspartate Metabolism
Riboflavin Metabolism
Arachidonic Acid Metabolism
Ibuprofen 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
5-Oxoprolinuria
Adenosine Deaminase Deficiency
Adenylosuccinate Lyase Deficiency
AICA-Ribosiduria
Alkaptonuria
Beta-Ketothiolase Deficiency
Canavan Disease
Cystathionine Beta-Synthase Deficiency
Dihydropyrimidine Dehydrogenase Deficiency (DHPD)
Gamma-Glutamyltransferase Deficiency
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
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
Glutathione Synthetase 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
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)
Methylmalonate Semialdehyde Dehydrogenase Deficiency
Citalopram Action Pathway
Azathioprine Action Pathway
Mercaptopurine Action Pathway
Disulfiram Action Pathway
Thioguanine Action Pathway
Nicotine Action Pathway
Cyclophosphamide Action Pathway
Ifosfamide Action Pathway
Ethanol Degradation
Degradation of Superoxides
Plasmalogen Synthesis
Dimethylglycine Dehydrogenase Deficiency
Hyperglycinemia, non-ketotic
Ureidopropionase Deficiency
Carnosinuria, carnosinemia
Tyrosinemia, transient, of the newborn
Dopamine beta-hydroxylase deficiency
5-oxoprolinase deficiency
Gamma-glutamyl-transpeptidase deficiency
Hypophosphatasia
Creatine deficiency, guanidinoacetate methyltransferase deficiency
Hyperornithinemia with gyrate atrophy (HOGA)
Hyperornithinemia-hyperammonemia-homocitrullinuria [HHH-syndrome]
L-arginine:glycine amidinotransferase deficiency
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
Homocystinuria-megaloblastic anemia due to defect in cobalamin metabolism, cblG complementation type
Pyridoxine dependency with seizures
Ibuprofen Metabolism Pathway
Cyclophosphamide Metabolism Pathway
Ifosfamide Metabolism Pathway
Clopidogrel Metabolism Pathway
Citalopram Metabolism Pathway
Nicotine Metabolism Pathway
Nevirapine Metabolism Pathway
Sorafenib Metabolism Pathway
Lamivudine Metabolism Pathway
Thyroid hormone synthesis
2-aminoadipic 2-oxoadipic aciduria
3-Phosphoglycerate dehydrogenase deficiency
StateNot Available
Water SolubilityNot Available
logP-0.45
logSNot Available
pKa (Strongest Acidic)11.52
pKa (Strongest Basic)-4.19
Hydrogen Acceptor Count2
Hydrogen Donor Count2
Polar Surface Area40.46 Ų
Rotatable Bond Count0
Physiological Charge0
Formal Charge0
Refractivity5.13 m³·mol⁻¹
Polarizability2.29

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