ACETONE

Relevant Data

Food Additives Approved by WHO:

Flavouring Substances Approved by European Union:

  • Acetone [show]

General Information

MaintermACETONE
Doc TypeASP
CAS Reg.No.(or other ID)67-64-1
Regnum 175.105
175.320
176.180
177.2600
176.300
73.30
173.210
73.1
73.345
73.615

From www.fda.gov

Computed Descriptors

Download SDF
2D Structure
CID180
IUPAC Namepropan-2-one
InChIInChI=1S/C3H6O/c1-3(2)4/h1-2H3
InChI KeyCSCPPACGZOOCGX-UHFFFAOYSA-N
Canonical SMILESCC(=O)C
Molecular FormulaC3H6O
Wikipediaacetone

From Pubchem

Computed Properties

Property Name Property Value
Molecular Weight58.08
Hydrogen Bond Donor Count0
Hydrogen Bond Acceptor Count1
Rotatable Bond Count0
Complexity26.3
CACTVS Substructure Key Fingerprint A A A D c Y B A I A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A G g A A A A A A C A S A g A A C A A A A A A A I A I A Q A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A = =
Topological Polar Surface Area17.1
Monoisotopic Mass58.042
Exact Mass58.042
XLogP3None
XLogP3-AA-0.1
Compound Is CanonicalizedTrue
Formal Charge0
Heavy Atom Count4
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Isotope Atom Count0
Covalently-Bonded Unit Count1

From Pubchem

Food Additives Biosynthesis/Degradation

ADMET Predicted Profile --- Classification

Model Result Probability
Absorption
Blood-Brain BarrierBBB+0.9818
Human Intestinal AbsorptionHIA+0.9959
Caco-2 PermeabilityCaco2+0.7526
P-glycoprotein SubstrateNon-substrate0.8012
P-glycoprotein InhibitorNon-inhibitor0.9272
Non-inhibitor0.9680
Renal Organic Cation TransporterNon-inhibitor0.9194
Distribution
Subcellular localizationMitochondria0.6207
Metabolism
CYP450 2C9 SubstrateNon-substrate0.8279
CYP450 2D6 SubstrateNon-substrate0.9116
CYP450 3A4 SubstrateNon-substrate0.7043
CYP450 1A2 InhibitorNon-inhibitor0.8238
CYP450 2C9 InhibitorNon-inhibitor0.9596
CYP450 2D6 InhibitorNon-inhibitor0.9614
CYP450 2C19 InhibitorNon-inhibitor0.9477
CYP450 3A4 InhibitorNon-inhibitor0.9847
CYP Inhibitory PromiscuityLow CYP Inhibitory Promiscuity0.9238
Excretion
Toxicity
Human Ether-a-go-go-Related Gene InhibitionWeak inhibitor0.9655
Non-inhibitor0.9569
AMES ToxicityNon AMES toxic0.9133
CarcinogensCarcinogens 0.7115
Fish ToxicityLow FHMT0.6453
Tetrahymena Pyriformis ToxicityLow TPT0.7916
Honey Bee ToxicityHigh HBT0.8176
BiodegradationReady biodegradable0.8501
Acute Oral ToxicityIII0.6238
Carcinogenicity (Three-class)Non-required0.7274

From admetSAR

ADMET Predicted Profile --- Regression

Model Value Unit
Absorption
Aqueous solubility0.1920LogS
Caco-2 Permeability1.5329LogPapp, cm/s
Distribution
Metabolism
Excretion
Toxicity
Rat Acute Toxicity1.5293LD50, mol/kg
Fish Toxicity3.2181pLC50, mg/L
Tetrahymena Pyriformis Toxicity-1.2451pIGC50, ug/L

From admetSAR

Toxicity Profile

Route of ExposureInhalation ; oral ; dermal ; eye contact
Mechanism of ToxicitySince acetone is highly water soluble, it is readily taken up by the blood and widely distributed to body tissues. Acetone may interfere with the composition of the membranes, altering their permeability to ions. Systemically, acetone is moderately toxic to the liver and produces hematological effects. The renal toxicity may be due to the metabolite, formate, which is known to be nephrotoxic and is excreted by the kidneys. One of the major effects of acetone is the potentiation of the toxicity of other chemicals. Pretreatment with acetone has been shown to potentiate the hepatotoxicity and nephrotoxicity of carbon tetrachloride and chloroform by inducing particular forms of cytochrome P-450, especially cytochrome P-45OIIE1, and associated enzyme activities.
MetabolismThe metabolic fate of acetone is independent of route of administration and involves three separate gluconeogenic pathways, with ultimate incorporation of carbon atoms into glucose and other products and substrates of intermediary metabolism with generation of carbon dioxide. The primary (major) pathway involves hepatic metabolism of acetone to acetol and hepatic metabolism of acetol to methylglyoxal, while two secondary (minor) pathways are partially extrahepatic, involving the extrahepatic reduction of acetol to L-1,2-propanediol. Subsequent conversion of acetol to methylglyoxal in microsomes is catalyzed by acetol monooxygenase (also called acetol hydroxylase), an activity also associated with cytochrome P-450IIE1, and also requires oxygen and NADPH. Methylglyoxal can then be converted to D-glucose by an unidentified pathway, and/or possibly by catalysis by glyoxalase I and II and glutathione to D-lactate, which is converted to D-glucose. Some of exogenous acetone is unmetabolized and is excreted primarily in the expired air with little acetone excreted in urine.
Toxicity ValuesLD50: 2400 mg/kg/day (Oral, Mouse)
Lethal DoseNone
Carcinogenicity (IARC Classification)No indication of carcinogenicity (not listed by IARC).
Minimum Risk LevelAcute Inhalation: 26 ppm Intermediate Inhalation: 13 ppm Chronic Inhalation: 13 ppm
Health EffectsPulmonary congestion and edema can follow inhalation of acetone, which irritates the mucosa. Gastrointestinal hemorrhage caused by repeated vomiting of blood has been reported. Neurobehavioral effects, indicative of narcosis, sedation, respiratory depression, ataxia, paresthesia and renal lesions can also result from acetone poisoning. (N004, A578)
TreatmentFollowing oral exposure to acetone, consider insertion of a nasogastric tube to aspirate stomach contents only after recent, large acetone ingestions; symptomatic and supportive treatment is generally all that is required. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes in case of eye exposure to acetone. In case of dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists.
Reference
  1. Iuliano L, Micheletta F, Maranghi M, Frati G, Diczfalusy U, Violi F: Bioavailability of vitamin E as function of food intake in healthy subjects: effects on plasma peroxide-scavenging activity and cholesterol-oxidation products. Arterioscler Thromb Vasc Biol. 2001 Oct;21(10):E34-7.[11597949 ]
  2. Subramanian A, Gupta A, Saxena S, Gupta A, Kumar R, Nigam A, Kumar R, Mandal SK, Roy R: Proton MR CSF analysis and a new software as predictors for the differentiation of meningitis in children. NMR Biomed. 2005 Jun;18(4):213-25.[15627241 ]
  3. Bairaktari E, Katopodis K, Siamopoulos KC, Tsolas O: Paraquat-induced renal injury studied by 1H nuclear magnetic resonance spectroscopy of urine. Clin Chem. 1998 Jun;44(6 Pt 1):1256-61.[9625050 ]
  4. Bales JR, Higham DP, Howe I, Nicholson JK, Sadler PJ: Use of high-resolution proton nuclear magnetic resonance spectroscopy for rapid multi-component analysis of urine. Clin Chem. 1984 Mar;30(3):426-32.[6321058 ]
  5. Kalapos MP: Possible physiological roles of acetone metabolism in humans. Med Hypotheses. 1999 Sep;53(3):236-42.[10580530 ]
  6. Robinson RC, Shorr RG, Varrichio A, Park SS, Gelboin HV, Miller H, Friedman FK: Human liver cytochrome P-450 related to a rat acetone-inducible, nitrosamine-metabolizing cytochrome P-450: identification and isolation. Pharmacology. 1989;39(3):137-44.[2587619 ]
  7. Yamane N, Tsuda T, Nose K, Yamamoto A, Ishiguro H, Kondo T: Relationship between skin acetone and blood beta-hydroxybutyrate concentrations in diabetes. Clin Chim Acta. 2006 Mar;365(1-2):325-9. Epub 2005 Oct 11.[16223475 ]
  8. Palamanda J, Feng WW, Lin CC, Nomeir AA: Stimulation of tolbutamide hydroxylation by acetone and acetonitrile in human liver microsomes and in a cytochrome P-450 2C9-reconstituted system. Drug Metab Dispos. 2000 Jan;28(1):38-43.[10611138 ]
  9. Crawley SC, Hindsgaul O, Alton G, Pierce M, Palcic MM: An enzyme-linked immunosorbent assay for N-acetylglucosaminyltransferase-V. Anal Biochem. 1990 Feb 15;185(1):112-7.[2160776 ]
  10. Inoue S, Sato Y, Hasegawa H, Noguchi A, Yamada A, Kurata T, Iwasaki T: Cross-reactive antigenicity of nucleoproteins of lyssaviruses recognized by a monospecific antirabies virus nucleoprotein antiserum on paraffin sections of formalin-fixed tissues. Pathol Int. 2003 Aug;53(8):525-33.[12895231 ]
  11. Meiser JB, Nelson HS: Comparing conventional and acetone-precipitated dog allergen extract skin testing. J Allergy Clin Immunol. 2001 Apr;107(4):744-5.[11295672 ]
  12. Baum HP, Reichrath J, Theobald A, Schock G: Fixation requirements for the immunohistochemical reactivity of PCNA antibody PC10 on cryostat sections. Histochem J. 1994 Dec;26(12):929-33.[7896568 ]
  13. Benz J: Antidiabetic agents and lactation. J Hum Lact. 1992 Mar;8(1):27-8.[1558654 ]
  14. Benfeldt E, Serup J, Menne T: Effect of barrier perturbation on cutaneous salicylic acid penetration in human skin: in vivo pharmacokinetics using microdialysis and non-invasive quantification of barrier function. Br J Dermatol. 1999 Apr;140(4):739-48.[10233334 ]
  15. Paweska JT, Barnard BJ, Williams R: The use of sucrose-acetone-extracted Rift Valley fever virus antigen derived from cell culture in an indirect enzyme-linked immunosorbent assay and haemagglutination-inhibition test. Onderstepoort J Vet Res. 1995 Dec;62(4):227-33.[8668320 ]
  16. Wittmann S, Gilg T, Dietz HG, Grantzow R, Peschel O, von Meyer L: [Isopropanol and acetone level in serum after preoperative surface disinfection with antiseptics containing isopropanol]. Blutalkohol. 1992 Sep;29(5):326-35.[1389018 ]
  17. Bird AR, Kossew B, Mulligan TP, Jacobs P: Regional thromboplastin standardisation using a human brain extract. S Afr Med J. 1989 Jun 3;75(11):538-40.[2727843 ]

From T3DB

Taxonomic Classification

KingdomOrganic compounds
SuperclassOrganic oxygen compounds
ClassOrganooxygen compounds
SubclassCarbonyl compounds
Intermediate Tree NodesNot available
Direct ParentKetones
Alternative Parents
Molecular FrameworkAliphatic acyclic compounds
SubstituentsKetone - Organic oxide - Hydrocarbon derivative - Aliphatic acyclic compound
DescriptionThis compound belongs to the class of organic compounds known as ketones. These are organic compounds in which a carbonyl group is bonded to two carbon atoms R2C=O (neither R may be a hydrogen atom). Ketones that have one or more alpha-hydrogen atoms undergo keto-enol tautomerization, the tautomer being an enol.

From ClassyFire

Targets

Target Details

Transient receptor potential cation channel subfamily A member 1

General Function:
Temperature-gated cation channel activity
Specific Function:
Receptor-activated non-selective cation channel involved in detection of pain and possibly also in cold perception and inner ear function (PubMed:25389312, PubMed:25855297). Has a central role in the pain response to endogenous inflammatory mediators and to a diverse array of volatile irritants, such as mustard oil, cinnamaldehyde, garlic and acrolein, an irritant from tears gas and vehicule exhaust fumes (PubMed:25389312, PubMed:20547126). Is also activated by menthol (in vitro)(PubMed:25389312). Acts also as a ionotropic cannabinoid receptor by being activated by delta(9)-tetrahydrocannabinol (THC), the psychoactive component of marijuana (PubMed:25389312). May be a component for the mechanosensitive transduction channel of hair cells in inner ear, thereby participating in the perception of sounds. Probably operated by a phosphatidylinositol second messenger system (By similarity).
Gene Name:
TRPA1
Uniprot ID:
O75762
Molecular Weight:
127499.88 Da
References
  1. Nilius B, Prenen J, Owsianik G: Irritating channels: the case of TRPA1. J Physiol. 2011 Apr 1;589(Pt 7):1543-9. doi: 10.1113/jphysiol.2010.200717. Epub 2010 Nov 15. [21078588 ]

From T3DB