Diacetyl
Relevant Data
Food Additives Approved in the United States:
Food Additives Approved by WHO:
General Information
| Chemical name | Diacetyl |
| CAS number | 431-03-8 |
| COE number | 752 |
| JECFA number | 408 |
| Flavouring type | substances |
| FL No. | 07.052 |
| Mixture | No |
| Purity of the named substance at least 95% unless otherwise specified | |
| Reference body | JECFA |
From webgate.ec.europa.eu
Computed Descriptors
Download SDF| 2D Structure | |
| CID | 650 |
| IUPAC Name | butane-2,3-dione |
| InChI | InChI=1S/C4H6O2/c1-3(5)4(2)6/h1-2H3 |
| InChI Key | QSJXEFYPDANLFS-UHFFFAOYSA-N |
| Canonical SMILES | CC(=O)C(=O)C |
| Molecular Formula | CH3COCOCH3 |
| Wikipedia | butane-2,3-dione |
From Pubchem
Computed Properties
| Property Name | Property Value |
|---|---|
| Molecular Weight | 86.09 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 1 |
| Complexity | 71.5 |
| CACTVS Substructure Key Fingerprint | A A A D c Y B g M 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 E 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 Area | 34.1 |
| Monoisotopic Mass | 86.037 |
| Exact Mass | 86.037 |
| Compound Is Canonicalized | True |
| Formal Charge | 0 |
| Heavy Atom Count | 6 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Isotope Atom Count | 0 |
| Covalently-Bonded Unit Count | 1 |
From Pubchem
Food Additives Biosynthesis/Degradation
ADMET Predicted Profile --- Classification
| Model | Result | Probability |
|---|---|---|
| Absorption | ||
| Blood-Brain Barrier | BBB+ | 0.9813 |
| Human Intestinal Absorption | HIA+ | 0.9922 |
| Caco-2 Permeability | Caco2+ | 0.6125 |
| P-glycoprotein Substrate | Non-substrate | 0.8244 |
| P-glycoprotein Inhibitor | Non-inhibitor | 0.8348 |
| Non-inhibitor | 0.8863 | |
| Renal Organic Cation Transporter | Non-inhibitor | 0.9307 |
| Distribution | ||
| Subcellular localization | Mitochondria | 0.7560 |
| Metabolism | ||
| CYP450 2C9 Substrate | Non-substrate | 0.8512 |
| CYP450 2D6 Substrate | Non-substrate | 0.9116 |
| CYP450 3A4 Substrate | Non-substrate | 0.7288 |
| CYP450 1A2 Inhibitor | Non-inhibitor | 0.9046 |
| CYP450 2C9 Inhibitor | Non-inhibitor | 0.9376 |
| CYP450 2D6 Inhibitor | Non-inhibitor | 0.9437 |
| CYP450 2C19 Inhibitor | Non-inhibitor | 0.9294 |
| CYP450 3A4 Inhibitor | Non-inhibitor | 0.9728 |
| CYP Inhibitory Promiscuity | Low CYP Inhibitory Promiscuity | 0.9484 |
| Excretion | ||
| Toxicity | ||
| Human Ether-a-go-go-Related Gene Inhibition | Weak inhibitor | 0.9727 |
| Non-inhibitor | 0.9653 | |
| AMES Toxicity | AMES toxic | 0.5873 |
| Carcinogens | Carcinogens | 0.6451 |
| Fish Toxicity | Low FHMT | 0.8654 |
| Tetrahymena Pyriformis Toxicity | High TPT | 0.6543 |
| Honey Bee Toxicity | High HBT | 0.7305 |
| Biodegradation | Ready biodegradable | 0.9040 |
| Acute Oral Toxicity | III | 0.8776 |
| Carcinogenicity (Three-class) | Non-required | 0.7465 |
From admetSAR
ADMET Predicted Profile --- Regression
| Model | Value | Unit |
|---|---|---|
| Absorption | ||
| Aqueous solubility | 0.6035 | LogS |
| Caco-2 Permeability | 1.2439 | LogPapp, cm/s |
| Distribution | ||
| Metabolism | ||
| Excretion | ||
| Toxicity | ||
| Rat Acute Toxicity | 1.7047 | LD50, mol/kg |
| Fish Toxicity | 2.9210 | pLC50, mg/L |
| Tetrahymena Pyriformis Toxicity | -0.2977 | pIGC50, ug/L |
From admetSAR
Toxicity Profile
| Route of Exposure | Oral ; inhalation ; dermal ; eye contact |
|---|---|
| Mechanism of Toxicity | Diacetyl is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen. |
| Metabolism | Diacetyl is reduced to 2,3-butanediol . |
| Toxicity Values | LD50: 1580 mg/kg (Oral, Rat) LD50: >5 gm/kg (Dermal, Rabbit) |
| Lethal Dose | |
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity (not listed by IARC). |
| Minimum Risk Level | |
| Health Effects | Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides. |
| Treatment | If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally. |
| Reference |
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From T3DB
Taxonomic Classification
| Kingdom | Organic compounds |
|---|---|
| Superclass | Organic oxygen compounds |
| Class | Organooxygen compounds |
| Subclass | Carbonyl compounds |
| Intermediate Tree Nodes | Ketones |
| Direct Parent | Alpha-diketones |
| Alternative Parents | |
| Molecular Framework | Aliphatic acyclic compounds |
| Substituents | Alpha-diketone - Organic oxide - Hydrocarbon derivative - Aliphatic acyclic compound |
| Description | This compound belongs to the class of organic compounds known as alpha-diketones. These are organic compounds containing two ketone groups on two adjacent carbon atoms. |
From ClassyFire
Targets
- General Function:
- Serine hydrolase activity
- Specific Function:
- Terminates signal transduction at the neuromuscular junction by rapid hydrolysis of the acetylcholine released into the synaptic cleft. Role in neuronal apoptosis.
- Gene Name:
- ACHE
- Uniprot ID:
- P22303
- Molecular Weight:
- 67795.525 Da
References
- Parkinson EI, Jason Hatfield M, Tsurkan L, Hyatt JL, Edwards CC, Hicks LD, Yan B, Potter PM: Requirements for mammalian carboxylesterase inhibition by substituted ethane-1,2-diones. Bioorg Med Chem. 2011 Aug 1;19(15):4635-43. doi: 10.1016/j.bmc.2011.06.012. Epub 2011 Jul 4. [21733699 ]
- General Function:
- Methylumbelliferyl-acetate deacetylase activity
- Specific Function:
- Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Shows high catalytic efficiency for hydrolysis of cocaine, 4-methylumbelliferyl acetate, heroin and 6-monoacetylmorphine.
- Gene Name:
- CES2
- Uniprot ID:
- O00748
- Molecular Weight:
- 61806.41 Da
References
- Parkinson EI, Jason Hatfield M, Tsurkan L, Hyatt JL, Edwards CC, Hicks LD, Yan B, Potter PM: Requirements for mammalian carboxylesterase inhibition by substituted ethane-1,2-diones. Bioorg Med Chem. 2011 Aug 1;19(15):4635-43. doi: 10.1016/j.bmc.2011.06.012. Epub 2011 Jul 4. [21733699 ]
- General Function:
- Triglyceride lipase activity
- Specific Function:
- Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Hydrolyzes aromatic and aliphatic esters, but has no catalytic activity toward amides or a fatty acyl-CoA ester. Hydrolyzes the methyl ester group of cocaine to form benzoylecgonine. Catalyzes the transesterification of cocaine to form cocaethylene. Displays fatty acid ethyl ester synthase activity, catalyzing the ethyl esterification of oleic acid to ethyloleate.
- Gene Name:
- CES1
- Uniprot ID:
- P23141
- Molecular Weight:
- 62520.62 Da
References
- Parkinson EI, Jason Hatfield M, Tsurkan L, Hyatt JL, Edwards CC, Hicks LD, Yan B, Potter PM: Requirements for mammalian carboxylesterase inhibition by substituted ethane-1,2-diones. Bioorg Med Chem. 2011 Aug 1;19(15):4635-43. doi: 10.1016/j.bmc.2011.06.012. Epub 2011 Jul 4. [21733699 ]
- 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
- 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