Propionic acid
Relevant Data
Food Additives Approved in the United States:
Food Additives Approved by WHO:
General Information
Chemical name | Propionic acid |
CAS number | 79-09-4 |
COE number | 3 |
JECFA number | 84 |
Flavouring type | substances |
FL No. | 08.003 |
Mixture | No |
Purity of the named substance at least 95% unless otherwise specified | |
Reference body | JECFA |
From webgate.ec.europa.eu
Computed Descriptors
Download SDF2D Structure | |
CID | 1032 |
IUPAC Name | propanoic acid |
InChI | InChI=1S/C3H6O2/c1-2-3(4)5/h2H2,1H3,(H,4,5) |
InChI Key | XBDQKXXYIPTUBI-UHFFFAOYSA-N |
Canonical SMILES | CCC(=O)O |
Molecular Formula | C3H6O2 |
Wikipedia | propionate |
From Pubchem
Computed Properties
Property Name | Property Value |
---|---|
Molecular Weight | 74.079 |
Hydrogen Bond Donor Count | 1 |
Hydrogen Bond Acceptor Count | 2 |
Rotatable Bond Count | 1 |
Complexity | 40.2 |
CACTVS Substructure Key Fingerprint | A A A D c Y B A 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 C A A A C A C A g A A C C A A A A g A I A A C Q C 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 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 = = |
Topological Polar Surface Area | 37.3 |
Monoisotopic Mass | 74.037 |
Exact Mass | 74.037 |
Compound Is Canonicalized | True |
Formal Charge | 0 |
Heavy Atom Count | 5 |
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+ | 0.9410 |
Human Intestinal Absorption | HIA+ | 0.9893 |
Caco-2 Permeability | Caco2+ | 0.6324 |
P-glycoprotein Substrate | Non-substrate | 0.7959 |
P-glycoprotein Inhibitor | Non-inhibitor | 0.9671 |
Non-inhibitor | 0.9909 | |
Renal Organic Cation Transporter | Non-inhibitor | 0.9624 |
Distribution | ||
Subcellular localization | Mitochondria | 0.5849 |
Metabolism | ||
CYP450 2C9 Substrate | Non-substrate | 0.7880 |
CYP450 2D6 Substrate | Non-substrate | 0.9394 |
CYP450 3A4 Substrate | Non-substrate | 0.8006 |
CYP450 1A2 Inhibitor | Non-inhibitor | 0.8922 |
CYP450 2C9 Inhibitor | Non-inhibitor | 0.9639 |
CYP450 2D6 Inhibitor | Non-inhibitor | 0.9667 |
CYP450 2C19 Inhibitor | Non-inhibitor | 0.9794 |
CYP450 3A4 Inhibitor | Non-inhibitor | 0.9763 |
CYP Inhibitory Promiscuity | Low CYP Inhibitory Promiscuity | 0.9876 |
Excretion | ||
Toxicity | ||
Human Ether-a-go-go-Related Gene Inhibition | Weak inhibitor | 0.9681 |
Non-inhibitor | 0.9778 | |
AMES Toxicity | Non AMES toxic | 0.9401 |
Carcinogens | Carcinogens | 0.6548 |
Fish Toxicity | Low FHMT | 0.5937 |
Tetrahymena Pyriformis Toxicity | Low TPT | 0.8365 |
Honey Bee Toxicity | High HBT | 0.7513 |
Biodegradation | Ready biodegradable | 0.9079 |
Acute Oral Toxicity | III | 0.9124 |
Carcinogenicity (Three-class) | Non-required | 0.7073 |
From admetSAR
ADMET Predicted Profile --- Regression
Model | Value | Unit |
---|---|---|
Absorption | ||
Aqueous solubility | 0.6067 | LogS |
Caco-2 Permeability | 1.1352 | LogPapp, cm/s |
Distribution | ||
Metabolism | ||
Excretion | ||
Toxicity | ||
Rat Acute Toxicity | 1.4864 | LD50, mol/kg |
Fish Toxicity | 3.5551 | pLC50, mg/L |
Tetrahymena Pyriformis Toxicity | -0.6348 | pIGC50, ug/L |
From admetSAR
Toxicity Profile
Route of Exposure | |
---|---|
Mechanism of Toxicity | In healthy individuals, the enzyme propionyl CoA carboxylase converts propionyl CoA to methylmalonyl CoA. This is one step in the process of converting certain amino acids and fats into sugar for energy. Individuals with propionic acidemia cannot perform this conversion because the enzyme propionyl CoA carboxylase is nonfunctional. The essential amino acids; isoleucine, valine, threonine, and methionine and odd-chain fatty acids are simply converted to propionyl CoA, before the process stops, leading to a buildup of propionyl CoA. Instead of being converted to methylmalonyl CoA, propionyl CoA is then converted into propionic acid, which builds up in the bloodstream. Propionyl-CoA, propionic acid, ketones, ammonia, and other toxic compounds accumulate in the blood, causing the signs and symptoms of propionic acidemia. Propionate acts as a metabolic toxin in liver cells by accumulating in mitochondria. Propanoate is metabolized oxidatively by glia, which suggests astrocytic vulnerability in propanoic acidemia when intramitochondrial propionyl-CoA may accumulate. Propanoic acidemia may alter both neuronal and glial gene expression by affecting histone acetylation . (Wikipedia) |
Metabolism | The metabolism of propanoic acid begins with its conversion to propionyl coenzyme A (propionyl-CoA), the usual first step in the metabolism of carboxylic acids. Since propanoic acid has three carbons, propionyl-CoA cannot directly enter either beta oxidation or the citric acid cycles. In most vertebrates, propionyl-CoA is carboxylated to D-methylmalonyl-CoA, which is isomerised to L-methylmalonyl-CoA. A vitamin B12-dependent enzyme catalyzes rearrangement of L-methylmalonyl-CoA to succinyl-CoA, which is an intermediate of the citric acid cycle and can be readily incorporated there. (Wikipedia) |
Toxicity Values | |
Lethal Dose | |
Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). |
Minimum Risk Level | |
Health Effects | Propionic acid occurs in chronically high levels in propionic acidemia. Propionic acidemia, also known as propionic aciduria, propionyl-CoA carboxylase deficiency and ketotic glycinemia, is an autosomal recessive metabolic disorder, classified as a branched-chain organic acidemia. The disorder presents in the early neonatal period with progressive encephalopathy. Death can occur quickly, due to secondary hyperammonemia, infection, cardiomyopathy, or basal ganglial stroke. In many cases, propionic acidemia can damage the brain, heart, and liver, cause seizures, and delays to normal development like walking and talking. (Wikipedia) |
Treatment | During times of illness the affected person may need to be hospitalized to prevent breakdown of proteins within the body. Each meal presents a challenge to those with propionic acidemia. If not constantly monitored, the effects would be devastating. Dietary needs must be closely managed by a metabolic geneticist or metabolic dietician. Patients with propionic acidemia should be started as early as possible on a low protein diet. In addition to a protein mixture that is devoid of methionine, threonine, valine, and isoleucine, the patient should also receive L-carnitine treatment and should be given antibiotics 10 days per month in order to remove the intestinal propiogenic flora. The patient should have diet protocols prepared for him with a “well day diet” with low protein content, a “half emergency diet” containing half of the protein requirements, and an “emergency diet” with no protein content. These patients are under the risk of severe hyperammonemia during infections that can lead to comatose states. Liver transplant is gaining a role in the management of these patients, with small series showing improved quality of life. (Wikipedia) |
Reference |
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From T3DB
Taxonomic Classification
Kingdom | Organic compounds |
---|---|
Superclass | Organic acids and derivatives |
Class | Carboxylic acids and derivatives |
Subclass | Carboxylic acids |
Intermediate Tree Nodes | Not available |
Direct Parent | Carboxylic acids |
Alternative Parents | |
Molecular Framework | Aliphatic acyclic compounds |
Substituents | Monocarboxylic acid or derivatives - Carboxylic acid - Organic oxygen compound - Organic oxide - Hydrocarbon derivative - Organooxygen compound - Carbonyl group - Aliphatic acyclic compound |
Description | This compound belongs to the class of organic compounds known as carboxylic acids. These are compounds containing a carboxylic acid group with the formula -C(=O)OH. |
From ClassyFire
Targets
- General Function:
- Molybdopterin molybdotransferase activity
- Specific Function:
- Microtubule-associated protein involved in membrane protein-cytoskeleton interactions. It is thought to anchor the inhibitory glycine receptor (GLYR) to subsynaptic microtubules (By similarity). Catalyzes two steps in the biosynthesis of the molybdenum cofactor. In the first step, molybdopterin is adenylated. Subsequently, molybdate is inserted into adenylated molybdopterin and AMP is released.
- Gene Name:
- GPHN
- Uniprot ID:
- Q9NQX3
- Molecular Weight:
- 79747.635 Da
References
- Berman HM, Westbrook J, Feng Z, Gilliland G, Bhat TN, Weissig H, Shindyalov IN, Bourne PE: The Protein Data Bank. Nucleic Acids Res. 2000 Jan 1;28(1):235-42. [10592235 ]
- General Function:
- Lipid binding
- Specific Function:
- G protein-coupled receptor that is activated by a major product of dietary fiber digestion, the short chain fatty acids (SCFAs), and that plays a role in the regulation of whole-body energy homeostasis and in intestinal immunity. In omnivorous mammals, the short chain fatty acids acetate, propionate and butyrate are produced primarily by the gut microbiome that metabolizes dietary fibers. SCFAs serve as a source of energy but also act as signaling molecules. That G protein-coupled receptor is probably coupled to the pertussis toxin-sensitive, G(i/o)-alpha family of G proteins but also to the Gq family (PubMed:12496283, PubMed:12711604, PubMed:23589301). Its activation results in the formation of inositol 1,4,5-trisphosphate, the mobilization of intracellular calcium, the phosphorylation of the MAPK3/ERK1 and MAPK1/ERK2 kinases and the inhibition of intracellular cAMP accumulation. May play a role in glucose homeostasis by regulating the secretion of GLP-1, in response to short-chain fatty acids accumulating in the intestine. May also regulate the production of LEP/Leptin, a hormone acting on the central nervous system to inhibit food intake. Finally, may also regulate whole-body energy homeostasis through adipogenesis regulating both differentiation and lipid storage of adipocytes. In parallel to its role in energy homeostasis, may also mediate the activation of the inflammatory and immune responses by SCFA in the intestine, regulating the rapid production of chemokines and cytokines. May also play a role in the resolution of the inflammatory response and control chemotaxis in neutrophils. In addition to SCFAs, may also be activated by the extracellular lectin FCN1 in a process leading to activation of monocytes and inducing the secretion of interleukin-8/IL-8 in response to the presence of microbes (PubMed:21037097). Among SCFAs, the fatty acids containing less than 6 carbons, the most potent activators are probably acetate, propionate and butyrate (PubMed:12496283, PubMed:12711604). Exhibits a SCFA-independent constitutive G protein-coupled receptor activity (PubMed:23066016).
- Gene Name:
- FFAR2
- Uniprot ID:
- O15552
- Molecular Weight:
- 37143.375 Da
References
- Wang Y, Jiao X, Kayser F, Liu J, Wang Z, Wanska M, Greenberg J, Weiszmann J, Ge H, Tian H, Wong S, Schwandner R, Lee T, Li Y: The first synthetic agonists of FFA2: Discovery and SAR of phenylacetamides as allosteric modulators. Bioorg Med Chem Lett. 2010 Jan 15;20(2):493-8. doi: 10.1016/j.bmcl.2009.11.112. Epub 2009 Nov 26. [20005104 ]
- General Function:
- Chloride peroxidase activity
- Gene Name:
- cpo
- Uniprot ID:
- O31158
- Molecular Weight:
- 29651.125 Da
- General Function:
- Hydrolase activity
- Gene Name:
- cumD
- Uniprot ID:
- P96965
- Molecular Weight:
- 31489.385 Da
- General Function:
- Pyridoxal phosphate binding
- Specific Function:
- Catalyzes the interconversion of L-alanine and D-alanine. Also weakly active on serine.
- Gene Name:
- alr
- Uniprot ID:
- P10724
- Molecular Weight:
- 43592.715 Da
From T3DB