M-CRESOL
Relevant Data
Food Additives Approved by WHO:
Flavouring Substances Approved by European Union:
General Information
| Mainterm | M-CRESOL |
| Doc Type | ASP |
| CAS Reg.No.(or other ID) | 108-39-4 |
| Regnum |
175.300 177.2410 |
From www.fda.gov
Computed Descriptors
Download SDF| 2D Structure | |
| CID | 342 |
| IUPAC Name | 3-methylphenol |
| InChI | InChI=1S/C7H8O/c1-6-3-2-4-7(8)5-6/h2-5,8H,1H3 |
| InChI Key | RLSSMJSEOOYNOY-UHFFFAOYSA-N |
| Canonical SMILES | CC1=CC(=CC=C1)O |
| Molecular Formula | C7H8O |
| Wikipedia | metacresol |
From Pubchem
Computed Properties
| Property Name | Property Value |
|---|---|
| Molecular Weight | 108.14 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Complexity | 70.8 |
| CACTVS Substructure Key Fingerprint | A A A D c c B g 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 w A A A A A A A A A A A B A A A A G g A A C A A A D A S A m A A y B o A A A g C A A i B C A A A C A A A g I A A I i A A G C I g I J i K C E R K A c A A k w B E I m A e A w B A O A A A B A A A A A A A A A A I A A A A A A A A A A A A A A A = = |
| Topological Polar Surface Area | 20.2 |
| Monoisotopic Mass | 108.058 |
| Exact Mass | 108.058 |
| Compound Is Canonicalized | True |
| Formal Charge | 0 |
| Heavy Atom Count | 8 |
| 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+ | 0.8911 |
| Human Intestinal Absorption | HIA+ | 0.9960 |
| Caco-2 Permeability | Caco2+ | 0.9256 |
| P-glycoprotein Substrate | Non-substrate | 0.7504 |
| P-glycoprotein Inhibitor | Non-inhibitor | 0.9753 |
| Non-inhibitor | 0.9910 | |
| Renal Organic Cation Transporter | Non-inhibitor | 0.8770 |
| Distribution | ||
| Subcellular localization | Mitochondria | 0.7469 |
| Metabolism | ||
| CYP450 2C9 Substrate | Non-substrate | 0.7251 |
| CYP450 2D6 Substrate | Non-substrate | 0.8554 |
| CYP450 3A4 Substrate | Non-substrate | 0.7152 |
| CYP450 1A2 Inhibitor | Inhibitor | 0.5105 |
| CYP450 2C9 Inhibitor | Non-inhibitor | 0.9606 |
| CYP450 2D6 Inhibitor | Non-inhibitor | 0.9789 |
| CYP450 2C19 Inhibitor | Non-inhibitor | 0.9343 |
| CYP450 3A4 Inhibitor | Non-inhibitor | 0.9324 |
| CYP Inhibitory Promiscuity | Low CYP Inhibitory Promiscuity | 0.8870 |
| Excretion | ||
| Toxicity | ||
| Human Ether-a-go-go-Related Gene Inhibition | Weak inhibitor | 0.8281 |
| Non-inhibitor | 0.9609 | |
| AMES Toxicity | Non AMES toxic | 0.9513 |
| Carcinogens | Non-carcinogens | 0.7350 |
| Fish Toxicity | High FHMT | 0.6839 |
| Tetrahymena Pyriformis Toxicity | High TPT | 0.9286 |
| Honey Bee Toxicity | High HBT | 0.8261 |
| Biodegradation | Ready biodegradable | 0.6121 |
| Acute Oral Toxicity | II | 0.7716 |
| Carcinogenicity (Three-class) | Non-required | 0.6111 |
From admetSAR
ADMET Predicted Profile --- Regression
| Model | Value | Unit |
|---|---|---|
| Absorption | ||
| Aqueous solubility | -0.6374 | LogS |
| Caco-2 Permeability | 1.6148 | LogPapp, cm/s |
| Distribution | ||
| Metabolism | ||
| Excretion | ||
| Toxicity | ||
| Rat Acute Toxicity | 2.5863 | LD50, mol/kg |
| Fish Toxicity | 1.3626 | pLC50, mg/L |
| Tetrahymena Pyriformis Toxicity | -0.2094 | pIGC50, ug/L |
From admetSAR
Toxicity Profile
| Route of Exposure | Oral ; inhalation ; dermal |
|---|---|
| Mechanism of Toxicity | m-Cresol 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 | Cresols can be absorbed following inhalation, oral, and dermal exposure. Once in the body they can distribute rapidly into many organs and tissues. Cresols undergo oxidative metabolism in the liver and are rapidly eliminated, mostly in the urine, as sulfate or glucuronide conjugates. The activation of cresols by oxidation involves tyrosinase and thyroid peroxidase, forming a reactive quinone methide. Experiments with recombinant P-450s demonstrated cresol metabolism was mediated by several P-450s including CYP2D6, 2C19, 1A2, 1A1, and 2E1. |
| Toxicity Values | LD50: 242 mg/kg (Oral, Rat) LD50: 168 mg/kg (Intraperitoneal, Mouse) LD50: 2050 mg/kg (Dermal, Rabbit) |
| Lethal Dose | None |
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). |
| Minimum Risk Level | Intermediate Oral: 0.1 mg/kg/day Chronic Oral: 0.1 mg/kg/day |
| 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 |
|
From T3DB
Taxonomic Classification
| Kingdom | Organic compounds |
|---|---|
| Superclass | Benzenoids |
| Class | Phenols |
| Subclass | Cresols |
| Intermediate Tree Nodes | Not available |
| Direct Parent | Meta cresols |
| Alternative Parents | |
| Molecular Framework | Aromatic homomonocyclic compounds |
| Substituents | M-cresol - 1-hydroxy-4-unsubstituted benzenoid - 1-hydroxy-2-unsubstituted benzenoid - Toluene - Monocyclic benzene moiety - Organic oxygen compound - Hydrocarbon derivative - Organooxygen compound - Aromatic homomonocyclic compound |
| Description | This compound belongs to the class of organic compounds known as meta cresols. These are aromatic compounds containing a meta-cresol moiety, which consists of a benzene ring bearing a methyl group and a hydroxyl group at ring positions 1 and 3, respectively. |
From ClassyFire
Targets
- General Function:
- Protease binding
- Specific Function:
- Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
- Gene Name:
- INS
- Uniprot ID:
- P01308
- Molecular Weight:
- 11980.795 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:
- 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
- Cardozo MG, Iimura Y, Sugimoto H, Yamanishi Y, Hopfinger AJ: QSAR analyses of the substituted indanone and benzylpiperidine rings of a series of indanone-benzylpiperidine inhibitors of acetylcholinesterase. J Med Chem. 1992 Feb 7;35(3):584-9. [1738151 ]
- General Function:
- Prostaglandin-endoperoxide synthase activity
- Specific Function:
- Converts arachidonate to prostaglandin H2 (PGH2), a committed step in prostanoid synthesis. Involved in the constitutive production of prostanoids in particular in the stomach and platelets. In gastric epithelial cells, it is a key step in the generation of prostaglandins, such as prostaglandin E2 (PGE2), which plays an important role in cytoprotection. In platelets, it is involved in the generation of thromboxane A2 (TXA2), which promotes platelet activation and aggregation, vasoconstriction and proliferation of vascular smooth muscle cells.
- Gene Name:
- PTGS1
- Uniprot ID:
- P23219
- Molecular Weight:
- 68685.82 Da
References
- Chan CP, Yuan-Soon H, Wang YJ, Lan WH, Chen LI, Chen YJ, Lin BR, Chang MC, Jeng JH: Inhibition of cyclooxygenase activity, platelet aggregation and thromboxane B2 production by two environmental toxicants: m- and o-cresol. Toxicology. 2005 Mar 1;208(1):95-104. [15664436 ]
- General Function:
- Prostaglandin-endoperoxide synthase activity
- Specific Function:
- Converts arachidonate to prostaglandin H2 (PGH2), a committed step in prostanoid synthesis. Constitutively expressed in some tissues in physiological conditions, such as the endothelium, kidney and brain, and in pathological conditions, such as in cancer. PTGS2 is responsible for production of inflammatory prostaglandins. Up-regulation of PTGS2 is also associated with increased cell adhesion, phenotypic changes, resistance to apoptosis and tumor angiogenesis. In cancer cells, PTGS2 is a key step in the production of prostaglandin E2 (PGE2), which plays important roles in modulating motility, proliferation and resistance to apoptosis.
- Gene Name:
- PTGS2
- Uniprot ID:
- P35354
- Molecular Weight:
- 68995.625 Da
References
- Chan CP, Yuan-Soon H, Wang YJ, Lan WH, Chen LI, Chen YJ, Lin BR, Chang MC, Jeng JH: Inhibition of cyclooxygenase activity, platelet aggregation and thromboxane B2 production by two environmental toxicants: m- and o-cresol. Toxicology. 2005 Mar 1;208(1):95-104. [15664436 ]
- 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