1,1,2-TRICHLOROETHANE
General Information
| Mainterm | 1,1,2-TRICHLOROETHANE |
| CAS Reg.No.(or other ID) | 79-00-5 |
| Regnum |
175.105 177.1650 |
From www.fda.gov
Computed Descriptors
Download SDF| 2D Structure | |
| CID | 6574 |
| IUPAC Name | 1,1,2-trichloroethane |
| InChI | InChI=1S/C2H3Cl3/c3-1-2(4)5/h2H,1H2 |
| InChI Key | UBOXGVDOUJQMTN-UHFFFAOYSA-N |
| Canonical SMILES | C(C(Cl)Cl)Cl |
| Molecular Formula | C2H3Cl3 |
| Wikipedia | 1,1,2-trichloroethane |
From Pubchem
Computed Properties
| Property Name | Property Value |
|---|---|
| Molecular Weight | 133.396 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 1 |
| Complexity | 18.9 |
| CACTVS Substructure Key Fingerprint | A A A D c Q B A A A A G 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 A I A A A A A A A O A 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 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 A = = |
| Topological Polar Surface Area | 0.0 |
| Monoisotopic Mass | 131.93 |
| Exact Mass | 131.93 |
| 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+ | 0.9863 |
| Human Intestinal Absorption | HIA+ | 0.9927 |
| Caco-2 Permeability | Caco2+ | 0.7342 |
| P-glycoprotein Substrate | Non-substrate | 0.8944 |
| P-glycoprotein Inhibitor | Non-inhibitor | 0.9782 |
| Non-inhibitor | 0.9543 | |
| Renal Organic Cation Transporter | Non-inhibitor | 0.8560 |
| Distribution | ||
| Subcellular localization | Mitochondria | 0.5751 |
| Metabolism | ||
| CYP450 2C9 Substrate | Non-substrate | 0.8291 |
| CYP450 2D6 Substrate | Non-substrate | 0.6461 |
| CYP450 3A4 Substrate | Non-substrate | 0.7348 |
| CYP450 1A2 Inhibitor | Non-inhibitor | 0.5216 |
| CYP450 2C9 Inhibitor | Non-inhibitor | 0.8290 |
| CYP450 2D6 Inhibitor | Non-inhibitor | 0.9497 |
| CYP450 2C19 Inhibitor | Non-inhibitor | 0.6450 |
| CYP450 3A4 Inhibitor | Non-inhibitor | 0.9466 |
| CYP Inhibitory Promiscuity | Low CYP Inhibitory Promiscuity | 0.8090 |
| Excretion | ||
| Toxicity | ||
| Human Ether-a-go-go-Related Gene Inhibition | Weak inhibitor | 0.9493 |
| Non-inhibitor | 0.9457 | |
| AMES Toxicity | AMES toxic | 0.7416 |
| Carcinogens | Carcinogens | 0.7964 |
| Fish Toxicity | High FHMT | 0.6050 |
| Tetrahymena Pyriformis Toxicity | High TPT | 0.9515 |
| Honey Bee Toxicity | High HBT | 0.8478 |
| Biodegradation | Not ready biodegradable | 0.8267 |
| Acute Oral Toxicity | III | 0.5156 |
| Carcinogenicity (Three-class) | Non-required | 0.6349 |
From admetSAR
ADMET Predicted Profile --- Regression
| Model | Value | Unit |
|---|---|---|
| Absorption | ||
| Aqueous solubility | -1.4174 | LogS |
| Caco-2 Permeability | 1.5600 | LogPapp, cm/s |
| Distribution | ||
| Metabolism | ||
| Excretion | ||
| Toxicity | ||
| Rat Acute Toxicity | 2.4732 | LD50, mol/kg |
| Fish Toxicity | 1.7865 | pLC50, mg/L |
| Tetrahymena Pyriformis Toxicity | 0.8513 | pIGC50, ug/L |
From admetSAR
Toxicity Profile
| Route of Exposure | Inhalation ; oral ; dermal |
|---|---|
| Mechanism of Toxicity | Acyl chlorides and free radicals formed during the metabolism of 1,1,2-trichloroethane are reactive metabolites that can bind to proteins and nucleic acids (DNA, RNA), and are suspected of being cytotoxic, mutagenic, and carginogenic. |
| Metabolism | After 1,1,2-trichloroethane enters the body, it is carried by the blood to organs and tissues such as the liver, kidney, brain, heart, spleen, and fat. The primary metabolites identified are chloroacetic acid, S-carboxymethylcysteine, and thiodiacetic acid. S-carboxymethycysteine and thiodiacetic acid are formed from 1,1,2-trichloroethane following conjugation with glutathione. Chloroacetic acid is formed by hepatic cytochrome P-450. This reaction is thought to proceed via the acyl chloride. Cytochrome P-450 can also produce free radicals from 1,1,2-trichloroethane. Experiments show that most 1,1,2-trichloroethane leaves the body unchanged in the breath and as other substances that it is changed into in the urine in about 1 day. |
| Toxicity Values | LD50: 837 mg/kg (Oral, Rat) LD50: 5.38 g/kg (Dermal, Rabbit) |
| Lethal Dose | None |
| Carcinogenicity (IARC Classification) | 3, not classifiable as to its carcinogenicity to humans. |
| Minimum Risk Level | Acute Oral: 0.3 mg/kg/day (Mouse) Intermediate Oral: 0.04 mg/kg/day (Mouse) 9L422) |
| Health Effects | Inhalation of high levels of 1,1,2-trichloroethanein can affect the nervous system and cause sleepiness. 1,1,2-Trichloroethane may also affect the liver, kidney, and digestive tract, produce skin irritation, and affect the body's ability to fight infections. (L422) |
| Treatment | Following ingestion, administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old. Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion. In case of seizures, administer a benzodiazepine IV. 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. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. |
| Reference |
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From T3DB
Taxonomic Classification
| Kingdom | Organic compounds |
|---|---|
| Superclass | Organohalogen compounds |
| Class | Organochlorides |
| Subclass | Not available |
| Intermediate Tree Nodes | Not available |
| Direct Parent | Organochlorides |
| Alternative Parents | |
| Molecular Framework | Aliphatic acyclic compounds |
| Substituents | Hydrocarbon derivative - Organochloride - Alkyl halide - Alkyl chloride - Aliphatic acyclic compound |
| Description | This compound belongs to the class of organic compounds known as organochlorides. These are compounds containing a chemical bond between a carbon atom and a chlorine atom. |
From ClassyFire
Targets
- General Function:
- Zinc ion binding
- Specific Function:
- Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Isoform 3 is involved in activation of NOS3 and endothelial nitric oxide production. Isoforms lacking one or several functional domains are thought to modulate transcriptional activity by competitive ligand or DNA binding and/or heterodimerization with the full length receptor. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3. Isoform 3 can bind to ERE and inhibit isoform 1.
- Gene Name:
- ESR1
- Uniprot ID:
- P03372
- Molecular Weight:
- 66215.45 Da
References
- Luft S, Milki E, Glustrom E, Ampiah-Bonney R, O'Hara P. Binding of Organochloride and Pyrethroid Pesticides To Estrogen Receptors α and β: A Fluorescence Polarization Assay. Biophysical Journal 2009;96(3):444a. [16531984 ]
- General Function:
- Zinc ion binding
- Specific Function:
- Nuclear hormone receptor. Binds estrogens with an affinity similar to that of ESR1, and activates expression of reporter genes containing estrogen response elements (ERE) in an estrogen-dependent manner (PubMed:20074560). Isoform beta-cx lacks ligand binding ability and has no or only very low ere binding activity resulting in the loss of ligand-dependent transactivation ability. DNA-binding by ESR1 and ESR2 is rapidly lost at 37 degrees Celsius in the absence of ligand while in the presence of 17 beta-estradiol and 4-hydroxy-tamoxifen loss in DNA-binding at elevated temperature is more gradual.
- Gene Name:
- ESR2
- Uniprot ID:
- Q92731
- Molecular Weight:
- 59215.765 Da
References
- Luft S, Milki E, Glustrom E, Ampiah-Bonney R, O'Hara P. Binding of Organochloride and Pyrethroid Pesticides To Estrogen Receptors α and β: A Fluorescence Polarization Assay. Biophysical Journal 2009;96(3):444a. [16531984 ]
- 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