<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">48</id>
  <title>T3D0047</title>
  <common-name>Carbon tetrachloride</common-name>
  <description>Grain fumigantCarbon tetrachloride has been shown to exhibit anesthetic, metal chelator and hepatoprotective functions (A7684, A7685, A7686).Carbon tetrachloride belongs to the family of Chlorocarbons. These are Any Compound consisting wholly of chlorine and carbon. (Reference: [1] IUPAC. Compendium of Chemical Terminology, 2nd ed. (the Gold Book). Compiled by A. D. McNaught and A. Wilkinson. Blackwell Scientific Publications, Oxford (1997). XML on-line corrected version: http://goldbook.iupac.org (2006-) created by M. Nic, J. Jirat, B. Kosata; updates compiled by A. Jenkins. ISBN 0-9678550-9-8. doi:10.1351/goldbook. (Or PAC, 1995, 67, 1307 (Glossary of class names of organic compounds and reactivity intermediates based on structure (IUPAC Recommendations 1995)) on page 1328)).</description>
  <cas>56-23-5</cas>
  <pubchem-id>5943</pubchem-id>
  <chemical-formula>CCl4</chemical-formula>
  <weight>151.875410</weight>
  <appearance>Clear liquid.</appearance>
  <melting-point>28.6°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>0.793 mg/mL at 25°C</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral (L129) ; inhalation (L129) ; dermal (L129)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Unmetabolized carbon tetrachloride, depresses the central nervous system. All other toxic effects of carbon tetrachloride are related to its biotransformation via cytochrome P-450 enzymes, specifically CYP2E1. Metabolism of carbon tetrachloride by CYP2E1 may result in the destruction of the enzyme during the metabolic process, either by direct attack of radicals on the cytochrome(s) or highly localized lipid peroxidation resulting in detachment of P-450 proteins from the microsomal membranes. Reactive metabolites of carbon tetrachloride causes hepatic damage via haloalkylation of cellular macromolecules and lipid peroxidation. Carbon tetrachloride also perturbs the intracellular calcium homeostasis. Increased cytosolic levels of calcium may result from an influx of extracellular calcium caused by plasma membrane damage and decreased intracellular calcium sequestering. Higher levels of calcium activate enzymes such as proteases, which hydrolyze proteins in neighboring cells, leading to a progression of the lesion. Carbon tetrachloride's carcinogenicity is likely the result of certain reactive metabolites that bind to nuclear proteins, lipids, and DNA. (T10, L129)</mechanism-of-toxicity>
  <metabolism>Carbon tetrachloride is absorbed readily from the gastrointestinal and respiratory tracts, and more slowly through the skin. It is distributed to all major organs, with highest concentrations in the fat, liver, bone marrow, adrenals, blood, brain, spinal cord, and kidney. Once carbon tetrachloride is absorbed, it is metabolized by cytochrome P-450 enzymes, with the production of the trichloromethyl radical. Aerobically, metabolism of the trichloromethyl radical can eventually form phosgene. Anaerobically, the radical can undergo reactions to form chloroform, hexachloroethane, or carbon monoxide. Carbon tetrachloride is excreted primarily in exhaled air and in the feces, with relatively minimal amounts in the urine. (L129)</metabolism>
  <toxicity>LD50: 2800 mg/kg (Oral, Rat) (T21)</toxicity>
  <lethaldose>1700 to 1800 mg/kg for an adult human. (T26)</lethaldose>
  <carcinogenicity>2B, possibly carcinogenic to humans. (L135)</carcinogenicity>
  <use-source>Carbon tetrachloride was used in the production of refrigeration fluid and propellants for aerosol cans, as a pesticide, as a cleaning fluid and degreasing agent, in fire extinguishers, and in spot removers. (L129)</use-source>
  <min-risk-level>Intermediate Inhalation: 0.03 ppm (L134)
Chronic Inhalation: 0.03 ppm (L134)
Acute Oral: 0.02 mg/kg/day (L134)
Intermediate Oral: 0.007 mg/kg/day (L134)</min-risk-level>
  <health-effects>High exposure to carbon tetrachloride can cause liver, kidney, and central nervous system damage. Single cell necrosis, which is evident after 5h to 6h after dosing, progresses to maximal centrilobular necrosis within 24h to 48h. Cellular regeneration is maximal 36h to 48h after dosing. The rate and extent of tissue repair are important determinants of the ultimate outcome of liver injury. In severe cases, coma and even death may occur. (T10, L129)</health-effects>
  <symptoms>Carbon tetrachloride exposure causes headaches, dizziness, sleepiness, nausea, and vomiting. (L129)</symptoms>
  <treatment nil="true"/>
  <created-at type="dateTime">2009-03-06T18:57:59Z</created-at>
  <updated-at type="dateTime">2026-03-26T23:43:53Z</updated-at>
  <interacting-proteins>Cytochrome P450 2E1 (P05181)
(L129)</interacting-proteins>
  <wikipedia>http://en.wikipedia.org/wiki/Carbon_tetrachloride</wikipedia>
  <uniprot-id nil="true"/>
  <kegg-compound-id>C07561</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>27385</chebi-id>
  <biocyc-id>CPD-842</biocyc-id>
  <ctd-id>D002251</ctd-id>
  <stitch-id>Carbon tetrachloride</stitch-id>
  <drugbank-id nil="true"/>
  <pdb-id nil="true"/>
  <actor-id>253</actor-id>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins>Cytochrome P450 2E1 (P05181)
(L129)</metabolizing-proteins>
  <transporting-proteins nil="true"/>
  <moldb-smiles>ClC(Cl)(Cl)Cl</moldb-smiles>
  <moldb-formula>CCl4</moldb-formula>
  <moldb-inchi>InChI=1S/CCl4/c2-1(3,4)5</moldb-inchi>
  <moldb-inchikey>VZGDMQKNWNREIO-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">153.823</moldb-average-mass>
  <moldb-mono-mass type="decimal">151.875410828</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>2.83</logp>
  <hmdb-id>HMDB31330</hmdb-id>
  <chembl-id>CHEMBL44814</chembl-id>
  <chemspider-id>5730</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference nil="true"/>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM000043</chemdb-id>
  <dsstox-id>DTXSID8020250</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00005620</susdat-id>
  <iupac>tetrachloromethane</iupac>
</compound>
