Tmic
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Record Information
Version2.0
Creation Date2009-03-06 18:58:13 UTC
Update Date2014-12-24 20:21:16 UTC
Accession NumberT3D0176
Identification
Common NameCarbon disulfide
ClassSmall Molecule
DescriptionCarbon disulfide is found in kohlrabi. Obsolete fumigant against insects in stored grain and potatoes.
Compound Type
  • Food Toxin
  • Industrial/Workplace Toxin
  • Metabolite
  • Natural Compound
  • Organic Compound
  • Pollutant
  • Solvent
Chemical Structure
Thumb
Synonyms
Synonym
Carbon bisulfide
Carbon bisulphide
Carbon disulphide
Carbon disulphide, BSI
Carbon sulfide (CS2)
Dithiocarbonic anhydride
Chemical FormulaCS2
Average Molecular Mass76.141 g/mol
Monoisotopic Mass75.944 g/mol
CAS Registry Number75-15-0
IUPAC Namemethanedithione
Traditional Namecarbon disulfide
SMILESS=C=S
InChI IdentifierInChI=1S/CS2/c2-1-3
InChI KeyInChIKey=QGJOPFRUJISHPQ-UHFFFAOYSA-N
Chemical Taxonomy
Description belongs to the class of inorganic compounds known as other non-metal sulfides. These are inorganic compounds containing a sulfur atom of an oxidation state of -2, in which the heaviest atom bonded to the oxygen belongs to the class of other non-metals.
KingdomInorganic compounds
Super ClassHomogeneous non-metal compounds
ClassOther non-metal organides
Sub ClassOther non-metal sulfides
Direct ParentOther non-metal sulfides
Alternative Parents
Substituents
  • Other non-metal sulfide
  • Inorganic sulfide
Molecular FrameworkNot Available
External Descriptors
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateLiquid
AppearanceNot Available
Experimental Properties
PropertyValue
Melting Point-111.6°C
Boiling Point46.3°C (115.3°F)
Solubility2.16 mg/mL at 20°C
LogP1.94
Predicted Properties
PropertyValueSource
Water Solubility1.3 g/LALOGPS
logP2.25ALOGPS
logP1.95ChemAxon
logS-1.8ALOGPS
Physiological Charge0ChemAxon
Hydrogen Acceptor Count0ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area0 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity22.37 m³·mol⁻¹ChemAxon
Polarizability6.79 ųChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash Key
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positivesplash10-004i-9000000000-1be1dd1539f07de91257View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-004i-9000000000-c32b774f5ef5f9e3b3b5View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-004i-9000000000-c32b774f5ef5f9e3b3b5View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-004i-9000000000-c32b774f5ef5f9e3b3b5View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-00di-9000000000-f8b0b78f7785ba1a8d02View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-00di-9000000000-f8b0b78f7785ba1a8d02View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-00di-9000000000-f8b0b78f7785ba1a8d02View in MoNA
MSMass Spectrum (Electron Ionization)splash10-004i-9000000000-4fd31585d55b0b9843c4View in MoNA
1D NMR13C NMR SpectrumNot AvailableView in JSpectraViewer
Toxicity Profile
Route of ExposureInhalation (12) ; oral (12) ; dermal (12) ; eye contact (12)
Mechanism of ToxicityCarbon disulfide is a potent nerve toxin and also affect liver enzymes, particularly those related to lipid metabolism. The increases in serum cholesterol that are sometimes seen following carbon disulfide exposure may be a result of increased hepatic cholesterol synthesis. The primary target of carbon disulfide appears to be the nervous system. Neurophysiological and behavioral effects as well as pathomorphology of peripheral nervous system structures have been reported in humans. Moreover, carbon disulfide metabolites of the thiocarbamate type inhibit aldehyde anhydrase. (11, 7)
MetabolismNitrogenase reduces carbon disulfide and can also be inhibited by this toxin. Carbon disulfide binds (in the form of AL CS2) mainly to hemoglobin and to a small extent to other blood proteins, such as albumin and gamma-globulin. Carbon disulfide is bioactivated by cytochrome P-450 to an unstable oxygen intermediate. The intermediate may either spontaneously degrade to atomic sulfur and carbonyl sulfide or hydrolyze to form atomic sulfur and monothiocarbonate. The atomic sulfur generated in these reactions may either covalently bind to macromolecules or be oxidized to products such as sulfate. The carbonyl sulfide formed may be converted to monothiocarbonate by carbonic anhydrase. Monothiocarbonate may further spontaneously degrade, regenerating carbonyl sulfide or forming carbon dioxide and sulfide bisulfide ion (HS-). The HS- formed can subsequently be oxidized to sulfate or other nonvolatile metabolites. Dithiocarbamates are the products of the reaction of carbon disulfide with amino acids. Most of the carbon disulfude absorbed is metabolized. Small traces of unchanged can be found in the urine. Carbon disulfide or carbonyl sulfide can conjugate with endogenous glutathione to yield thiazolidine-2-thione-4-carboxylic acid and 2-oxythiazolidine-4-carboxylic acid, respectively. Carbonic anhydrase 2 mediates the metabolism of carbon disulfide. (11, 2, 3, 4, 5, 6)
Toxicity ValuesLD50: 3020 mg/kg/day (Oral, Mouse) (11)
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesSeveral industries use carbon disulfide as a raw material to make such things as rayon, cellophane, and carbon tetrachloride. Exposure to carbon disulfide can results from breathing air, drinking water, or eating foods that contain it. One can also be exposed by skin contact with soil, water, or other substances that contain it. (11)
Minimum Risk LevelChronic Inhalation: 0.3 ppm (11) Acute Oral: 0.01 mg/kg/day (11)
Health EffectsFollowing inhalation, subtle and transient changes in pulmonary function can be manifested as reduced vital capacity and decreased partial pressure of arterial oxygen. Patients can developed normochromic and normocytic anemia, eosinopenia, and an increase in reticulocyte cell numbers after oral exposure . Carbon disulfide poisoning can result in central nervous system depression, coma, respiratory paralysis, and death. It also may accelerate coronary artery disease. Peripheral neuropathies, cranial nerve dysfunction, and neuropsychiatric changes are present in over 70% of chronic carbon sulfide victims. (11)
SymptomsDizziness, headache, nausea, shortness of breath, vomiting, weakness, irritability and hallucination can result from inhalation, ingestion or skin exposure to carbon disultfide. Skin and eye exposure can lead to pain, redness. Moreover, dermal exposure can lead to dryness of the skin; the carbon disulfide may be absorbed. Weak pulse, palpitations, fatigue, weakness in the legs, unsteady gait, vertigo, hyperesthesia, agitation, mania, hallucinations of sight, hearing, taste, and smell in acute are other symtoms of carbon disulfide poisoning. (12, 8)
TreatmentFollowing oral exposure, administer charcoal as a slurry (240 mL water/30 g charcoal). Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Intravenous urea (0.5 to 1.5 g/kg) has been recommended to inactivate free carbon disulfide in the blood. The efficacy of this treatment is unknown. 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. If the exposure occurred through eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If the exposure occurred through dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water. (9)
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDHMDB36574
PubChem Compound ID6348
ChEMBL IDCHEMBL1365180
ChemSpider ID6108
KEGG IDC19033
UniProt IDNot Available
OMIM ID
ChEBI ID23012
BioCyc IDCPD-844
CTD IDNot Available
Stitch IDCarbon disulfide
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkCarbon disulfide
References
Synthesis ReferenceNot Available
MSDSLink
General References
  1. Sams C, Loizou GD, Cocker J, Lennard MS: Metabolism of ethylbenzene by human liver microsomes and recombinant human cytochrome P450s (CYP). Toxicol Lett. 2004 Mar 7;147(3):253-60. [15104117 ]
  2. Haritos VS, Dojchinov G: Carbonic anhydrase metabolism is a key factor in the toxicity of CO2 and COS but not CS2 toward the flour beetle Tribolium castaneum [Coleoptera: Tenebrionidae]. Comp Biochem Physiol C Toxicol Pharmacol. 2005 Jan;140(1):139-47. [15792633 ]
  3. Masuda Y, Yasoshima M, Nakayama N: Early, selective and reversible suppression of cytochrome P-450-dependent monooxygenase of liver microsomes following the administration of low doses of carbon disulfide in mice. Biochem Pharmacol. 1986 Nov 15;35(22):3941-7. [3778518 ]
  4. Ryle MJ, Lee HI, Seefeldt LC, Hoffman BM: Nitrogenase reduction of carbon disulfide: freeze-quench EPR and ENDOR evidence for three sequential intermediates with cluster-bound carbon moieties. Biochemistry. 2000 Feb 8;39(5):1114-9. [10653657 ]
  5. Seefeldt LC, Rasche ME, Ensign SA: Carbonyl sulfide and carbon dioxide as new substrates, and carbon disulfide as a new inhibitor, of nitrogenase. Biochemistry. 1995 Apr 25;34(16):5382-9. [7727396 ]
  6. Lam CW, DiStefano V: Characterization of carbon disulfide binding in blood and to other biological substances. Toxicol Appl Pharmacol. 1986 Nov;86(2):235-42. [3787622 ]
  7. Schreiner E, Freundt KJ: Behaviour of epoxide hydrolase, glutathione S-transferase, alcohol dehydrogenase, and aldehyde dehydrogenase, respectively, under the influence of carbon disulfide studies with rats in vivo and in vitro. G Ital Med Lav. 1984 May-Jul;6(3-4):131-3. [6242047 ]
  8. Thompson TS and Vorster SJ (2000). Attempted suicide by ingestion of methoxychlor. J Anal Toxicol 24:377-380.
  9. Rumack BH (2009). POISINDEX(R) Information System. Englewood, CO: Micromedex, Inc. CCIS Volume 141, edition expires Aug, 2009.
  10. Yannai, Shmuel. (2004) Dictionary of food compounds with CD-ROM: Additives, flavors, and ingredients. Boca Raton: Chapman & Hall/CRC.
  11. ATSDR - Agency for Toxic Substances and Disease Registry (1996). Toxicological profile for carbon disulfide. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  12. International Programme on Chemical Safety (IPCS) INCHEM (2000). Poison Information Monograph for Carbon Disulfide. [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

General Function:
Vitamin d 24-hydroxylase activity
Specific Function:
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics.
Gene Name:
CYP1A1
Uniprot ID:
P04798
Molecular Weight:
58164.815 Da
References
  1. Gyamfi MA, Kocsis MG, He L, Dai G, Mendy AJ, Wan YJ: The role of retinoid X receptor alpha in regulating alcohol metabolism. J Pharmacol Exp Ther. 2006 Oct;319(1):360-8. Epub 2006 Jul 7. [16829625 ]
  2. Dalvi PS, Wilder-Kofie T, Mares B, Dalvi RR, Billups LH. Toxicologic implications of the metabolism of thiram, dimethyldithiocarbamate and carbon disulfide mediated by hepatic cytochrome P450 isozymes in rats. Pesticide Biochemistry and Physiology Oct 2002;74(2):85-90.
General Function:
Steroid hydroxylase activity
Specific Function:
Metabolizes several precarcinogens, drugs, and solvents to reactive metabolites. Inactivates a number of drugs and xenobiotics and also bioactivates many xenobiotic substrates to their hepatotoxic or carcinogenic forms.
Gene Name:
CYP2E1
Uniprot ID:
P05181
Molecular Weight:
56848.42 Da
References
  1. Gyamfi MA, Kocsis MG, He L, Dai G, Mendy AJ, Wan YJ: The role of retinoid X receptor alpha in regulating alcohol metabolism. J Pharmacol Exp Ther. 2006 Oct;319(1):360-8. Epub 2006 Jul 7. [16829625 ]
  2. Dalvi PS, Wilder-Kofie T, Mares B, Dalvi RR, Billups LH. Toxicologic implications of the metabolism of thiram, dimethyldithiocarbamate and carbon disulfide mediated by hepatic cytochrome P450 isozymes in rats. Pesticide Biochemistry and Physiology Oct 2002;74(2):85-90.
General Function:
L-ascorbic acid binding
Specific Function:
Conversion of dopamine to noradrenaline.
Gene Name:
DBH
Uniprot ID:
P09172
Molecular Weight:
69064.45 Da
References
  1. McKenna MJ, DiStefano V: Carbon disulfide. II. A proposed mechanism for the action of carbon disulfide on dopamine beta-hydroxylase. J Pharmacol Exp Ther. 1977 Aug;202(2):253-66. [886465 ]