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Name Description
id 34
T3DB ID T3D0038
Name Disulfoton
Class SmallMolecule
Description Disulfoton is a manufactured organophosphate used as a pesticide. It is used mainly in agriculture to protect field and vegetable crops. (L123)
Categories "Pesticide", "Household Toxin", "Synthetic Toxin"
Types "Organic Compound", "Pesticide", "Organophosphate", "Ether", "Ester", "Household Toxin", "Synthetic Compound"
Synonyms "Di-syston", "Disipton", "Disulfoton mixture", "Disyston FE-10", "Disystox", "Dithiodemeton", "Dithiosystox", "Dution", "Ekatin TD", "Ekatine", "Ethyl thiometon", "Ethylthiodemeton", "Ethylthiometon", "Ethylthiometon b", "Glebofos", "Insyst-d", "O,O-Diaethyl-S-(2-aethylthio-aethyl)-dithiophosphat", "O,O-diethyl 2-(ethylthio)ethyl dithiophosphate", "O,O-Diethyl 2-ethylthioethyl phosphorodithioate", "O,O-Diethyl S-(2-(ethylthio)ethyl) dithiophosphate", "O,O-Diethyl S-(2-(ethylthio)ethyl)phosphorodithioate", "O,O-Diethyl S-(2-eththioethyl) phosphorodithioate", "O,O-Diethyl S-(2-eththioethyl) thiothionophosphate", "O,O-Diethyl S-(2-ethylmercaptoethyl) dithiophosphate", "O,O-Diethyl S-2-(ethylthio)ethyl phosphorodithioate", "O,O-Diethyl S-[2-(ethylsulfanyl)ethyl] dithiophosphate", "O,O-Diethyl S-[2-(Ethylthio)ethyl] dithiophosphate", "O,O-Diethyl S-[2-(ethylthio)ethyl] phosphorodithioate", "O,o-diethyl-s-ethylmercapto-ethyl dithiophosphate", "O,O-Ethyl S-2(ethylthio)ethyl phosphorodithioate", "S-[2-(ethylsulfanyl)ethyl] O,O-dimethyl dithiophosphate", "Solvigran", "Solvirex", "Thiodemeton", "Thiodemetron"
CAS Number 298-04-4
Chemical Formula C8H19O2PS3
Average Molecular Mass 274.40
Monoisotopic Mass 274.03
IUPAC Name O,O-diethyl {[2-(ethylsulfanyl)ethyl]sulfanyl}phosphonothioate
Traditional Name O,O-diethyl [2-(ethylsulfanyl)ethyl]sulfanylphosphonothioate
SMILES CCOP(=S)(OCC)SCCSCC
InChI Identifier InChI=1S/C8H19O2PS3/c1-4-9-11(12,10-5-2)14-8-7-13-6-3/h4-8H2,1-3H3
InChI Key InChIKey=DOFZAZXDOSGAJZ-UHFFFAOYSA-N
Kingdom Organic Compounds
Super Class Organophosphorus Compounds
Class Organothiophosphorus Compounds
Sub Class Organic Dithiophosphoric Acids and Derivatives
Direct Parent Thia Fatty Acids
Alternate Parents "Dithiophosphate Esters", "Sulfenyl Compounds", "Dialkylthioethers", "Organooxygen Compounds"
Geometric Description Aliphatic Acyclic Compounds
Substituents "thioether", "organosulfur compound", "Organooxygen Compound", "Aliphatic Acyclic Compound", "Dialkylthioether", "Sulfenyl Compound", "Dithiophosphate S-Ester", "Dithiophosphate Ester"
Descriptors "organic thiophosphate (ChEBI)", "organothiophosphate insecticide (ChEBI)", "Organophosphorus insecticides (KEGG)"
Status Detected and Not Quantified
Origin Exogenous
Cellular Locations "Membrane"
Biofluids
Tissues
Pathways
State Liquid
Appearance Colorless (pure) or dark yellow (technical grade) oil.
Melting Point -25°C
Boiling Point
Solubility 0.0163 mg/mL at 20 °C [BOWMAN,BT & SANS,WW (1983A)]
LogP
Route of Exposure Oral (L123) ; inhalation (L123) ; dermal (L123)
Mechanism of Toxicity Disulfoton 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 Metabolism of organophosphates occurs principally by oxidation, by hydrolysis via esterases and by reaction with glutathione. Demethylation and glucuronidation may also occur. Oxidation of organophosphorus pesticides may result in moderately toxic products. In general, phosphorothioates are not directly toxic but require oxidative metabolism to the proximal toxin. The glutathione transferase reactions produce products that are, in most cases, of low toxicity. Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of organophosphate exposure.
Toxicity LD50: 25 mg/kg (Dermal, Rat) (T23) LD50: 6.8 mg/kg (Oral, Rat) (T23) LD50: 9.4 mg/kg (Intraperitoneal, Rat) (T23)
Lethal Dose
Carcinogenicity No indication of carcinogenicity to humans (not listed by IARC).
Uses/Sources Disulfoton is used mainly in agriculture to protect field and vegetable crops, as well as some fruit and nut crops. It may also be used in smaller quantities on home and garden plants and for mosquito control in swamps. (L123)
Minimum Risk Level Acute Inhalation: 0.006 mg/m3 (L134) Intermediate Inhalation: 0.0002 mg/m3 (L134) Acute Oral: 0.001 mg/kg/day (L134) Intermediate Oral: 0.00009 mg/kg/day (L134) Chronic Oral: 0.00006 mg/kg/day (L134)
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.
Symptoms Depending on the amount of disulfoton that enters the body, effects on the nervous system, such as narrowing of the pupils, vomiting, diarrhea, drooling, difficulty in breathing, tremors, convulsions, and even death may occur. Skin contact with disulfoton may cause weakness and fatigue. (L123)
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.
DrugBank ID
HMDB ID
PubChem Compound ID 3118
ChEMBL ID CHEMBL1332314
ChemSpider ID 3006
KEGG Compound ID C18400
UniProt ID 0
OMIM ID 0
ChEBI ID 38661
BioCyc ID
CTD ID D004222
Stitch ID Disulfoton
PDB ID
ACToR ID 1916
Wikipedia Link http://en.wikipedia.org/wiki/Disulfoton
Creation Date 2009-03-06 18:57:58
Update Date 2014-12-24 20:20:56