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Name Description
id 27
T3DB ID T3D0031
Name Toxaphene
Class SmallMolecule
Description Toxaphene is an insecticide mixture of compounds. It was once widenly used, but it is now banned in most areas due to its toxicity and tendency to bioaccumulate in the environment. (L107) The structure displayed is a generic structure of toxaphene components.
Categories "Pesticide", "Pollutant", "Airborne Pollutant", "Synthetic Toxin"
Types "Organic Compound", "Organochloride", "Pesticide", "Pollutant", "Synthetic Compound"
Synonyms "Camphechlor", "Chlorcamphene", "Chlorinated camphene", "Polychlorochamphene"
CAS Number 8001-35-2
Chemical Formula C10H8Cl8
Average Molecular Mass 411.80
Monoisotopic Mass 407.81
IUPAC Name 1,4,5,6,7,7-hexachloro-2,2-bis(chloromethyl)-3-methylidenebicyclo[2.2.1]heptane
Traditional Name toxaphene
SMILES ClCC1(CCl)C(=C)C2(Cl)C(Cl)C(Cl)C1(Cl)C2(Cl)Cl
InChI Identifier InChI=1S/C10H8Cl8/c1-4-7(2-11,3-12)9(16)6(14)5(13)8(4,15)10(9,17)18/h5-6H,1-3H2
Kingdom Organic Compounds
Super Class Organohalogen Compounds
Class Organochlorides
Sub Class
Direct Parent Bicyclic Monoterpenes
Alternate Parents "Alkyl Chlorides"
Geometric Description Aliphatic Homopolycyclic Compounds
Substituents "organochloride", "alkyl chloride", "Alkyl Halide", "Aliphatic Homopolycyclic Compound"
Status Detected and Not Quantified
Origin Exogenous
Cellular Locations "Membrane"
State Solid
Appearance Yellow solid.
Melting Point 77°C
Boiling Point
Solubility 0.00055 mg/mL at 20 °C [MURPHY,TJ et al. (1987)]
Route of Exposure Oral (L107) ; inhalation (L107)
Mechanism of Toxicity Toxaphene 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 Toxaphene is absorbed through the intestines and lungs, then distributed mainly to fat tissues. Due to the complex composition of toxaphene, it requires various metabolic pathways to degrade, which involve dechlorination, dehydrodechlorination, and oxidation. Metabolism occurs primarily by hepatic mixed-function oxidases, and metabolites are excreted in the urine and faeces. (L107)
Toxicity LD50: 50 mg/kg (Oral, Rat) (L147) LD50: 600 mg/kg (Dermal, Rat) (L147)
Lethal Dose 2 to 7 grams for an adult human. (183)
Carcinogenicity 2B, possibly carcinogenic to humans. (L135)
Uses/Sources Toxaphene was used as an insecticide. (L107)
Minimum Risk Level Acute Oral: 0.005 mg/kg/day (L134) Intermediate Oral: 0.001 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 Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include 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. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.
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
PubChem Compound ID 5284469
ChemSpider ID 4447533
KEGG Compound ID C15470
UniProt ID 0
BioCyc ID
CTD ID D014112
Stitch ID Toxaphene
ACToR ID 1399
Wikipedia Link
Creation Date 2009-03-06 18:57:57
Update Date 2014-12-24 20:20:55