O,P'-DDD (CHEM000139)

Record Information
Version1.0
Creation Date2009-03-06 18:58:10 UTC
Update Date2026-05-14 16:45:01 UTC
Accession NumberCHEM000139
Identification
Common NameO,P'-DDD
ClassSmall Molecule
Description
DDD, O,P'- is an isomer of dichlorodiphenyldichloroethane, an organochlorine insecticide. It is a component of commercial mixtures of DDT. DDT was once a widely used pesticide, but today its agricultural use has been banned worldwide due to its toxicity and tendency to bioaccumulate. However, it still has limited use in disease vector control. (1). It is a derivative of the insecticide dichlorodiphenyldichloroethane that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression. [PubChem]
Contaminant Sources
  • HMDB Contaminants - Urine
  • My Exposome Chemicals
  • STOFF IDENT Compounds
  • T3DB toxins
  • ToxCast & Tox21 Chemicals
Contaminant Type
  • Antineoplastic Agent, Hormonal
  • Drug
  • Organic Compound
  • Organochloride
  • Pesticide
  • Synthetic Compound
Chemical Structure
MOLSDFPDBSMILESInChI
Synonyms
ValueSource
LysodrenKegg
Bristol myers squibb brand OF mitotaneMeSH, HMDB
KhloditanMeSH, HMDB
ortho,Para-DDDMeSH, HMDB
ChloditanMeSH, HMDB
Bristol-myers squibb brand OF mitotaneMeSH, HMDB
O,P-DDDMeSH, HMDB
ortho,Para DDDMeSH, HMDB
ChlodithaneMeSH, HMDB
MytotanMeSH, HMDB
Chemical FormulaC14H10Cl4
Average Molecular Mass320.041 g/mol
Monoisotopic Mass317.954 g/mol
CAS Registry Number53-19-0
IUPAC Name1-chloro-4-[2,2-dichloro-1-(2-chlorophenyl)ethyl]benzene
Traditional Namemitotane
SMILESClC(Cl)C(C1=CC=C(Cl)C=C1)C1=CC=CC=C1Cl
InChI IdentifierInChI=1S/C14H10Cl4/c15-10-7-5-9(6-8-10)13(14(17)18)11-3-1-2-4-12(11)16/h1-8,13-14H
InChI KeyJWBOIMRXGHLCPP-UHFFFAOYSA-N
Chemical Taxonomy
Description Belongs to the class of organic compounds known as diphenylmethanes. Diphenylmethanes are compounds containing a diphenylmethane moiety, which consists of a methane wherein two hydrogen atoms are replaced by two phenyl groups.
KingdomOrganic compounds
Super ClassBenzenoids
ClassBenzene and substituted derivatives
Sub ClassDiphenylmethanes
Direct ParentDiphenylmethanes
Alternative Parents
Substituents
  • Diphenylmethane
  • Halobenzene
  • Chlorobenzene
  • Aryl halide
  • Aryl chloride
  • Hydrocarbon derivative
  • Organochloride
  • Organohalogen compound
  • Alkyl halide
  • Alkyl chloride
  • Aromatic homomonocyclic compound
Molecular FrameworkAromatic homomonocyclic compounds
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Membrane
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point77°C
Boiling PointNot Available
Solubility0.1 mg/L (at 25°C)
Predicted Properties
PropertyValueSource
Water Solubility9.4e-06 g/LALOGPS
logP6.08ALOGPS
logP6.11ChemAxon
logS-7.5ALOGPS
Physiological Charge0ChemAxon
Hydrogen Acceptor Count0ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area0 ŲChemAxon
Rotatable Bond Count3ChemAxon
Refractivity79.97 m³·mol⁻¹ChemAxon
Polarizability29.93 ųChemAxon
Number of Rings2ChemAxon
BioavailabilityYesChemAxon
Rule of FiveNoChemAxon
Ghose FilterNoChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleNoChemAxon
Spectra
Spectra
Toxicity Profile
Route of ExposureOral (2); about 40% oral Lysodren is absorbed.
Mechanism of ToxicityDDD toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDD reduces potassium transport across the membrane. DDD inhibits the inactivation of voltaged-gated sodium channels. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization and resulting in a state of hyperexcitability. DDD inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDD also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDD is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (7, 2)
MetabolismDDD is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDD occurs mainly via cytochrome P-450 enzymes in the liver and kidney. Its metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), are excreted in the urine. (2) Route of Elimination: A variable amount of metabolite (1%-17%) is excreted in the bile and the balance is apparently stored in the tissues. Half Life: 18-159 days
Toxicity ValuesLD50: 113 mg/kg (Oral, Rat) (4)
Lethal Dose5 g/kg for an adult human. (4)
Carcinogenicity (IARC Classification)Not directly listed by IARC, but carcinogenicity studies of this DDT metabolite are discussed in connection with DDT (6).
Uses/SourcesDDD is found in DDT, which is used as a pesticide and in disease vector control. (1). It is also used for treatment of inoperable adrenocortical tumours; Cushing's syndrome
Minimum Risk LevelNot Available
Health EffectsDDT has been shown to cause mild anemia. Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted. (7)
SymptomsDDT exposure causes ataxia and abnormal stepping. Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli. (7)
TreatmentTreatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (5)
Concentrations
Not Available
External Links
DrugBank IDDB00648
HMDB IDHMDB0259550
FooDB IDNot Available
Phenol Explorer IDNot Available
KNApSAcK IDNot Available
BiGG IDNot Available
BioCyc IDNot Available
METLIN IDNot Available
PDB IDNot Available
Wikipedia LinkMitotane
Chemspider ID4066
ChEBI IDNot Available
PubChem Compound IDNot Available
Kegg Compound IDNot Available
YMDB IDNot Available
ECMDB IDNot Available
References
Synthesis ReferenceNot Available
MSDSNot Available
General References