Absorption, Distribution and Excretion
DDT and ... DDE have high fat:water partition coefficient and therefore tend to accumulate in adipose tissue.
... There is a close correspondence between lipid content of organs and concentration of DDE, DDT, and dieldrin in blood, kidney, liver, and adipose tissue. ... Does not apply to brain, an organ that include almost no neutral fat, although its lipid content is relatively high.
DDE concentrations from various tissues from 44 autopsies of people in general population: concentration (ppm) spleen 0.0305; lung 0.0585; gonad 0.0688; brain 0.0831; liver 0.200; kidney 0.209; adrenal 0.875; lymph node 1.38; bone marrow 2.08; panniculus fat 4.48; mesenteric fat 4.40; perirenal fat 4.64. /From table/
... /It has been found/ that excretory products of a wide range of chlorinated hydrocarbon insecticides are detectable in urine of people in the general population. ... /frequently/ 2 isomers of DDT, one each of DDE and DDD /were found/ ... .
For more Absorption, Distribution and Excretion (Complete) data for DDE (16 total), please visit the HSDB record page.

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Metabolism / Metabolites
... Rats dosed with p,p'-DDE (about 800 mg/kg) excreted 3 phenols ... in one ... the phenolic hydroxy-group is sited at the position of original p-chloro-substituent, and the Cl atom has migrated to adjacent position. Detection of this metabolite provides strong support for formation from p,p'-DDE of arene oxides ... .
DDT is metabolized in variety of mammalian species primarily by series of alternate reductive dechlorinations and/or dehydrochlorinations ... to yield in 1st step TDE ... or DDE... In rats, further conversion of DDE in liver proceeds slowly via DDMU (1-chloro-2,2-bis(p-chlorophenyl)ethylene) to DDNU (2,2-bis(bis(p-chlorophenyl)ethylene) ... Further metabolism of 2,2-bis(bis(p-chlorophenyl)ethylene seems to occur primarily in kidney ... to yield DDCHO (2,2-bis(p-chlorophenyl)acetaldehyde) ... or DDA (2,2-bis(p-chlorophenyl)acetic acid) ... .
DDE is converted /by dehydrochlorination/ to 2,2-bis(bis(p-chlorophynyl)ethylene, also by successive oxidation-reduction of respective ethylene analogues; thereafter it follows the DDOH to DDA pathway. This metabolism proceeds slowly which accounts for persistence of DDE residues in mammalian adipose tissues.
... DDT ... degradative changes ... /such as/ dehydrochlorination to form DDE ... DDT ... reductively chlorinated in biologic systems to form DDD. DDD is less stable than DDT or DDE. DDD is dehydrochlorinated to 1-chloro-2,2-bis(p-chlorophenyl)ethylene, or 2,2-bis-(p-chlorophenyl)-1-chloroethylene; reduced to DDMS ... 2,2-bis- (p-chlorophenyl)-1-chloroethane ... DDMS ... is dehydrochlorinated to 2,2-bis(bis(p-chlorophynyl)ethylene ... 2,2-bis-(p-chlorophenyl)-ethylene; reduced to 1,1-bis-(p-chlorophenyl) ethane ... Eventually oxidized to bis(p-chlorophenyl)-acetic acid ... Bis-(p-chlorophenyl)-acetic acid.
For more Metabolism/Metabolites (Complete) data for DDE (9 total), please visit the HSDB record page.
DDE 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 DDE 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. (L85)

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Biological Half-Life
DDE is eliminated /from human body/ ... slowly, with a biologic half-life of about 8 yr.
A comparison of DDT & methoxychlor accumulation & depletion in sheep at dosages of 250 ppm in the diet revealed that residues of latter are at least one hundredth those of DDT. The half-life of elimination of methoxychlor in sheep was calculated to be 10 days; /while the values for/ DDT, DDD, & DDE ... were 90, 26, & 223 days, /respectively/.

Toxicity Summary
DDE toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDE reduces potassium transport across the membrane. DDE 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. DDE inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDE 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. DDE is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (T10, L85)

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Interactions
.... The effects of the perinatal, combined exposure to 1,4-dichlorobenzene (DCB) and p,p'-DDE on the female reproductive system have been investigated in mature rat female offspring of dams ingesting 25 ppm. DCB (approximately 2 mg/kg) and 125 ppm. p,p'-DDE (approximately 10 mg/kg) during the gestational and lactational period. Sexual maturation was fully developed in the rat female offspring perinatally exposed to DCB and/or p,p'-DDE through maternal exposure. The combined effect of DCB and p,p'-DDE was observed, and the ovarian weight was seen to decrease to approximately 80% of the control rat in matured female offspring following perinatal exposure to DCB and p,p'-DDE. This alteration might lead to reproductive dysfunction in matured female offspring...
As little as 10 ug of DDT (combined DDT and DDE) per g of fat is associated with enhanced metabolism of pentobarbital in the rat.
Bovine liver is susceptible to induction /of microsomal enzymes/, and treatment of cattle with barbiturates has been shown to accelerate the metabolic clearance of DDE.
In quail, chronic dosage with ... DDE ... effectively inhibited pentobarbitone metabolism.
For more Interactions (Complete) data for DDE (14 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral 880 mg/kg
LD50 Mouse oral 700 mg/kg

[1]. Persistent DDT metabolite p,p'-DDE is a potent androgen receptor antagonist. Nature. 1995;375(6532):581-585.

DDE (Dichlorodiphenyldichloroethylene) can cause cancer according to an independent committee of scientific and health experts. It can cause developmental toxicity and male reproductive toxicity according to The Environmental Protection Agency (EPA).
P,p'-dde appears as white crystalline solid or white powder. (NTP, 1992)
DDE is a chlorophenylethylene that is ethylene substituted by two 4-chlorophenyl groups at position 1 and two chlorine atoms at position 2. It has a role as a persistent organic pollutant and a human xenobiotic metabolite. It is a member of monochlorobenzenes and a chlorophenylethylene.
1,1-Dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE) is a breakdown product of DDT, which was used in the past as an insecticide. No information is available on the acute (short-term) or chronic (long-term) effects of DDE. Acute, oral exposure to high doses of DDT in humans results in central nervous system (CNS) effects, such as headaches, nausea, and convulsions. The only effect noted in epidemiologic studies of workers exposed to DDT and other pesticides was an increase in activity of liver enzymes. Animal studies have reported effects on the liver, immune system, and CNS from chronic oral exposure to DDT. Human studies are inconclusive regarding DDE and cancer. Animal studies have reported an increased incidence of liver tumors in mice and hamsters, and thyroid tumors in female rats from oral exposure to DDE. EPA has classified DDE as a Group B2, probable human carcinogen.
p,p'-DDE has been reported in Euglena gracilis with data available.
DDE, P,P'- is an isomer of dichlorodiphenyldichloroethylene, an organochlorine insecticide. It is one of the components 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. (L84)
An organochlorine pesticide, it is the ethylene metabolite of DDT.

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Mechanism of Action
Eight chlorinated hydrocarbons were tested for their ability to compete with (3)H-estradiol-17beta for specific binding proteins in uterine cytoplasm from immature rats. o,p'-DDE (0.14 mmol) competed with (3)H-estradiol-17beta for binding to '8s receptor' in uterine cytoplasm but p,p'-DDE and p,p'-DDT did not compete. o,p'-DDT and o,p'-DDE act as estrogens at high concentrations as measured by their ability to compete with estradiol-17beta for binding to uterine cytoplasmic receptor in the transfer and binding of estradiol in nuclei of uterine cells.
In a strain of ducks sensitive to eggshell-thinning effects of DDE, admin of 40 mg/kg in food for 45 days reduced eggshell index (EI) by 13% & content of calcium in the fluid of the shell gland forming an eggshell by 36%, & raised the calcium content of the shell gland mucosa by 19%, compared with control values. DDE inhibited the translocation (secretion) of calcium between the gland mucosa & the uterine cavity. ATP-dependent binding of calcium to microsomal subfraction (FI) rich in fragments of the plasma membrane was reduced by 16%, whereas that to a subfraction FIII which bound calcium at a very high rate was decreased to 36%. DDE may interfere with the stimulus-secretion mechanism of the eggshell gland in ducks through its effect on calcium binding.
In vitro DDE at 2 to 16 ng/L of an homogenate of the eggshell gland of ducks (Anas platyrhynchos) inhibited the Ca(2+)-Mg(2+)-activated ATPase in a concentration-dependent manner, whereas Mg(2+)-activated ATPase was not affected by these concentrations. Since calcium is transported against a concentration gradient between blood plasma & lumen of the eggshell gland, it is suggested that DDE, by inhibiting the Ca(2+)-Mg(2+)-activated ATPase, decreased the calcium translocation over the eggshell gland mucosa.
As for the mechanism of this eggshell thinning phenomenon, no adequate, or generally accepted, explanation exists. There are many reports that claim inhibition of carbonic anhydrase, generally acknowledged to play an important role in forming eggshells, by DDT, /DDE/ & some other derivatives, but there are just as many that deny this. ... Thus one is left with two alternatives to explain the phenomenon: 1) the carbonic anhydrase in the shell gland of avian species is unusually sensitive to chlorinated hydrocarbon insecticides, or 2) the in vivo inhibition observed is a result of some other effect, such as reduced enzyme production or the production of substances that suppress the activity of the enzyme.
For more Mechanism of Action (Complete) data for DDE (6 total), please visit the HSDB record page.

C14H8CL4

318.018

315.938

72-55-9

p,p'-DDE-d8;93952-19-3

3035

White to off-white solid powder

1.4±0.1 g/cm3

383.1±37.0 °C at 760 mmHg

88-90 °C(lit.)

183.7±23.9 °C

0.0±0.8 mmHg at 25°C

1.622

6.37

0

0

2

18

269

0

UCNVFOCBFJOQAL-UHFFFAOYSA-N

InChI=1S/C14H8Cl4/c15-11-5-1-9(2-6-11)13(14(17)18)10-3-7-12(16)8-4-10/h1-8H

1-chloro-4-[2,2-dichloro-1-(4-chlorophenyl)ethenyl]benzene

DDE 4,4'-DDE DDT dehydrochloride CCRIS 193 p,p'-DDE

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~314.44 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.86 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (7.86 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)