Absorption, Distribution and Excretion
DDT and DDE have high lipid-water partition coefficients, thus they tend to accumulate in adipose tissue. …The lipid content of organs is closely related to the concentrations of DDE, DDT, and dieldrin in blood, kidneys, liver, and adipose tissue. …This does not apply to the brain, as it contains almost no neutral fats, although its lipid content is relatively high. DDE concentrations in various tissues from 44 autopsies of ordinary individuals: Concentration (ppm) Spleen 0.0305; Lung 0.0585; Gonads 0.0688; Brain 0.0831; Liver 0.200; Kidney 0.209; Adrenal gland 0.875; Lymph nodes 1.38; Bone marrow 2.08; Subcutaneous fat 4.48; Mesenteric fat 4.40; Perirenal fat 4.64. /Excerpt from table/ …/Found/ Excretion products of various chlorinated hydrocarbon pesticides can be detected in the urine of ordinary individuals. .../frequently/two isomers of DDT, one each of DDE and DDD/... For more complete data on the absorption, distribution, and excretion of DDEs (16 in total), please visit the HSDB record page.

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Metabolism/Metabolites
...Rats administered p,p'-DDE (approximately 800 mg/kg) excreted three phenolic compounds...one of which...the phenolic hydroxyl group was located at the original para-chlorine substituent position, with the chlorine atom migrating to an adjacent position. The detection of this metabolite provides strong evidence for the formation of p,p'-DDE from aromatic oxides...
DDT is metabolized in many mammals primarily through a series of alternating reductive dechlorination and/or dehydrochlorination reactions… The first step produces TDE… or DDE… In rats, DDE is slowly converted in the liver via DDMU (1-chloro-2,2-bis(p-chlorophenyl)ethylene) to DDNU (2,2-bis(p-chlorophenyl)ethylene)… Further metabolism of 2,2-bis(p-chlorophenyl)ethylene appears to occur primarily in the kidneys… producing DDCHO (2,2-bis(p-chlorophenyl)acetaldehyde)… or DDA (2,2-bis(p-chlorophenyl)acetic acid)…
DDE can be converted to 2,2-bis(p-chlorophenyl)ethylene via dehydrochlorination, or via a series of redox reactions of the corresponding ethylene analogues; thereafter, it follows the DDOH to DDA metabolic pathway. This metabolic process is slow, which explains the persistence of DDE residues in mammalian adipose tissue.
...DDT...degradation changes.../e.g./dehydrochlorination to DDE...DDT...is reduced and chlorinated in biological systems to DDD. DDD is more unstable than DDT or DDE. DDD dehydrochlorinates 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...dehydrochlorinates to 2,2-bis(bis(p-chlorophenyl)ethylene...2,2-bis-(p-chlorophenyl)ethylene; reduced to 1,1-bis-(p-chlorophenyl)ethane...finally oxidized to bis(p-chlorophenyl)acetic acid...bis(p-chlorophenyl)acetic acid.
More metabolism/metabolism of DDE (9 metabolites in total) For complete data, please visit the HSDB record page. DDE is absorbed in the stomach and intestines, enters the lymphatic system, and is transported throughout the body, eventually integrating into adipose tissue. DDE is primarily metabolized by cytochrome P-450 enzymes in the liver and kidneys. Its metabolite, mainly DDA (bis(p-chlorophenyl)acetic acid), is excreted in the urine. (L85)

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Biological Half-Life
DDE is slowly eliminated from the human body, with a biological half-life of approximately 8 years.
A comparison of the accumulation and depletion of DDT and methoxydiphenyltriglyceride in sheep diets at a dose of 250 ppm revealed that the latter had a residual amount of at least… The elimination half-life of methoxydiphenyltriglyceride in sheep was calculated to be 10 days; while the elimination half-lives of DDT, DDD, and DDE were 90 days, 26 days, and 223 days, respectively.

Toxicity Summary
DDE toxicity occurs through at least four mechanisms, possibly all simultaneously. DDE reduces transmembrane potassium transport. DDE inhibits the inactivation of voltage-gated sodium channels. These channels are normally activated (open) but inactivate (close) slowly, interfering with the active transport of sodium ions out of nerve axons during repolarization, leading to neuronal hyperexcitability. DDE inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase and Ca2+-ATPase, which play crucial roles in neuronal repolarization. DDE also inhibits the ability of calmodulin (a calcium mediator) in neurons to transport calcium ions, which are essential for neurotransmitter release. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to weak stimuli that would not elicit a response in fully depolarized neurons. DDE is also thought to have adverse effects on the reproductive system by mimicking endogenous hormones and binding to estrogen and androgen receptors. (T10, L85)

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Interaction
.... This study investigated the effects of perinatal exposure to 1,4-dichlorobenzene (DCB) and p,p'-DDE on the reproductive system of adult female rat offspring. These female rats were exposed to 25 ppm DCB (approximately 2 mg/kg) during pregnancy and 125 ppm p,p'-DDE (approximately 10 mg/kg) during lactation. The results showed that female rat offspring exposed to DCB and/or p,p'-DDE maternally reached full sexual maturity. The combined effect of DCB and p,p'-DDE was observed, with ovarian weight in mature female offspring decreasing to approximately 80% of that in control rats after perinatal exposure to DCB and p,p'-DDE. This change may lead to reproductive dysfunction in mature female offspring…
Even 10 micrograms of DDT (a mixture of DDT and DDE) per gram of fat enhanced the metabolism of pentobarbital in rats.
Bovine liver is susceptible to microsomal enzyme induction; treatment of cattle with barbiturates has been shown to accelerate the metabolic clearance of DDE.
In quail, long-term administration of DDE effectively inhibits the metabolism of pentobarbital.
For more complete data on DDE interactions (14 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats: 880 mg/kg
Oral LD50 in mice: 700 mg/kg

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

According to an independent committee of scientific and health experts, DDE (dichlorodiphenyl dichloroethylene) may be carcinogenic. According to the U.S. Environmental Protection Agency (EPA), it may cause developmental toxicity and male reproductive toxicity. P,p'-DDE is a white crystalline solid or white powder. (NTP, 1992) DDE is a chlorophenylethylene compound with an ethylene molecule having two 4-chlorophenyl atoms substituted at position 1 and two chlorine atoms substituted at position 2. It is a persistent organic pollutant and a human exogenous metabolite. It belongs to the monochlorobenzene and chlorophenylethylene groups. 1,1-Dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) is a degradation product of DDT, which was once used as an insecticide. Currently, there is no information on the acute (short-term) or chronic (long-term) effects of DDE. Acute oral administration of high doses of DDT in humans can cause damage to the central nervous system (CNS), such as headache, nausea, and convulsions. Epidemiological studies have found that the only symptom affecting workers exposed to DDT and other pesticides is elevated liver enzyme activity. Animal studies have shown that long-term oral DDT can affect the liver, immune system, and central nervous system. The relationship between DDE and cancer is currently inconclusive. Animal studies have shown that oral DDE increases the incidence of liver tumors in mice and hamsters, and increases the incidence of thyroid tumors in female rats. The U.S. Environmental Protection Agency (EPA) has classified DDE as a Group B2 carcinogen, meaning it is a possible human carcinogen. p,p'-DDE has been reported in Euglena gracilis, and relevant data are available. p,p'-DDE is an isomer of dichlorodiphenyl dichloroethylene (an organochlorine pesticide) and is also a component of commercial DDT mixtures. DDT was once a widely used pesticide, but due to its toxicity and bioaccumulation, it is now banned globally for use in agriculture. However, it still has limited applications in disease vector control. (L84)
DDT is an organochlorine pesticide and is an ethylene metabolite of DDT.

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Mechanism of Action
We tested the ability of eight chlorinated hydrocarbons to competitively bind to specific binding proteins in the cytoplasm of immature rat uterine cells with (3)H-estradiol-17β. o,p'-DDE (0.14 mmol) competitively bound to the "8S receptor" in the uterine cytoplasm with (3)H-estradiol-17β, while p,p'-DDE and p,p'-DDT did not. o,p'-DDT and o,p'-DDE exhibit estrogenic activity at high concentrations, as evidenced by their ability to competitively bind to estradiol-17β receptors in the uterine cytoplasm, thereby inhibiting the transport and binding of estradiol to the uterine cell nucleus. In duck breeds sensitive to the eggshell thinning effect of DDE, the addition of 40 mg/kg DDE to the diet for 45 consecutive days resulted in a 13% decrease in eggshell index (EI) and a 36% decrease in calcium content in the shell gland fluid, while increasing the calcium content in the shell gland mucosa by 19%, compared to the control group. DDE inhibited calcium transport (secretion) between the gland mucosa and the uterine cavity. ATP-dependent calcium binding to the microsomal subfraction (FI), rich in plasma membrane fragments, decreased by 16%, while binding to the highly calcium-binding subfraction FIII decreased by 36%. DDE may interfere with the stimulation-secretion mechanism of duck shell glands by affecting calcium binding. In vitro experiments showed that DDE at concentrations of 2 to 16 ng/L could, in a concentration-dependent manner, inhibit Ca(2+)-Mg(2+)-activated ATPase in duck (Anas platyrhynchos) shell gland homogenate, while Mg(2+)-activated ATPase was unaffected by these concentrations. Because calcium ions are transported against their concentration gradient between the plasma and the shell gland lumen, it is hypothesized that DDE reduces calcium ion transport on the shell gland mucosa by inhibiting Ca²⁺-Mg²⁺-activated ATPase. As for the mechanism of eggshell thinning, there is currently no fully or universally accepted explanation. Many reports claim that DDT, DDE, and certain derivatives inhibit carbonic anhydrase (which plays an important role in eggshell formation), but many others deny this. Therefore, we are left with only two explanations for this phenomenon: 1) carbonic anhydrase in bird shell glands is abnormally sensitive to chlorinated hydrocarbon pesticides; or 2) the observed in vivo inhibition is caused by other factors, such as reduced enzyme production or the production of substances that inhibit enzyme activity. For more complete data on the mechanisms of action of DDEs (6 in 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.)