Absorption, Distribution and Excretion
In chronic feeding experiments DDD, like DDT, is stored in body fat, but it is mobilized and excreted faster than DDT when a normal diet is resumed.
Sheep were orally dosed for 28 consecutive days with ... DDD ... DDE appeared as a metabolite of DDD ... in fat. ... DDD showed 2 maxima /in blood; one occurring/ at 8 hr and /the other at/ 32 hr after dosing.
Tetrachlorodiphenyl ethane (p,p-DDD) ... was found in urine of New Zealand red rabbits ... exposed to cigarette smoke containing labeled TDE. In fat, vital organs, and other tissues, tetrachlorodiphenyl ethane and TDEE were found.
DDD was quantified in specimens of maternal blood, placenta, and umbilical cord blood from women experiencing stillbirth and live birth. Specimens of stillbirth cases had higher organochlorine insecticide contents as compared to matched controls.
For more Absorption, Distribution and Excretion (Complete) data for DDD (15 total), please visit the HSDB record page.

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Metabolism / Metabolites
In pigeons (Columba liva) ... feeding of DDD ... /gave/ rise to small residues of DDE. The DDD was rapidly metabolized exclusively to 2,2-bis(p-chlorophenyl-1-chloroethylene.
... DDD ... in peanut oil ... was injected into fertile leghorn eggs or fed in the diet to chicks hatched from untreated eggs. No significant differences ... between two treatments were observed. ... p,p'-DDD gave rise to o,p'-DDD, 2,2-bis(p-chlorophenyl)-1-chloroethylene (DDMU), 2,2-bis(p-chlorophenyl)-1-chloroethane (DDMS), 2,2-bis(p-chlorophenyl)ethylene (DDNU), 2,2-bis(p-chlorophenyl)ethanol (DDOH), bis(p-chlorophenyl)-acetic acid (DDA), DDM, and dichlorobenzophenone (DBP).
The mexican bean beetle, Epilachna varivestis muls, contained DDT-dehydrochlorinase activity in its tissues and was able to dehydrochlorinate DDD.
After ingestion of ... DDD by adult volunteers, bis(p-chlorophenyl)-acetic acid (DDA) was excreted in urine ... DDD readily degrades ... through a series of intermediates to DDA and is rarely found as a stored metabolite in the general population.
For more Metabolism/Metabolites (Complete) data for DDD (15 total), please visit the HSDB record page.
DDD 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. (L85)

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Biological Half-Life
...The t/2 of elimination of methoxychlor in sheep was calculated to be 10 days; /while the values for/ DDT, DDD, and DDE ... were 90, 26, & 223 days, /respectively/.

Toxicity Summary
DDD 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. (T10, L85)

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Toxicity Data
LD50: 113 mg/kg (Oral, Rat) (L138)

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Interactions
... At a dosage of 50 mg/kg/day for 14 days, o,p'-DDD caused a gradually progressive hypotensive failure in dogs injected with epinepherine or norepinepherine, while leaving unchanged the cardioaccelerator and immediate pressor response of these drugs. The hypotensive failure was associated with weakening of the contractile force of the heart and with a reduction in plasma volume. The latter may have been caused by loss of fluid from the intravascular compartment and was not caused by release of histamine. The hypotensive state could be prevented to a significant degree by pretreatment with prednisolone.
If cortisol is taken ... DDD ... increased the formation of hydroxylated metabolites, and cause changes in patterns of excretion from glucuronides to other conjugates. ... With testosterone, DDD again gives rise to increased formation of hydroxylated metabolites ...

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Non-Human Toxicity Values
LD50 Rat percutaneous >10,000 mg/kg
LD50 Mouse oral 1466 mg/kg
LD50 Rat oral 113 mg/kg
LD50 Rat oral 3,400 mg/kg
LD50 Rabbit dermal 1,200 mg/kg

[1]. Conversion of p,p' -DDT to p,p' -DDD by intestinal flora of the rat. Science. 1966;151(3717):1527-1528.

[2]. Cytogenetic status of human lymphocytes after exposure to low concentrations of p,p'-DDT, and its metabolites (p,p'-DDE, and p,p'-DDD) in vitro. Chemosphere. 2012;87(11):1288-1294.

DDD (Dichlorodiphenyldichloroethane) can cause cancer according to an independent committee of scientific and health experts.
Dichlorodiphenyldichloroethane appears as a colorless crystalline solid. Insoluble in water and sinks in water. Toxic by inhalation, skin absorption or ingestion. Used as a pesticide.
DDD is a chlorophenylethane that is 2,2-bis(p-chlorophenyl)ethane substituted by two chloro groups at position 1. It is a metabolite of the organochlorine insecticide, DDT. It has a role as a xenobiotic metabolite. It is an organochlorine insecticide, a member of monochlorobenzenes and a chlorophenylethane.
DDD, P,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. (L84)
An organochlorine insecticide that is slightly irritating to the skin. (From Merck Index, 11th ed, p482)

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Mechanism of Action
... Following ... dosage of (60 mg/kg, iv), all of the isomers of TDE inhibited ACTH-induced steroid production in the dog, but the inhibition reached 50% of the control only 27 min after dosing with the m,p'-isomer compared with 87 min with the o,p'-isomer and 4-18 hr with the p,p'-isomer. There was marked temporal correlation between the percentage inhibition of adrenocorticotropic hormone (ACTH)-induced steroid production, the disruption of normal cellular structure of the fascicular and reticular zones of the adrenal cortex, and the severity of the damage to mitochondria in these zones caused by the three isomers.
In this study, we determined whether the DDT isomers p,p'-DDT [1,1,1,-trichloro-2,2-bis(p-chlorophenyl)ethane], o,p'-DDT [1,1,1-trichloro-2(p-chlorophenyl)-2-(o-chlorophenyl)ethane], and their metabolites p,p'-DDD [1,1-dichloro-2,2-bis(p-chlorophenyl)ethane], o,p'-DDD [1,1-dichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl)ethane], p,p'-DDE [1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene], o,p'-DDE [1,1-dichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl)ethylene], and p,p'-DDA [2,2-bis(p-chlorophenyl)acetic acid], could bind to and transcriptionally activate the human estrogen receptor (hER). Novel results from competitive binding assays showed that o,p'-DDD, o,p'-DDE, and p,p'-DDT, as well as the established environmental estrogen o,p'-DDT, were able to bind specifically to the hER with approximately 1000-fold weaker affinities for the hER than that of estradiol. In contrast, only o,p'-DDT, but not p,p'-DDT, bound to the rat estrogen receptor. Moreover, two yeast expression-reporter systems, constructed to test if the DDT isomers and metabolites could transcriptionally activate the hER, demonstrated that an o,p'-DDT metabolite could transactivate the hER or LexA-hER fusion protein with just a 140- to 300-fold weaker potency than that of estradiol. The DDT isomers and metabolites that bound the hER in vitro triggered estrogen receptor-mediated transcription of the lacZ reporter gene in the yeast systems. Furthermore, the DDT isomers and metabolites that transactivated the hER elicited an additive response when given together or with estradiol. The DDT isomers and metabolites that triggered transcription of the yeast expression-reporter systems also stimulated two estrogenic endpoints in estrogen-responsive MCF-7 cells: the induction of the progesterone receptor and the down-regulation of the hER. Thus, in MCF-7 cells and in yeast expression-reporter systems, certain DDT isomers and metabolites act directly as agonists and transactivate the hER at concentrations found in human tissues.
Using a combination of in vitro assays we have evaluated whether DDT metabolites can interact with the progesterone receptor pathway in yeast expressing human progesterone receptor (hPR) and in T47D human breast cancer cells which express endogenous hPR. In transactivation assays using both yeast and T47D cells, o,p'-DDT and the metabolites p,p'-DDT, o,p'-DDD, p,p'-DDD, o,p'-DDE, p,p'-DDE, p,p'-DDA, and DDOH inhibited progesterone-induced reporter gene activity in a dose-dependent manner. None of the DDT metabolites functioned as hPR agonists. Whole cell competition binding assays using T47D cells indicated that the inhibitory effects of DDT metabolites on progesterone-dependent activites may occur through both hPR-dependent and hPR-independent pathways. Our results and previous reports of DDT metabolites interacting with estrogen and androgen receptors suggests that this class of environmental chemicals may interact with numerous hormone receptor signaling pathways.
The mechanisms of action of o,p'-DDD on adrenal steroidogenesis were investigated in vitro in rainbow trout (Oncorhynchus mykiss). Acute exposures to o,p'-DDD inhibited ACTH-stimulated cortisol secretion while cell viability decreased significantly only at the highest concentration tested (200 microM o,p'-DDD). Stimulation of cortisol secretion with a cAMP analogue (dibutyryl-cAMP) was inhibited at a higher concentration than that needed to inhibit ACTH-stimulated cortisol synthesis in cells exposed to o,p'-DDD. Forskolin-stimulated cortisol secretion and cAMP production, and NaF-stimulated cAMP production were inhibited in a concentration-dependent manner by o,p'-DDD. In contrast, basal cortisol secretion was stimulated while basal cAMP production was unaffected by o,p'-DDD. Pregnenolone-stimulated cortisol secretion was enhanced by o,p'-DDD at a physiologically relevant pregnenolone concentration, while o,p'-DDD inhibited cortisol secretion when a pharmacological concentration of pregnenolone was used. /These/ results suggest that the cAMP generation step is a target in o,p'-DDD-mediated disruption of ACTH-stimulated adrenal steroidogenesis in rainbow trout but that other downstream targets such as steroidogenic enzymes responsible for cortisol synthesis might also be affected.

C14H10CL4

320.034

317.953

72-54-8

p,p'-DDD-d8;93952-20-6

6294

White to off-white solid powder

1.4±0.1 g/cm3

405.7±40.0 °C at 760 mmHg

94-96 °C

199.3±24.7 °C

0.0±0.9 mmHg at 25°C

1.599

5.39

0

0

0

3

18

218

0

AHJKRLASYNVKDZ-UHFFFAOYSA-N

InChI=1S/C14H10Cl4/c15-11-5-1-9(2-6-11)13(14(17)18)10-3-7-12(16)8-4-10/h1-8,13-14H

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

Rothane; Dilene; TDE

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中（例如氮气保护），避免吸湿/受潮和光照。

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 (~312.46 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (7.81 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
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