p,p'-DDE
(Synonyms: 2，2-双（4-氯苯基）-1，1-二氯乙烯,4,4'-DDE; p,p'-Dichlorodiphenyldichloroethylene) 目录号 : GC44527
A metabolite and degradation product of the pesticide DDT
Cas No.:72-55-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
p,p'-DDE is a metabolite and degradation product of the organochlorine pesticide DDT. It accumulates in smallmouth buffalo, channel catfish, and largemouth bass as well as sediment in the Huntsville Spring Branch-Indian Creek tributary system surrounding a DDT manufacturing plant where it is considered a persistent organic pollutant (POP). p,p'-DDE inhibits estrogen binding to rainbow trout estrogen receptors (rtERs) with an IC50 value of 8 µM. It induces concentration-dependent secretion of estradiol by granulosa and theca cell co-cultures isolated from porcine ovarian follicles. p,p'-DDE (50-100 µM) also decreases ATP levels, the proportion of sperm with high mitochondrial membrane potential, and motility of human sperm in vitro.
| Cas No. | 72-55-9 | SDF | |
| 别名 | 2，2-双（4-氯苯基）-1，1-二氯乙烯,4,4'-DDE; p,p'-Dichlorodiphenyldichloroethylene | ||
| Canonical SMILES | ClC1=CC=C(/C(C2=CC=C(Cl)C=C2)=C(Cl)\Cl)C=C1 | ||
| 分子式 | C14H8Cl4 | 分子量 | 318 |
| 溶解度 | DMSO : 100 mg/mL (314.44 mM; Need ultrasonic) | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.1447 mL | 15.7233 mL | 31.4465 mL |
| 5 mM | 0.6289 mL | 3.1447 mL | 6.2893 mL |
| 10 mM | 0.3145 mL | 1.5723 mL | 3.1447 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Temporal and latitudinal trends of p,p'-DDE in eggs and carcasses of North American birds from 1980 to 2005
Environ Toxicol Chem 2016 Jun;35(6):1340-8.PMID:26753749DOI:10.1002/etc.3360.
The use of 1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane (DDT) in agriculture in the United States and Canada was prohibited in the early 1970s; however, it continued to be used restrictively in Mexico until 2000. Forty years later, 1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene (p,p'-DDE), continues to be detected in eggs and bird carcasses in North America. The use of DDE has been associated with reproductive failure of several avian species, primarily through eggshell thinning. To assess the temporal and latitudinal distribution of p,p'-DDE in North America, the authors examined DDE concentrations reported in bird tissues in the scientific literature published between 1980 and 2009. Overall, the majority of supported models suggested that DDE concentrations in birds were greater in the upper mid-latitudes (38°-48°) than in other parts of North America. However, spatial trends of DDE seemed to be influenced by regions with large amounts of data, such as the Great Lakes area. Concentrations of p,p'-DDE in eggs averaged 2.5 μg/g, 3.2 μg/g, and 29.5 μg/g wet weight in 1980 and decreased to 1.64 μg/g, 0.87 μg/g, and 1.01 μg/g wet weight by the mid-2000s for the central, eastern, and western North America regions, respectively. The results indicate that, over time, all DDE residues observed in birds have decreased significantly in North America. Environ Toxicol Chem 2016;35:1340-1348. © 2016 SETAC.
Association between Exposure to p,p'-DDT and Its Metabolite p,p'-DDE with Obesity: Integrated Systematic Review and Meta-Analysis
Environ Health Perspect 2017 Sep 18;125(9):096002.PMID:28934091DOI:10.1289/EHP527.
Background: The prevalence of obesity is increasing in all countries, becoming a substantial public health concern worldwide. Increasing evidence has associated obesity with persistent pollutants such as the pesticide DDT and its metabolite p,p'-DDE. Objectives: Our objective was to systematically review the literature on the association between exposure to the pesticide DDT and its metabolites and obesity to develop hazard identification conclusions. Methods: We applied a systematic review-based strategy to identify and integrate evidence from epidemiological, in vivo, and in vitro studies. The evidence from prospective epidemiological studies was quantitatively synthesized by meta-analysis. We rated the body of evidence and integrated the streams of evidence to systematically develop hazard identification conclusions. Results: We identified seven epidemiological studies reporting prospective associations between exposure to p,p'-DDE and adiposity assessed by body mass index (BMI) z-score. The results from the meta-analysis revealed positive associations between exposure to p,p'-DDE and BMI z-score (β=0.13 BMI z-score (95% CI: 0.01, 0.25) per log increase of p,p'-DDE). Two studies constituted the primary in vivo evidence. Both studies reported positive associations between exposure to p,p'-DDT and increased adiposity in rodents. We identified 19 in vivo studies and 7 in vitro studies that supported the biological plausibility of the obesogenic effects of p,p'-DDT and p,p'-DDE. Conclusions: We classified p,p'-DDT and p,p'-DDE as "presumed" to be obesogenic for humans, based on a moderate level of primary human evidence, a moderate level of primary in vivo evidence, and a moderate level of supporting evidence from in vivo and in vitro studies. https://doi.org/10.1289/EHP527.
DDE-induced eggshell thinning in birds: effects of p,p'-DDE on the calcium and prostaglandin metabolism of the eggshell gland
Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 1997 Oct;118(2):113-28.PMID:9490182DOI:10.1016/s0742-8413(97)00105-9.
1. The focus of this review is the effects and mechanism of action of p,p'-DDE on eggshell formation in birds. Inhibition of prostaglandin synthesis in the eggshell gland mucosa is a probable mechanism for p,p'-DDE-induced eggshell thinning. 2. The duck is sensitive to p,p'-DDE-induced eggshell thinning but the domestic fowl is not, and studies comparing the two species in regard to the calcium and prostaglandin metabolism of the eggshell gland have shown that eggshell thinning induced by p,p'-DDE in ducks is accompanied by reduced activity of prostaglandin synthetase, reduced levels of prostaglandin E2, and reduced uptake of 45Ca by the eggshell gland mucosa. The content of calcium, bicarbonate, chloride, sodium, and potassium are also reduced in the eggshell gland lumen in ducks exhibiting eggshell thinning. None of these effects are seen in the domestic fowl. 3. Inhibition of prostaglandin synthesis is a specific effect of p,p'-DDE. The detrimental effects of p,p'-DDE on the eggshell gland seem to be unique when comparing the compound with structurally related substances, i.e., similar treatment regimens with o,p'-DDE, p,p'-DDT, o,p'-DDT, and p,p'-DDD do not cause eggshell thinning in ducks. Neither do they inhibit prostaglandin synthesis in the eggshell gland mucosa. 4. Administration of other compounds that do inhibit prostaglandin synthesis, e.g., indomethacin, does cause the same effects as those seen with p,p'-DDE, i.e., eggshell thinning and the described effects on the calcium and prostaglandin metabolism of the eggshell gland.
Unravelling the Effect of p,p'-Dichlorodiphenyldichloroethylene (DDE) in Hypertension of Wistar Rats
J Agric Food Chem 2018 Dec 5;66(48):12847-12854.PMID:30415545DOI:10.1021/acs.jafc.8b05001.
Hypertension is a multifactorial disease with limited knowledge of the involved mechanisms. p,p'-DDE ( p,p'-dichlorodiphenyldichloroethylene) is a pollutant commonly found in tissues that interferes with endocrine signaling. This study aimed to evaluate the mechanism of hypertension triggered by p,p'-DDE exposure in the presence or absence of a HF (high-fat) diet in rats. The renin-angiotensin system (RAS) was evaluated by qPCR in liver and adipose tissue (AT), and a transcriptome analysis comparing visceral AT of HF diet and HF/DDE groups was performed. HF diet influenced RAS, but the p,p'-DDE effect was more evident in liver than in AT (interaction between the diet and p,p'-DDE treatment affected aldosterone receptor and angiotensin converting enzyme 2 expression in liver, p < 0.05, two-way ANOVA). p,p'-DDE induced a decrease in the expression of genes involved in the retinoid acid biosynthesis pathway (Crabp1; -2.07-fold; p = 0.018), eNOS activation (Nos1; -1.64-fold; p = 0.012), and regulation and urea cycle (Ass1; -2.07-fold; p = 0.02). This study suggested that p,p'-DDE may play a fundamental role in the pathogenesis of hypertension, not exclusively in RAS but also by induction of hyperuricemia and increased oxidative stress, which may lead to endoplasmic reticulum stress and vascular injury.
Metabolic effects of p,p'-DDE on Atlantic salmon hepatocytes
J Appl Toxicol 2018 Apr;38(4):489-503.PMID:29148584DOI:10.1002/jat.3556.
Decades after being banned in many countries, DDT and its metabolites are still considered major environmental hazards. The p,p'-DDE isomer, the DDT metabolite found in highest concentration in aquaculture feeds, is an endocrine disruptor with demonstrated ability to induce epigenetic effects. This study aimed at examining the impact of p,p'-DDE on Atlantic salmon. Primary hepatocytes were exposed to four concentrations of p,p'-DDE (0.1, 1, 10, 100 μm) for 48 hours, and endpoints included cytotoxicity, global DNA methylation, targeted transcription and metabolomics profiling (100 μm). p,p'-DDE was moderately cytotoxic at 100 μm. No impact was seen on global DNA methylation. Vtg1 and esr1 transcription, markers of endocrine disruption, was most strongly induced at 10 μm p,p'-DDE, while ar showed strongest response at 100 μm. Metabolomics profiling showed that p,p'-DDE at 100 μm most strongly affected carbohydrate metabolism, primary bile acid metabolism, leucine, isoleucine and valine metabolism, diacylglycerol and sphingolipid metabolism. Observed changes in lipid levels suggest that p,p'-DDE interferes with phospholipid membrane biosynthesis. Elevation of bile acid levels in p,p'-DDE-exposed hepatocytes indicates upregulation of synthesis of bile acids after cytochrome P450 activation. Pathway analysis showed that the superpathway of methionine degradation was the most significantly affected pathway by p,p'-DDE exposure, while endocrine system disorder topped the diseases and disorder ranking. In conclusion, this work predicts an endocrine response to p,p'-DDE exposure, and demonstrates how this legacy pesticide might interfere with mechanisms linked to DNA methylation in Atlantic salmon hepatocytes.