Decabromodiphenyl ethane   中文名称: 十溴二苯乙烷

Absorption, Distribution and Excretion
Male rats were orally administrated with corn oil containing 100 mg/kg bw/day of DBDPE or BDE-209 for 90 days, after which the levels of DBDPE and BDE-209 in the liver, kidney, and adipose were measured. Biochemical parameters, including thyroid hormone levels, 13 clinical chemistry parameters, and the mRNA expression levels of certain enzymes were also monitored. Results showed DBDPE was found in all tissues with concentrations 3-5 orders of magnitude lower than BDE-209.
/MILK/ We have examined several emerging brominated flame retardants (BFRs) including 2-ethyl-1-hexyl-2,3,4,5-tetrabromobenzoate (TBB), bis(2-ethylhexyl) tetrabromophthalate (TBPH), 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE), 4,5,6,7-tetrabromo-1,1,3-trimethyl-3-(2,3,4,5-tetrabromophenyl)-indane (OBIND), and decabromodiphenyl ethane (DBDPE) in paired human maternal serum (n = 102) and breast milk (n = 105) collected in 2008-2009 in the Sherbrooke region in Canada. Three legacy BFRs were also included in the study for comparison: decabromobiphenyl (BB-209), 2,2',4,4',5,5'-hexabromobiphenyl (BB-153), and 2,2',4,4',5,5'-hexabromodiphenyl ethers (BDE-153). TBB, BB-153, and BDE-153 had detection frequencies greater than 55% in both serum and milk samples. Their lipid weight (lw) adjusted median concentrations (ng g(-1) lw) in serum and milk were 1.6 and 0.41 for TBB, 0.48 and 0.31 for BB-153, and 1.5 and 4.4 for BDE-153, respectively. The detection frequencies for the other BFRs measured in serum and milk were 16.7% and 32.4% for TBPH, 3.9% and 0.0% for BTBPE, 2.0% and 0.0% for BB-209, 9.8% and 1.0% for OBIND, and 5.9% and 8.6% for DBDPE. The ratio of TBB over the sum of TBB and TBPH (fTBB) in serum (0.23) was lower than that in milk (0.46), indicating TBB has a larger tendency than TBPH to be redistributed from blood to milk. Overall, these data confirm the presence of non-PBDE BFRs in humans, and the need to better understand their sources, routes of exposure, and potential human health effects
Decabromodiphenyl ethane (DBDPE), a replacement for decabromodiphenyl ether (deca-BDE), was investigated in captive Chinese alligators from China. DBDPE was detected in adult tissues, neonates and eggs of Chinese alligators with concentrations ranging from 4.74-192, 0.24-1.94, and 0.01-0.51 ng g(-1) lipid weight, respectively. Compared to PBDEs and PCBs, DBDPE contamination was limited in Chinese alligators. Additionally, DBDPE concentrations in adult muscles were one to three orders of magnitude higher than those in neonates and eggs, suggesting the limited maternal transfer potential of DBDPE in Chinese alligators. ...
Hen muscle, eggs, and newborn chick tissues (muscle and liver) were collected from an electronic waste recycling site in southern China. The authors examined the maternal transfer, potential metabolism, and tissue distribution of several halogenated flame retardants (HFRs) during egg formation and chicken embryo development. The pollutant composition changes significantly from hen muscle to eggs and from eggs to tissues of newborn chicks. Higher-halogenated chemicals, such as octa- to deca-polybrominated diphenyl ether (PBDE) congeners, deca-polybrominated biphenyl (PBB209), and dechlorane plus (DP), are less readily transferred to eggs compared with lower-halogenated chemicals. During embryo development, PBDEs are the most likely to be metabolized, whereas decabromodiphenyl ethane (DBDPE) is the least. The authors also observed selective maternal transfer of anti-DP and stereoselective metabolism of syn-DP during chicken embryo development. During tissue development, liver has greater affinity than the muscle for chemcials with a high log octanol-water partition coefficient, with the exception of DBDPE. The differences in metabolism potential of different chemicals in chicken embryos cause pollutant composition alterations. Halogenated flame retardant from maternal transfer and tissue distribution also exhibited chemical specificity, especially for DBDPE. Levels of DBDPE were elevated along with the full process from hen muscle to eggs and from eggs to chick tissues. ...
The extensive use of polybrominated diphenyl ethers (PBDEs) and decabromodiphenyl ethane (DBDPE) has made them widespread contaminants in abiotic environments, but data regarding their bioavailability to benthic organisms are sparse. The bioaccumulation potential of PBDEs and DBDPE from field-collected sediment was evaluated in the oligochaete Lumbriculus variegatus using a 49-d exposure, including a 28-d uptake and a 21-d elimination phase. All PBDEs and DBDPE were bioavailable to the worms with biota-sediment accumulation factors (BSAFs) ranging from 0.0210 g organic carbon/g lipid to 4.09 g organic carbon/g lipid. However, the bioavailability of highly brominated compounds (BDE-209 and DBDPE) was poor compared with that of other PBDEs, and this was confirmed by their relatively low freely dissolved concentrations (C(free)) measured by solid-phase microextraction. The inverse correlation between BSAFs and hydrophobicity was explained by their uptake (k(s)) and elimination (k(e)) rate constants. While ke changed little for PBDEs, ks decreased significantly when chemical hydrophobicity increased. The difference in bioaccumulation kinetics of brominated flame retardants in fish and the worms was explained by their physiological difference and the presence of multiple elimination routes. The appropriateness of 28-d bioaccumulation testing for BSAF estimation was validated for PBDEs and DBDPE. In addition, C(free) was shown to be a good indicator of bioavailability.

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Metabolism / Metabolites
At least seven unknown compounds were observed in the DBDPE-exposed rats, indicating that DBDPE biotransformation occurred in rats. These compounds were identified by comparing relative retention times and full-scan mass spectra of DBDPE debrominated products from a photolytic degradation experiment using GC/EI-MS and GC/ECNI-MS analysis. The results showed that debromination of DBDPE to lower brominated BDPEs were not the primary metabolic pathway observed in rats. Two of the metabolites were proposed tentatively as MeSO(2)-nona-BDPE and EtSO(2)-nona-BDPE using GC/EI-MS, but their structures require further confirmation by other techniques and authentic standards. In addition, evidence of a biological response to DBDPE and BDE-209 and their metabolites in rats are different.
The present study assessed and compared the oxidative and reductive biotransformation of brominated flame retardants, including established polybrominated diphenyl ethers (PBDEs) and emerging decabromodiphenyl ethane (DBDPE) using an in vitro system based on liver microsomes from various arctic marine-feeding mammals: polar bear (Ursus maritimus), beluga whale (Delphinapterus leucas), and ringed seal (Pusa hispida), and in laboratory rat as a mammalian model species. Greater depletion of fully brominated BDE209 (14-25% of 30 pmol) and DBDPE (44-74% of 90 pmol) occurred in individuals from all species relative to depletion of lower brominated PBDEs (BDEs 99, 100, and 154; 0-3% of 30 pmol). No evidence of simply debrominated metabolites was observed. Investigation of phenolic metabolites in rat and polar bear revealed formation of two phenolic, likely multiply debrominated, DBDPE metabolites in polar bear and one phenolic BDE154 metabolite in polar bear and rat microsomes. For BDE209 and DBDPE, observed metabolite concentrations were low to nondetectable, despite substantial parent depletion. These findings suggested possible underestimation of the ecosystem burden of total-BDE209, as well as its transformation products, and a need for research to identify and characterize the persistence and toxicity of major BDE209 metabolites. Similar cause for concern may exist regarding DBDPE, given similarities of physicochemical and environmental behavior to BDE209, current evidence of biotransformation, and increasing use of DBDPE as a replacement for BDE209.

Toxicity Summary
IDENTIFICATION AND USE: Decabromodiphenyl ethane (DBDPE) has been used as a substitute for decabrominated diphenyl ether (BDE-209) and therefore it is currently used in more or less the same applications as BDE-209, such as manufacture of plastics (including polyester and vinyl ester resins) and rubber products, as well as in different applications related to manufacture of textiles and leather. This compound is also found in polymers used for electronic and electrical applications. DBDPE could also be used in adhesives and sealants. HUMAN STUDIES: When tested in vitro in HepG2 cells, DBDPE was cytotoxic with anti-proliferation effect and apoptosis was accompanied with overproduction of reactive oxygen species. ANIMAL STUDIES: Male rats were orally administrated with 100 mg/kg DBDPE for 90 days. Results showed DBDPE was found in all tissues. At least seven unknown compounds were observed in the DBDPE-exposed rats, indicating that DBDPE biotransformation occurred in rats. In mice treated with DBDPE for 30 days the levels of alanine aminotransferase or ALT and aspartate aminotransferase or AST of higher dose treatment groups were markedly increased. Blood glucose levels of treatment groups were higher than those of control group. There was also an induction in TSH, T3, and fT3. Uridinediphosphoglucuronosyltransferase (UDPGT), 7-pentoxyresorufin O-depentylase (PROD), and ethoxyresorufin-O-deethylase (EROD) activities were found to have been increased significantly in the high dose group. Histopathologic liver changes were characterized by hepatocyte hypertrophy and cytoplasmic vacuolization. In rats, DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, PROD activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. No evidence of maternal toxicity, developmental toxicity, or teratogenicity was observed in rats or rabbits treated with DBDPE at dosage levels up to 1,250 mg/kg-day. DBDPE was not genotoxic in bacterial assays (Ames/Salmonella typhimurium and Escherichia coli WP2 reverse mutation assays) and no chromosomal aberrations were reported in Chinese hamster lung cells. ECOTOXICITY STUDIES: In Grass carp (Ctenopharyngodon idella) 5 miRNAs were significantly down-regulated and 36 miRNAs were significantly up-regulated after DBDPE exposure indicating that miRNAs have potential for use as biomarkers. The fish hepatocyte assay, based on the synthesis and secretion of vitellogenin from isolated male liver cells produced a clear dose-response curve in the presence of DBDPE. DBDPE induced the induction of hepatic EROD activity at low test concentrations, but started to inhibit the activity at higher concentrations. Also, the induction of the hepatocyte conjugation activity, UDPGT, was induced with no signs of inhibition even at the highest test concentration. The reduced EROD activity resulted in a drop in the production of vitellogenin by the cells. In vivo tests showed that DBDPE was acutely toxic to water fleas, the 48 hr EC-50 value being 19 ug/L. Moreover, DBDPE reduced the hatching rates of exposed zebra-fish eggs and raised significantly the mortality of hatched larvae. Treatment-related effects were identified for E. fetida reproduction, C. sativa survival, and L. esculentum and A. cepa height and dry weight. The most sensitive endpoints were decreased height and dry weight for A. cepa and decreased reproduction for E. fetida.

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Non-Human Toxicity Values
LD50 Rat oral 5000 mg/kg bw[ECHA; 1,1'-(ethane-1,2-diyl)bis
LD50 Rabbit dermal 2000 mg/kg bw[ECHA; 1,1'-(ethane-1,2-diyl)bis

C14H6BR10

973.24

961.214

84852-53-9

10985889

White powder

2.8±0.1 g/cm3

676.2±50.0 °C at 760 mmHg

345°C

346.6±24.8 °C

0.0±2.0 mmHg at 25°C

1.727

11.09

0

0

0

3

24

352

0

BrC1C(Br)=C(Br)C(CCC2C(Br)=C(Br)C(Br)=C(Br)C=2Br)=C(Br)C=1Br

BZQKBFHEWDPQHD-UHFFFAOYSA-N

InChI=1S/C14H4Br10/c15-5-3(6(16)10(20)13(23)9(5)19)1-2-4-7(17)11(21)14(24)12(22)8(4)18/h1-2H2

1,2,3,4,5-pentabromo-6-[2-(2,3,4,5,6-pentabromophenyl)ethyl]benzene

DeBDethane DBDPE Decabromodiphenyl ethane

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。