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

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

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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