Absorption, Distribution and Excretion
Male rats were orally administered corn oil containing 100 mg/kg body weight/day of DBDPE or BDE-209 for 90 consecutive days. The levels of DBDPE and BDE-209 in liver, kidney, and adipose tissue were then measured. Simultaneously, biochemical indicators, including thyroid hormone levels, 13 clinical chemistry indicators, and the mRNA expression levels of certain enzymes were monitored. Results showed that DBDPE was detected in all tissues, at concentrations 3-5 orders of magnitude lower than that of BDE-209.
/MILK/ We tested 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). The samples tested were paired human maternal serum (n = 102) and breast milk (n = 105) collected in Sherbrooke, Canada in 2008–2009. This study also included a comparison of three traditional brominated flame retardants: decabromobiphenyl (BB-209), 2,2',4,4',5,5'-hexabromobiphenyl (BB-153), and 2,2',4,4',5,5'-hexabromodiphenyl ether (BDE-153). The detection rates of TBB, BB-153, and BDE-153 were all above 55% in serum and milk samples. After lipid weight (lw) correction, the median concentrations (ng g⁻¹ lw) of these three substances 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. The detection frequencies of other brominated flame retardants (BFRs) in serum and breast milk were as follows: TBPH 16.7% and 32.4%, BTBPE 3.9% and 0.0%, BB-209 2.0% and 0.0%, OBIND 9.8% and 1.0%, and DBDPE 5.9% and 8.6%. The ratio of TBB to the sum of TBB and TBPH in serum (fTBB) (0.23) was lower than that in breast milk (0.46), indicating that TBB is more likely to redistribute from blood to breast milk than TBPH. Overall, these data confirm the presence of non-polybrominated diphenyl ether brominated flame retardants in the human body and highlight the need for a better understanding of their sources, exposure pathways, and potential human health effects. Decabromodiphenyl ethane (DBDPE), an alternative to decabromodiphenyl ether (deca-BDE), was investigated in captive Chinese alligators in this study. DBDPE was detected in adult tissues, newborn juveniles, and eggs of the Chinese alligator, with concentrations ranging from 4.74–192 ng g(⁻¹) fat weight, 0.24–1.94 ng g(⁻¹) fat weight, and 0.01–0.51 ng g(⁻¹) fat weight, respectively. The level of DBDPE contamination in Chinese alligators was lower than that in newborn juveniles and eggs. Furthermore, the concentration of DBDPE in the muscle of adult Chinese alligators was one to three orders of magnitude higher than that in newborn juveniles and eggs, indicating a limited potential for maternal transfer of DBDPE in Chinese alligators. …
Researchers collected hen muscle, eggs, and tissues (muscle and liver) from an e-waste recycling plant in southern China. They investigated the maternal transfer, potential metabolism, and tissue distribution of several halogenated flame retardants (HFRs) during egg formation and chicken embryo development. The composition of contaminants changed significantly from hen muscle to eggs, and then from eggs to newborn chick tissues. Compared to low-halogenated compounds, high-halogenated compounds, such as octabromo-decabromodiphenyl ether (PBDE) homologues, decabromobiphenyl (PBB209), and decachlorobiphenyl (DP), are less likely to be transferred into eggs. During embryonic development, PBDEs are most readily metabolized, while decabromobiphenyl ethane (DBDPE) is metabolized the least. The authors also observed selective maternal transfer of trans-DP during chicken embryonic development, while cis-DP exhibits stereoselective metabolism. During tissue development, except for DBDPE, the liver has a higher affinity for chemicals with high octanol-water partition coefficients than muscle. Differences in the metabolic potential of different chemicals in chicken embryos lead to variations in contaminant composition. Halogenated flame retardants exhibiting maternal transfer and tissue distribution also show chemical specificity, especially DBDPE. The content of DBDPE increases throughout the entire process from hen muscle to egg and from egg to chick tissue. …
The widespread use of polybrominated diphenyl ethers (PBDEs) and decabromodiphenyl ethane (DBDPEs) has made them ubiquitous pollutants in the abiotic environment, but data on their bioavailability to benthic organisms are scarce. This study assessed the bioaccumulation potential of PBDEs and DBDPEs in the field-collected sediments of the oligochaete Lumbriculus variegatus using a 49-day exposure study (including a 28-day absorption period and a 21-day elimination period). All PBDEs and DBDPEs were bioavailable to earthworms, with bioaccumulation factors (BSAFs) ranging from 0.0210 g organic carbon/g lipids to 4.09 g organic carbon/g lipids. However, the bioavailability of the high-brominated compounds (BDE-209 and DBDPEs) was lower compared to other PBDEs, as evidenced by their relatively low free dissolved concentrations (C(free)) determined by solid-phase microextraction. The negative correlation between bioaccumulation factors (BSAFs) and hydrophobicity can be explained by their absorption rate constant (k(s)) and elimination rate constant (k(e)). The ke values of PBDEs did not change significantly, while the ks values decreased significantly with increasing chemohydrophobicity. The differences in the bioaccumulation kinetics of brominated flame retardants in fish and worms can be attributed to their physiological differences and the presence of multiple elimination pathways. A 28-day bioaccumulation assay for estimating BSAFs of PBDEs and DBDPE has been validated. Furthermore, C(free) has proven to be a good indicator of bioavailability. At least seven unknown compounds were observed in rats exposed to DBDPE, indicating that DBDPE underwent biotransformation in rats. These compounds were identified by comparing the relative retention times and full-scan mass spectra of DBDPE debromination products in a photodegradation assay, and by GC/EI-MS and GC/ECNI-MS analysis. The results showed that the debromination of DBDPE to generate low-brominated BDPE was not the major metabolic pathway observed in rats. Using GC/EI-MS, two metabolites were preliminarily identified as MeSO(2)-nona-BDPE and EtSO(2)-nona-BDPE, but their structures require further confirmation using other techniques and standards. Furthermore, the evidence for the biological responses of rats to DBDPE and BDE-209 and their metabolites differed. This study evaluated and compared the oxidative and reductive biotransformations of brominated flame retardants (including known polybrominated diphenyl ethers (PBDEs) and the emerging decabromodiphenyl ethane (DBDPE)) using an in vitro system based on liver microsomes from various Arctic marine mammals (polar bear (Ursus maritimus), beluga whale (Delphinapterus leucas), and ringed seal (Pusa hispida)) and laboratory rats as the mammalian model species. Compared to low-brominated polybrominated diphenyl ethers (BDE 99, 100, and 154; 0–3% at 30 pmol), the consumption of fully brominated BDE209 (14–25% at 30 pmol) and DBDPE (44–74% at 90 pmol) was significantly higher in individuals across all species. No simple debrominated metabolites were observed. Studies of phenolic metabolites in rats and polar bears revealed the formation of two phenolic compounds, likely polybrominated DBDPE metabolites, in polar bears; and one phenolic compound, the BDE154 metabolite, in the microsomes of both polar bears and rats. Despite the large consumption of parent compounds, the observed concentrations of BDE209 and DBDPE metabolites were very low or even undetectable. These findings suggest that the burden of total BDE209 and its transformation products in ecosystems may be underestimated, thus necessitating further research to identify and characterize the persistence and toxicity of major BDE209 metabolites. Given the similarities between DBDPE and BDE209 in physicochemical properties and environmental behavior, existing evidence of biotransformation, and the increasing use of DBDPE as a substitute for BDE209, similar concerns may also exist regarding DBDPE.

Toxicity Summary
Identification and Uses: Decabromodiphenyl ethane (DBDPE) was once used as a substitute for decabromodiphenyl ether (BDE-209), and therefore its current uses are largely the same as BDE-209, such as in the manufacture of plastics (including polyester and vinyl ester resins) and rubber products, as well as various applications related to textile and leather manufacturing. This compound is also present in polymers used in electronic and electrical applications. DBDPE is also used in adhesives and sealants. Human Studies: In in vitro HepG2 cell assays, DBDPE exhibited cytotoxicity, antiproliferative activity, and was associated with apoptosis and excessive production of reactive oxygen species. Animal Studies: Male rats were orally administered 100 mg/kg DBDPE for 90 days. Results showed that DBDPE was detected in all tissues. At least seven unknown compounds were detected in rats exposed to DBDPE, indicating that DBDPE underwent biotransformation in rats. In mice treated with DBDPE for 30 days, the high-dose group showed significantly elevated levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Blood glucose levels in all treatment groups were higher than in the control group. Levels of thyroid-stimulating hormone (TSH), triiodothyronine (T3), and free triiodothyronine (fT3) were also elevated. The high-dose group showed significantly elevated activities of uridine diphosphate glucuronide transferase (UDPGT), 7-pentoxyhalogen O-depentylase (PROD), and ethoxyhalogen O-deethylase (EROD). Histopathological changes in the liver were characterized by hepatocyte hypertrophy and cytoplasmic vacuolation. In rats, DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, and PROD activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzyl ether debenzylate (LBD) activity. No maternal toxicity, developmental toxicity, or teratogenicity was observed in rats or rabbits at DBDPE treatment at doses up to 1250 mg/kg·d. DBDPE did not show genotoxicity in bacterial assays (Ames/Salmonella typhimurium and Escherichia coli WP2 reverse mutation assays), and no chromosomal aberrations were observed in Chinese hamster lung cells. Ecotoxicity studies: In grass carp (Ctenopharyngodon idella), DBDPE exposure significantly downregulated 5 miRNAs and significantly upregulated 36 miRNAs, indicating the potential of miRNAs as biomarkers. Fish hepatocyte assays based on isolated male hepatocyte vitellogenin synthesis and secretion showed a clear dose-response curve in the presence of DBDPE. DBDPE induced hepatic EROD activity at low concentrations but began to inhibit this activity at high concentrations. Furthermore, even at the highest concentrations, hepatocyte-binding UDPGT activity was not inhibited. The decrease in EROD activity led to a decrease in cellular vitellogenin production. In vivo studies showed that DBDPE was acutely toxic to Daphnia davidii, with a 48-hour EC50 of 19 μg/L. Furthermore, DBDPE reduced the hatching rate of exposed zebrafish eggs and significantly increased the mortality rate of hatched fry. Treatment-related effects were observed on the reproduction of E. fetida, the survival rate of Canna indica (C. sativa), and the plant height and dry weight of Lettuce (L. esculentum) and Onion (A. cepa). The most sensitive endpoints were the reduction in Onion plant height and dry weight and the decrease in E. fetida reproductive capacity.

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Non-human toxicity values
Oral LD50 in rats: 5000 mg/kg body weight [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.)