Decabromodiphenyl ethane
Based on 1 Customer Validation
Decabromodiphenyl ethane (DBDPE) is a brominated flame retardant. Decabromodiphenyl ethane induces ROS-related cytotoxicity and apoptosis in human hepatoma cells, causes hepatocyte damage through oxidative stress, endoplasmic reticulum stress and decreased CYP3A expression, and accumulates and undergoes biotransformation in animal tissues. Decabromodiphenyl ethane can be used to study the environmental toxicology and biological effects of brominated flame retardants.
For research use only. We do not sell to patients.
- Purity: 98.0%
- CAS No.: 84852-53-9
- Formula: C14H4Br10
- Molecular Weight:971.22
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Decabromodiphenyl ethane (DBDPE) (12.5-100 mg/L; 48 or 72 h) reduces HepG2 cell viability, induces apoptosis, and increases ROS production in a dose- and time-dependent manner. Treatment with NAC decreases DBDPE-induced ROS levels and restores cell viability[3].
Exposure to decabromodiphenyl reduces the viability of L-02 hepatocytes, induces LDH release and apoptosis, increases ROS levels, elevates MDA levels, decreases GSH content, reduces SOD activity, lowers mitochondrial membrane potential, and alters the expression of endoplasmic reticulum stress-related proteins such as PERK and IRE-1α[4]
Decabromodiphenyl ethane (50 μM; 24 h) induces oxidative stress in L-02 cells, which is characterized by increased levels of ROS and MDA, as well as decreased GSH content, SOD activity and mitochondrial membrane potential; pretreatment with NAC alleviates the above changes.
Decabromodiphenyl ethane (6.25-100 μM; 24 h) reduces the viability of L-02 human normal hepatocytes in a concentration-dependent manner and increases the release of LDH and transaminases, indicating hepatocyte injury.
Exposure to decabromodiphenyl ethane reduces CYP3A expression in L-02 cells, while pretreatment with NAC or 4-PBA can ameliorate the changes in CYP3A expression induced by DBDPE.
Exposure to decabromodiphenyl ethane induces endoplasmic reticulum stress in L-02 cells, characterized by increased expression of PERK and IRE-1α; 4-PBA, an endoplasmic reticulum stress inhibitor, reduces endoplasmic reticulum stress and apoptosis induced by DBDPE.
Decabromodiphenyl ethane (12.5-100 mg/L; 48 or 72 h) induces apoptosis in HepG2 cells, accompanied by excessive production of ROS; the ROS scavenger NAC reduces the related effects induced by DBDPE.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human normal hepatocyte L-02 cells
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Concentration:6.25 μM, 12.5 μM, 25.0 μM, 50.0 μM, 100.0 μM
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Incubation Time:24 h
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Result:Caused a dose-dependent decrease in L-02 cell viability.
Reduced viability significantly at concentrations of 25.0-100.0 μM compared to control.
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Cell Line:human normal hepatocyte L-02 cells
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Concentration:50.0 μM
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Incubation Time:24 h
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Result:Increased PERK and IRE-1α protein expression levels significantly in L-02 cells.
Showed no significant effect on ATF-6 expression.
Pretreatment with 4-phenylbutyric acid attenuated the induced increases in PERK and IRE-1α.\nDecreased CYP3A protein expression significantly in L-02 cells.
Pretreatment with NAC or 4-PBA attenuated this induced decrease.
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Cell Line:human normal hepatocyte L-02 cells
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Concentration:50.0 μM
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Incubation Time:24 h
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Result:Increased the apoptosis rate of L-02 cells significantly.
Pretreatment with NAC or 4-PBA significantly reduced this induced apoptosis.
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Cell Line:human HepG2 hepatoma cells
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Concentration:3.125 mg/L, 6.25 mg/L, 12.5 mg/L, 25.0 mg/L, 50.0 mg/L, 100.0 mg/L
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Incubation Time:24 h, 48 h, 72 h
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Result:Failed to significantly alter HepG2 cell viability relative to controls at 3.125, 6.25 mg/L across all incubation times.
Inhibited HepG2 viability in a time- and dose-dependent manner at 12.5, 25.0, 50.0, 100.0 mg/L at 48 h and 72 h, with viability decreasing as both concentration and incubation time increased.
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Cell Line:human HepG2 hepatoma cells
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Concentration:12.5 mg/L, 25.0 mg/L, 50.0 mg/L, 100.0 mg/L
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Incubation Time:48 h, 72 h
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Result:Induced apoptosis in HepG2 cells in a time- and dose-dependent manner, with significantly higher apoptotic rates compared to control groups at 12.5, 25.0, 50.0, 100.0 mg/L after 48 h and 72 h.
Exhibited higher apoptotic rates after 72 h than after 48 h at equivalent concentrations.
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Cell Line:human HepG2 hepatoma cells
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Concentration:12.5 mg/L, 25.0 mg/L, 50.0 mg/L, 100.0 mg/L (with 10 min pretreatment with 5 mmol/L NAC)
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Incubation Time:72 h
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Result:Improved HepG2 cell viability that was reduced by DBDPE exposure at 12.5, 25.0, 50.0, 100.0 mg/L after 72 h when pretreated with 5 mmol/L NAC, with significant effects observed.
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Cell Line:human HepG2 hepatoma cells
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Concentration:12.5 mg/L, 25.0 mg/L, 50.0 mg/L, 100.0 mg/L (with 10 min pretreatment with 5 mmol/L NAC)
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Incubation Time:72 h
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Result:Reduced the rate of apoptosis induced by DBDPE exposure at 12.5, 25.0, 50.0, 100.0 mg/L after 72 h when pretreated with 5 mmol/L NAC, with significant effects observed.
Decabromodiphenyl ethane ([14C]-DBDPE; 100 nmol/kg; oral administration; single dose; 72 h observation) exhibits low oral absorption in male B6C3F1/Tac mice, with the administered radioactivity mainly excreted in feces in unchanged form; mice show faster fecal excretion rates compared to female Sprague Dawley rats, but the overall in vivo disposition characteristics are similar in the two animal models[2].
Decabromodiphenyl ethane (100 mg/kg bw/day; p.o.; daily administration; consecutive 90 days) is detectable and undergoes biotransformation in the liver, kidney, and adipose tissue of male Sprague Dawley rats. At least 7 unknown metabolites are detected after exposure, some of which are speculated to be sulfur-containing nona-BDPE derivatives, while the debromination pathway producing lower-brominated BDPEs is not the major metabolic pathway. DBDPE exposure affects some clinical biochemical parameters, thyroid hormone levels, and the expression of related enzymes in rats[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague Dawley (female, 10 weeks old, ~200 g)[2]
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Dosage:100 nmol/kg
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Administration:p.o.; single dose; 72 h observation
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Result:More than 98% of radioactivity was recovered in feces, approximately 1% was recovered in urine, and approximately 1% was detected in assayed tissues at 72 h after oral dosing.
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Animal Model:Rat (female Sprague Dawley, 10 weeks old, ~200 g)[2]
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Dosage:100 nmol/kg
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Administration:p.o.; repeated dosing for 10 days; 24 h post-final dose observation
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Result:Radioactivity concentration in adrenal tissue was increased approximately 8-fold, and liver radioactivity concentration reached 10 pmol-eq/g after repeated oral dosing compared with 0.7 pmol-eq/g after a single dose.
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Animal Model:Rat (female Sprague Dawley, 10 weeks old, ~200 g)[2]
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Dosage:100 nmol/kg
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Administration:i.v.; single dose; 72 h observation
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Result:Approximately 26% of radioactivity was recovered in feces, and the highest tissue concentrations were observed in lung (1223 pmol-eq/g), spleen (1096 pmol-eq/g), and liver (366 pmol-eq/g).
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Animal Model:Rat (female Sprague Dawley, 10 weeks old, ~200 g)[2]
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Dosage:2.7 nmol/cm2
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Administration:Dermal; single dose; 24 h observation
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Result:Approximately 5% of radioactivity penetrated through skin, and most radioactivity was retained in muscle (3%) and adipose tissue (0.8%).
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Animal Model:Mouse (male B6C3F1/Tac, 10 weeks old, ~20 g)[2]
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Dosage:100 nmol/kg
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Administration:p.o.; single dose; 72 h observation
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Result:Radioactivity was mainly eliminated through feces, and fecal elimination was faster than that in female Sprague Dawley rats, while overall disposition characteristics were similar.
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Animal Model:Rat (male Sprague Dawley)[1]
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Dosage:100 mg/kg bw/day
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Administration:p.o.; daily dosing for 90 days
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Result:Concentrations were detected in liver, kidney, and adipose tissues, and at least seven unknown metabolites were observed after exposure.
Two metabolites were tentatively proposed as MeSO2-nona-BDPE and EtSO2-nona-BDPE, while debromination to lower brominated BDPEs was not the primary metabolic pathway.
Changes in thyroid hormone levels, clinical chemistry parameters, and enzyme mRNA expression levels were also observed.
Chemical Information
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CAS No. 84852-53-9
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Appearance Solid
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Molecular Weight 971.22
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Formula C14H4Br10
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Color White to off-white
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SMILES
BrC1=C(Br)C(Br)=C(CCC2=C(Br)C(Br)=C(Br)C(Br)=C2Br)C(Br)=C1Br
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Synonyms
DBDPE; 1,2-Bis(perbromophenyl)ethane
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
H2O : < 0.1 mg/mL (insoluble)
Purity & Documentation
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Data Sheet (290 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Decabromodiphenyl ethane Related Classifications
HY-W013058 Related Classifications
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