JOURNAL OF HAZARDOUS MATERIALS
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2021
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IF 10.588
Shutao Wang,Wanlun Li,Lu Liu,Hong Qi,Hong You
Decabromodiphenyl ethane (DBDPE) can pose a potential toxic threat to human beings and the environment. P. ostreatus , as one of the typical white-rot fungi, can effectively degrade various refractory pollutants. The biodegradable characteristics of DBDPE by P. ostreatus , as well as the mechanisms, and toxicological response were investigated in this study. The removal rate reached 47.73% and 43.20%, respectively, for 5 and 20 mg/L DBDPE after 120-h degradation by P. ostreatus . As a coexisting substance, Pb could inhibit the biodegradation. It is found that both the intracellular enzyme (P450) and extracellular enzymes (manganese peroxidase (MnP), lignin peroxidase (LiP), and laccase (Lac)) played a very important role in the biodegradation of DBDPE, of which Lac dominated the degradation. The toxic response was monitored during the degradation. The activities of SOD and CAT were enhanced to eliminate excess ROS in P. ostreatus triggered by DBDPE. In addition, debromination, hydroxylation, and oxidation were inferred as the main degradation pathways preliminarily. The findings provide a theoretical basis for the application of microbial degradation of DBDPE contamination.
研究领域:
环境科学
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微生物学
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高影响因子
CHEMICAL ENGINEERING SCIENCE
·
2026
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IF 5.1
Wenping Jiang,Wenyue Zhang,Cheng Peng,Yuejin Zhang,Wei Zhang,Jizhang Chen,Xiaoxia Wang
Decabromodiphenyl ethane (DBDPE) is an efficient novel brominated flame retardant (NBFR) widely used in electronics, plastics, textiles, and other industries. DBDPE tends to permeate into surrounding environments during its synthesis, utilization, and disposal processes, accumulating in organisms and causing biomagnification effects. In this study, sodium persulfate (Na 2 S 2 O 8 , PS) was employed for the degradation of DBDPE in soil and indicated that elevated reaction temperature and increased initial alkalinity could both enhance the degradation efficiency of DBDPE. Under the optimal conditions (60°C, pH 11), DBDPE degradation efficiency reached 83.01% within 24 h. It was found that the system’s initial alkalinity exhibited negligible effects on the enhancement of activation by temperature, while chloride ions and weakly acidic conditions significantly inhibited DBDPE degradation. This study showed that hydroxyl radicals (HO•) played a dominant role in the degradation process, supplemented by sulfate radicals (SO 4 • − ). ECOSAR predictions revealed a marked reduction in the ecotoxicity of the seven potential degradation products relative to DBDPE, some of which were characterized by lower bromine content and oxygen incorporation. This study provides insights into the mechanisms of DBDPE degradation and a potential remediation strategy for contaminated soil.
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高影响因子
ENVIRONMENTAL TOXICOLOGY
·
2023
·Vol. 38
·期 4
·844-856
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IF 4.5
Yanting Wang,Yushun Yang,Chenyuan Dang,Bin Lu,Yin Luo,Jie Fu
In this paper, the hepatocytotoxicity and aryl hydrocarbon receptor (AHR) activity of decabromodiphenyl ethane (DBDPE), decabromodiphenyl ether (BDE209) and other 18 analogues were evaluated in vitro using human normal liver cell L02. These dioxin-like compounds showed differential hepatocytotoxicity (EC 50 = 0.38–17.87 mg/L) and AHR activity (EROD activity = 4.53–46.35 U/μg). In silico study indicated the distance of π-π bonds between the benzene ring of compounds and residue Phe234 of AHR played a key role in the binding of AHR, and the substituents on the benzene ring also influenced the activity. Combining molecular biology and bioomics, the comprehensive investigations on the hepatotoxic mechanisms have demonstrated the AHR signaling pathway was the key mediation mechanism for the hepatotoxicity of DBDPE/BDE209. The cytochrome P450s (CYP2 family) mediated formation of reactive oxygenated intermediates might be the dominant toxic mechanism, which could produce oxidative stress or cause genotoxicity. Although the experimental toxicity of DBDPE was smaller relative to BDE209, the health risk of DBDPE may be much greater than we expected, due to the high potential to form a variety of dioxin-like intermediates by microbial oxidation of ethyl group. Therefore, whether it is really safe to replace BDE209 with DBDPE is a debatable question, and more ecotoxicological and health data are needed to clarify this issue.
研究领域:
毒理学
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环境健康
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分子生物学
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生物信息学
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PubMed
高影响因子
ENVIRONMENT INTERNATIONAL
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2026
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IF 10.2
Wei Shi,Yuanteng Sun,Kejia Liu,Ying Zhang,Lu Lu,Qian Zhou,Yuepu Pu,Rongli Sun,Lihong Yin
Decabromodiphenyl ethane (DBDPE), a widely used novel brominated flame retardant, has been increasingly detected across environmental matrices and human samples. Owing to its marked persistence and bioaccumulation potential, DBDPE was designated as a Substance of Very High Concern (SVHC) by the European Chemicals Agency in 2025. However, evidence regarding its potential reproductive hazards remains limited. Here, we systematically investigated the molecular mechanisms underlying DBDPE-induced spermatogenic disorder using an integrated approach that combines network toxicology, machine learning, and in vivo validation. Intersecting 564 DBDPE-associated targets with 1,743 NOA-related differentially expressed genes identified 33 overlapping candidates that may mediate DBDPE-induced spermatogenic disorder. Enrichment analyses implicated the HIF-1 signaling and gap junction pathways in DBDPE-induced spermatogenic disorder. Machine learning prioritized five core genes, including PRKACG, WDR5, AURKC, PFKP, and ASGR1, all of which were downregulated in NOA patients. Molecular docking demonstrated stable binding between DBDPE and these core targets. In vivo , DBDPE exposure disrupted testicular structure, reduced sperm concentration and motility, and decreased expression of the five core proteins, confirming the predicted mechanisms. Additionally, we proposed an adverse outcome pathway (AOP) framework describing key events leading to DBDPE-induced spermatogenic impairment. Collectively, our findings revealed the reproductive toxicity of DBDPE and provided a mechanistic foundation for developing strategies to safeguard male fertility.
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高影响因子
Journal of Zhejiang University-SCIENCE B
·
2018
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IF 1.815
Mei-qing Jin,Dong Zhang,Ying Zhang,Shan-shan Zhou,Xian-ting Lu,Hong-ting Zhao
Decabromodiphenylethane (DBDPE) has been widely used as an alternative flame retardant due to the restriction or phase-out of traditional polybrominated diphenyl ethers (PBDEs), and is of increasing concern regarding its ubiquity, persistence, and potential adverse effects. In the present study, the toxicological effects of DBDPE were evaluated using zebrafish as an in vivo model. Upon being exposed to DBDPE-polluted sediments for a short term, it was found that the mortality and malformation of zebrafish (including edema, bent notochord, and bent tail) were not affected even at the highest concentration tested (1000.0 µg/kg dry sediment). Regarding behavioral responses, it was found that zebrafish larvae of 48 hours post fertilization (hpf) in all groups escaped successfully with a touch to the dorsal fin. However, when exposed to the highest DBDPE concentration, the larvae of 120 hpf exhibited significantly smaller distances as compared to the control. Moreover, the results of the acetylcholinesterase (AChE) activity, the expression levels of two important nerve-related genes, and the cell apoptosis all indicated that DBDPE posed low neurotoxicity in embryo-larval zebrafish. The results in this study shed some light on the potential risks of DBDPE in the real environment and highlight the application of the sediment exposure route in the future.
研究领域:
环境毒理学
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水生生物学
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神经科学
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高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2025
·
IF 6.1
Jianwei Cui,Liting Zhou,Xuehan Ding,Hui Ye,Tianyou Wang,Wen Qi
Decabromodiphenyl ethane (DBDPE) is a kind of commonly used novel brominated flame retardants, and widely exists in environments. DBDPE could be enriched in the liver, but its effects on lipid metabolism in liver and underlying mechanisms remain largely unknown. In the present study, firstly, we investigated the impact of DBDPE on the liver in rats and L02 cells. We found that DBDPE exposure could induce lipid metabolism disorders, up-regulate the expressions of Notch pathway genes, and promote Arrestin domain containing protein 1-mediated microvesicles (ARMMs)-derivation. Subsequently, siRNAs were used to inhibit the Notch pathway and the ARMMs-derivation in L02 cells respectively. It demonstrated that inhibition of Notch or ARMMs-derivation could reverse the lipid accumulation induced by DBDPE, and the inhibition of ARMMs-derivation could suppress the activation of the Notch pathway. Extracellular vesicles from L02 cells exposed to DBDPE co-culture with L02 cells confirmed that ARMMs can directly activate the Notch signaling pathway and induce lipid accumulation. In conclusion, our study is the first to explore the role of ARMMs in lipid metabolism disorders caused by environmental pollutants. We found that exposure to DBDPE increases the levels of ARMMs, which directly activates the Notch signaling pathway and triggers disruptions of liver lipid metabolism.
研究领域:
毒理学
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环境健康
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分子生物学
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细胞生物学
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代谢
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高影响因子
JOURNAL OF HAZARDOUS MATERIALS
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2025
·
IF 11.3
Run Ling,Xin Yin,Liyao Ma,Yan Zhang,Yidan Ma,Rufei Gao,Yanqing Geng,Xinyi Mu,Xuemei Chen,Fangfang Li,Junlin He
Decabromodiphenyl ethane (DBDPE) is a brominated flame retardant widely used for its high flame retardancy and low bioavailability. However, DBDPE exhibits bioaccumulative potential. The placental vasculature, critical for the exchange between maternal and fetal circulation, is susceptible to environmental factors. We aimed to understand the potential toxicity of DBDPE to the placental vasculature. Gestational CD-1 mice and human umbilical vein endothelial cells (HUVECs) were exposed to 0, 0.5, 5, 50 mg/kg·bw·day or 0, 6.25, 12.5, 25, 50 μmol/L DBDPE, respectively. DBDPE exposure impaired placental angiogenesis and inhibited the proliferation and invasion of HUVECs by activating the endothelial-to-mesenchymal transition (EndMT) through the TGF-β1/Smad pathway, in vivo and in vitro . DBDPE upregulated the transcription factor TWIST2 and mRNA acetyltransferase NAT10. Knockdown or overexpression of TWIST2 reversed the vascular dysfunction and EndMT mechanism. DBDPE facilitated the recruitment of NAT10 by TWIST2, promoting N4-acetylcytidine (ac4C) RNA modifications and stabilizing the TGF-β1 mRNA. NAT10 inhibition rescued the effects caused by DBDPE. These findings uncover molecular mechanisms linking DBDPE exposure to adverse pregnancy outcomes, highlighting potential risks to pregnant women.
研究领域:
毒理学
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生殖生物学
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分子生物学
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环境健康
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细胞生物学
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RNA修饰
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发育生物学
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DOI
PubMed
高影响因子
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