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.
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.
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.
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