Lebeuf Michel, Couillard Catherine M, Légaré Benoît, Trottier Steve
Department of Fisheries and Oceans, Maurice Lamontagne Institute, P.O. Box 1000, Mont-Joli, Quebec, Canada G5H 3Z4.
Environ Sci Technol. 2006 May 15;40(10):3211-6. doi: 10.1021/es0521829.
The biotransformation of high bromosubstituted polybrominated diphenyl ethers (PBDEs) congeners contained in a commercial deca mixture (DeBDE) is of environmental concern because it might lead to the increase of toxic low brominated PBDEs in biota. A few studies have reported that freshwater fish dietary exposed to DeBDE or its main constituent, decabrominated PBDE congener (BDE-209), had their tissues enriched with PBDEs not initially present in fish or feed. In the present study, Atlantic tomcod (Microgadus tomcod) were intraperitoneally (IP) injected with DeBDE to assess hepatic concentration changes of PBDEs and methoxy polybrominated diphenyl ethers (MeO-PBDEs) in a marine fish species. Tomcod were also IP injected with polychlorinated biphenyl (PCB)-126 to evaluate the impact of cytochrome P4501A (CYP1A) induction on the biotransformation of injected PBDEs contained in DeBDE and PBDEs initially present in fish. Besides BDE-209, concentrations of BDE-203 and three other unidentified octabrominated PBDEs and the nonabrominated PBDEs (BDE-206, -207, and -208) were enriched in the liver of fish injected with DeBDE. All these PBDE congeners, essentially absent in control fish, were identified as impurities in DeBDE, and, thus, their presence could not be attributed exclusivelyto biotransformation. Despite a 4.3times increase of EROD activity in the liver of tomcod injected with both PCB-126 and DeBDE, compared to DeBDE alone, no further increases of PBDE hepatic concentrations were observed. However, depleted concentrations of BDE-17 (x 1.5) and 6-MeO-BDE-47 (x 1.4) were found in fish IP injected with DeBDE compared to control fish, likely due to activated hepatic metabolic enzymes other than CYP1A. Fish injected with PCB-126 showed an even more significant depletion of BDE-17 hepatic concentrations (x 3.5) than the one associated with the DeBDE treatment and a significantly lower proportion of fish with quantifiable concentrations of BDE-203. Thus, CYP1A inducers can promote the biotransformation of PBDEs in fish liver. This study shows that exposure of fish to DeBDE is expected to result in the enrichment of high brominated PBDEs in fish liver and that metabolic activities in fish can affect their PBDE bioaccumulation pattern and possibly the toxicity of PBDEs to fish.
商业十溴混合物（DeBDE）中含有的高溴取代多溴二苯醚（PBDEs）同系物的生物转化引起了环境关注，因为这可能导致生物群中有毒低溴化PBDEs的增加。一些研究报告称，淡水鱼通过饮食接触DeBDE或其主要成分十溴代多溴二苯醚同系物（BDE-209）后，其组织中富集了鱼类或饲料中最初不存在的PBDEs。在本研究中，对大西洋小鳕（Microgadus tomcod）进行腹腔注射DeBDE，以评估海洋鱼类中PBDEs和甲氧基多溴二苯醚（MeO-PBDEs）的肝脏浓度变化。还对小鳕腹腔注射多氯联苯（PCB）-126，以评估细胞色素P4501A（CYP1A）诱导对DeBDE中注射的PBDEs以及鱼类中最初存在的PBDEs生物转化的影响。除了BDE-209外，注射DeBDE的鱼肝脏中还富集了BDE-203以及其他三种未鉴定的八溴代PBDEs和九溴代PBDEs（BDE-206、-207和-208）。所有这些PBDE同系物在对照鱼中基本不存在，被鉴定为DeBDE中的杂质，因此，它们的存在不能完全归因于生物转化。尽管与单独注射DeBDE相比，同时注射PCB-126和DeBDE的小鳕肝脏中EROD活性增加了4.3倍，但未观察到PBDE肝脏浓度的进一步增加。然而，与对照鱼相比，腹腔注射DeBDE的鱼中BDE-17（x 1.5）和6-MeO-BDE-47（x 1.4）的浓度降低，这可能是由于除CYP1A外的肝脏代谢酶被激活。注射PCB-126的鱼肝脏中BDE-17的浓度下降更为显著（x 3.5），比与DeBDE处理相关的下降幅度更大，且可定量检测到BDE-203的鱼的比例显著更低。因此，CYP1A诱导剂可促进鱼肝中PBDEs的生物转化。本研究表明，鱼类接触DeBDE预计会导致鱼肝中高溴化PBDEs的富集，并且鱼类的代谢活动会影响其PBDE生物累积模式，可能还会影响PBDEs对鱼类的毒性。
