Abstract：
To investigate the mechanisms of BDE-47 on hepatotoxicity in fish, this study examined the effects of dietary exposure to BDE-47 (40 and 4000 ng/g) on carp for 42 days. The results showed that BDE-47 significantly increased carp\'s condition factor and hepatosomatic index. Pathological results revealed unclear hepatic cord structure, hepatocytes swelling, cellular vacuolization, and inflammatory cell infiltration in the hepatopancreas of carp. Further investigation showed that ROS levels significantly increased on days 7, 14, and 42. Moreover, the activities of antioxidant enzymes SOD, GSH, CAT, and GST increased significantly from 1 to 7 days, and the transcription levels of antioxidant enzymes CAT, Cu-Zn SOD, Mn-SOD, GST, and GPX, and antioxidant pathway genes Keap1, Nrf2, and HO-1 changed significantly at multiple time-points during the 42 days. The results of apoptosis pathway genes showed that the mitochondrial pathway genes Bax, Casp3, and Casp9 were significantly upregulated and Bcl2 was significantly downregulated, while the transcription levels of FADD and PERK were significantly enhanced. These results indicate that BDE-47 induced oxidative damage in hepatopancreas, then it promoted cell apoptosis mainly through the mitochondrial pathway. This study provides a foundation for analyzing the mechanism of hepatotoxicity induced by BDE-47 on fish.
摘要：
探讨BDE-47对鱼类肝毒性的作用机制,这项研究调查了42天饮食中接触BDE-47（40和4000纳克/克）对鲤鱼的影响。结果表明,BDE-47能显著提高鲤鱼的病情因子和肝细胞指数。病理结果提示肝索结构不清,肝细胞肿胀，细胞空泡化，鲤鱼肝胰腺的炎症细胞浸润。进一步的调查显示，ROS水平在第7、14和42天显著增加。此外，抗氧化酶SOD的活性，GSH,CAT,GST从1天到7天显着增加，和抗氧化酶CAT的转录水平，Cu-Zn超氧化物歧化酶,Mn-SOD,GST,和GPX,抗氧化途径基因Keap1，Nrf2和HO-1在42天的多个时间点显着变化。凋亡通路基因检测结果显示，线粒体通路基因Bax、Casp3和Casp9显著上调，Bcl2显著下调，而FADD和PERK的转录水平显著增强。这些结果表明，BDE-47诱导肝胰腺氧化损伤，然后主要通过线粒体途径促进细胞凋亡。本研究为分析BDE-47对鱼类的肝毒性作用机制奠定了基础。
