中文摘要：

利用模式动物斑马鱼（Danio rerio）的运动行为实验,评价了在光照-黑暗周期刺激下BDE17（2,2′,4-tribromodiphenyl ether）和4′-OH-BDE17（4′-Hydroxy-2,2′,4-tribromodiphenyl ether）暴露对幼鱼运动行为效应,并利用分子对接技术和荧光素酶报告基因实验探讨了这两种化合物与斑马鱼视黄酸受体的相互作用关系,试图揭示运动行为效应的机制.BDE17暴露没有改变斑马鱼幼鱼的运动行为,而50μg·L-14′-OH-BDE17暴露却造成斑马鱼幼鱼在光照和黑暗条件下均出现运动活跃现象.分子对接结果表明,BDE17和4′-OH-BDE17与斑马鱼视黄酸受体的结合能力都不如视黄酸（Retinoic acid,RA）强.荧光素酶报告基因实验结果表明,与对照组相比,50μg·L-14′-OH-BDE17暴露组荧光素酶活性均显著增加（P〈0.05）;而BDE17暴露组荧光素酶活性则无显著性差异.这表明4′-OH-BDE17通过直接与视黄酸受体（Retinoic acid receptors,RARs）结合来诱导视黄酸受体转录活性,而BDE17则不能直接与视黄酸受体发生相互作用.本研究结果表明4′-OH-BDE17暴露可能通过诱导视黄酸受体转录活性,干扰视黄酸动态平衡,造成神经系统发育损伤,进而改变斑马鱼幼鱼的运动行为,而BDE17暴露则不能.

英文摘要：

Locomotor activity in zebrafish （Danio rerio） larvae was assessed under alternating light and dark conditions after exposure to BDE17 （2,2＇ ,4-tribromodiphenyl ether） and 4＇-OH-BDE17 （4＇-hydroxy-2,2＇, 4-tribromodiphenyl ether）. Molecular docking and luciferase reporter gene assay were used to explore the interaction between the two compounds and zebrafish retinoic acid receptors （RARs）. BDE17 exposure did not cause alteration in locomotor behavior in zebrafish larvae, while 50 μg· L^-1 4＇-OH-BDE17 exposure did cause hyperactivity both in dark and light conditions. The results of molecular docking suggested that BDE17 and 4＇-OH-BDE17 do not bind with zebrafish RARs as strongly as retinoic acid （RA）. The results of luciferase reporter gene assay showed that the luciferase activity of 50μg·L^-1 4＇-OH-BDE17 treatment was significantly higher than in the control group （P〈O.05）, while the luciferase activities of BDE17 treatment was not significantly different from that of the control group. These results indicated that 4＇-OH-BDE17 could induce RAR transcriptional activity by binding directly with RAR, and BDE17 could not directly interact with the RAR. This study showed that 4＇-OH-BDE17 exposure could disturb the homeostasis of RA by inducing RAR transcriptional activity, resulting in damage in nervous system and ultimately behavioral effects in zebrafish larvae and BDE17 could not.