双酚AF对海水青鳉仔鱼心血管和神经系统毒性效应  

Toxic effects of bisphenol AF on cardiovascular and nervous systems in marine medaka larvae

作　　者：周天洋 陈月碧 高佳豪 王中铎[1,2] 郭昱嵩 董忠典[1,2] ZHOU Tian-yang;CHEN Yue-bi;GAO Jia-hao;WANG Zhong-duo;GUO Yu-song;DONG Zhong-dian(Key Laboratory of Aquaculture in the South China Sea for Aquatic Economic Animal of Guangdong Higher Education Institutes/Fisheries College,Guangdong Ocean University,Zhanjiang 524088,China;Guangdong Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy Culture,Zhanjiang 524088,China)

机构地区：[1]广东海洋大学水产学院,南海水产经济动物增养殖重点实验室,广东湛江524088 [2]广东省水产动物病害防控与健康养殖重点实验室,广东湛江524088

出　　处：《中国环境科学》2024年第5期2724-2732,共9页China Environmental Science

基　　金：国家自然科学基金资助项目(41806195);广东海洋大学南海学者青年项目(QNXZ201903);广东海洋大学本科生创新团队项目(CXTD2023004)。

摘　　要：为研究BPAF对海水青鳉仔鱼生长发育的毒性效应以及毒性效应是否在环境恢复后可逆,本研究将海水青鳉仔鱼在7.96和82.91μg/L BPAF中暴露7d随后恢复7d,探讨了BPAF对海水青鳉仔鱼存活、生长、心率和游泳行为的影响,并结合仔鱼神经系统、心血管系统和抗氧化系统相关基因转录水平的变化探究了BPAF对海水青鳉仔鱼的毒性效应.结果表明,82.91μg/L BPAF暴露显著降低了仔鱼的存活率;7.96和82.91μg/L BPAF暴露均显著抑制了仔鱼的生长、游泳行为和心率,恢复7d后仔鱼的生长得以恢复,但游泳行为和心率仍被抑制;在分子水平上,7.96μg/LBPAF暴露导致神经系统基因ache、心血管统基因tbx2b和抗氧化系统基因cat的表达水平显著下调30%、47%和56%,恢复后对ache和cat的抑制效应消失,而82.91μg/L BPAF暴露则显著下调了神经系统基因syn2a(80%)、shha(58%)、xdh(59%)、gap43(47%)、elav13(54%),心血管统基因,atp2a1(44%)、crhr1(84%)、tbx2b(60%)、arnt2(32%)、tbx6(68%)的表达水平,恢复7d后elav13的表达恢复正常水平,而gap43的表达则显著上调,抗氧化系统基因cat、sod、cox和gpx的表达水平分别比对照组低61%、71%、51%和53%.本研究为BPAF的海洋生态安全风险评估和水质基准制定提供了重要参考.To assess the toxic impacts of bisphenol AF(BPAF)on the growth and development of marine medaka(Oryzias melastigma)larvae and whether these effects could recover when environmental restored,the larvae were exposed to BPAF at the concentrations of 7.96 and 82.91μg/L for 7 days,followed by a 7-day recovery in BPAF-free seawater.The survival,growth,heart rate,and swimming behavior,as well as transcription levels of genes related to nervous,cardiovascular,and antioxidant system,were examined.The results showed that exposure to 82.91μg/L BPAF significantly reduced the survival rate;exposure to both of 7.96 and 82.91μg/L BPAF significant inhibited the growth,swimming behavior,and heart rate.After a 7-day recovery,the growth of the larvae recstored,but swimming behavior and heart rate remained suppressed.The results of gene expression analysis showed that,exposure to 7.96μg/L of BPAF significantly downregulated the expression of the neurological gene ache(30%),cardiovascular gene tbx2b(47%),and antioxidant system gene cat(56%),with the inhibitory effects on ache and cat dissipating following recovery;exposure to 82.91μg/L of BPAF significantly reduced the expression of neurological genes syn2a(80%),shha(58%),xdh(59%),gap43(47%),and elav13(54%),as well as cardiovascular genes atp2a1(44%),crhr1(84%),tbx2b(60%),arnt2(32%),and tbx6(68%);following a 7 day recovery,elav13 normalized while gap43 was upregulated,and antioxidant genes cat,sod,cox,and gpx were decreased by 61%,71%,51%,and 53%relative to controls.This study provides important data for the assessment of marine ecological risks of BPAF and the establishment of water quality standards.

关 键 词：海水青鳉 BPAF 仔鱼 行为 发育毒性 

分 类 号：X174[环境科学与工程—环境科学] X503.225