Zheng Jia-Lang, Zhu Qing-Ling, Wu Chang-Wen, Zhu Ai-Yi, Shen Bin, Zeng Lin
National Engineering Research Center of Marine Facilities Aquaculture, Zhejiang Ocean University, Zhoushan 316022, PR China.
Postgraduate Work Department, Zhejiang Ocean University, Zhoushan 316022, PR China.
Aquat Toxicol. 2016 Mar;172:21-9. doi: 10.1016/j.aquatox.2015.12.009. Epub 2015 Dec 23.
The hypothesis tested in the present study was that Zn acclimation will alleviate high Zn induced oxidative stress in large yellow croaker Pseudosciaena crocea. To the end, fish were pre-exposed to 0 and 2mgZnL(-1) for 48h and then exposed to 0 and 10mgZnL(-1) for 48h. Lipid peroxidation, activities and mRNA levels of antioxidant enzyme genes (Cu/Zn-SOD, CAT, GPx and GR), and gene expressions of Nrf2-Keap1 signaling molecules at different exposure time (12h, 24h and 48h) were determined in the liver and spleen of large yellow croaker. 10mgZnL(-1) exposure alone enhanced lipid peroxidation in the liver during 12-48h and in the spleen during 24-48h. Although 2mgZnL(-1) pre-exposure did not affect lipid peroxidation, 2mgZnL(-1) pre-exposure mitigated high Zn induced oxidative stress. The positive effect of Zn acclimation could be attributed to the up-regulated expression and activities of antioxidant enzyme genes under high Zn stress. Obtained results also showed a coordinated transcriptional regulation of antioxidant genes, suggesting that Nrf2 is required for the protracted induction of these genes. Besides, the sharp increase in Keap1 expression levels would support its role in switching off Nrf2 response. In conclusion, Zn acclimation mitigated high Zn-induced oxidative stress in large yellow croker, emphasizing a central role of transcription factor Nrf2 in the process.
本研究中所检验的假设是，锌驯化将减轻高锌诱导的大黄鱼（Pseudosciaena crocea）氧化应激。为此，将鱼预先暴露于0和2mgZnL(-1) 48小时，然后暴露于0和10mgZnL(-1) 48小时。测定了大黄鱼肝脏和脾脏在不同暴露时间（12小时、24小时和48小时）的脂质过氧化、抗氧化酶基因（铜/锌超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶）的活性和mRNA水平，以及Nrf2-Keap1信号分子的基因表达。单独暴露于10mgZnL(-1)会在12 - 48小时内增强肝脏中的脂质过氧化，并在24 - 48小时内增强脾脏中的脂质过氧化。虽然预先暴露于2mgZnL(-1)不影响脂质过氧化，但预先暴露于2mgZnL(-1)减轻了高锌诱导的氧化应激。锌驯化的积极作用可归因于高锌胁迫下抗氧化酶基因表达和活性的上调。所得结果还显示了抗氧化基因的协同转录调控，表明Nrf2是这些基因长期诱导所必需的。此外，Keap1表达水平的急剧增加将支持其在关闭Nrf2反应中的作用。总之，锌驯化减轻了大黄鱼中高锌诱导的氧化应激，强调了转录因子Nrf2在此过程中的核心作用。
