Estuarine environmental have been reported to undergo significant fluctuations in oxygen concentrations with hypoxic conditions and subsequent re-oxygenation events being of significant concern for resident fish populations. In this study we assessed the toxicological effects of hypoxia and re-oxygenation on the liver of hypoxia-sensitive spotted sea bass (Lateolabrax maculatus) that were exposed to hypoxia (1.17 mg/L dissolved oxygen) for 12 h and then re-oxygenated for 12 h. The activities of glutamic-pyruvic transaminase and glutamic-oxalacetic transaminase in serum significantly increased under hypoxia (p < 0.05) and continued to increase during re-oxygenation (p < 0.05), indicating that normal liver function might be disrupted by hypoxia and might become worse during re-oxygenation for 12h. Total protein, albumin, and globulin levels in serum decreased under hypoxia but began to return to normal during re-oxygenation, showing that protein synthesis in the liver decreased during hypoxia but could be restored by re-oxygenation. We also used RNA-Seq technology to identify changes in gene expression in the liver during hypoxia and re-oxygenation. Transcriptome sequencing revealed that the hypoxia-inducible factor (HIF-1) signaling pathway, apoptosis, and purine metabolism transcripts were significantly enriched under hypoxia and re-oxygenation conditions. A total of 15 and 16 apoptosis-related genes were induced by hypoxia and re-oxygenation stress, respectively. The apoptosis index increased from the normal to the hypoxic condition and was highest under re-oxygenation. Additionally, 19 and 29 genes, that are involved in purine metabolism in the liver of L. maculatus during hypoxia and re-oxygenation, respectively, were dysregulated. Unexpectedly, the serum uric acid level significantly increased during hypoxia and significantly decreased under re-oxygenation, indicating the presence of purine metabolic disorder in the liver of L. maculatus. These results illustrate that hypoxia poses a pronounced threat to hepatocyte function in L. maculatus and that liver damage is difficult to reverse with 12 h of re-oxygenation, and it may actually become worse when re-oxygenation is established.

据报道，在缺氧条件下，河口环境中的氧气浓度会发生明显波动，随后的再充氧事件引起了居民鱼类种群的极大关注。在这项研究中，我们评估了缺氧和再充氧对缺氧敏感的斑点鲈鱼（Lateolabrax maculatus）暴露于缺氧（1.17 mg / L溶解氧）12 h然后再充氧的肝脏的毒理作用。12小时 在低氧条件下，血清中的谷氨酸-丙酮酸转氨酶和谷氨酸-草酰乙酸转氨酶的活性显着增加（p <0.05），而在复氧过程中则继续增加（p<0.05），表明正常的肝功能可能会因缺氧而中断，并可能在再充氧12小时后变得更糟。缺氧条件下血清总蛋白，白蛋白和球蛋白水平降低，但在复氧过程中开始恢复正常，表明肝脏中的蛋白质合成在低氧条件下下降，但可以通过复氧作用恢复。我们还使用RNA-Seq技术来识别缺氧和复氧期间肝脏中基因表达的变化。转录组测序表明，在缺氧和复氧条件下，缺氧诱导因子（HIF-1）信号传导途径，细胞凋亡和嘌呤代谢转录本显着富集。缺氧和复氧应激分别诱导了15和16个凋亡相关基因。从正常状态到缺氧状态，细胞凋亡指数均升高，在复氧条件下凋亡指数最高。此外，有19和29个基因参与了肝脏肝脏嘌呤的代谢L.斑缺氧和复氧过程中，分别失调。出乎意料的是，低氧期间显著增加和显著血清尿酸水平下重新氧合降低，表明嘌呤代谢紊乱的中的肝脏中的存在L.斑。这些结果表明缺氧造成在肝细胞功能的显着的威胁L.斑和肝损伤是困难的重新氧合的12小时扭转，并建立重新氧合，当它实际上可能变得更糟。