Guangxi Key Laboratory of Tumor Immunology and Microenvironmental Regulation, Guilin Medical University, Guilin, PR China; Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, Beibu Gulf University, Qinzhou, PR China; Department of Chemistry, City University of Hong Kong, Hong Kong, PR China; State Key Laboratory of Marine Pollution, City University of Hong Kong, Hong Kong, PR China.
Department of Chemistry, City University of Hong Kong, Hong Kong, PR China.
Aquat Toxicol. 2020 Jul;224:105520. doi: 10.1016/j.aquatox.2020.105520. Epub 2020 May 19.
Hypoxia, a low environmental oxygen level, is a common problem in the ocean globally. Hypoxia has been known to cause disruption to the endocrine system of marine organisms in both laboratory and field studies. Our previous studies have demonstrated the sex-specific response to hypoxia in the neural and reproductive systems of marine fish. In the current report, we aim to study the sex-specific hepatic response of fish at the transcriptome level to hypoxic stress. By using a comparative transcriptome analysis, followed by a systematic bioinformatics analysis including Database for Annotation, Visualization and Integrated Discovery (DAVID) and Ingenuity Pathway Analysis (IPA), we found that hypoxia altered expression of genes related to cell proliferation and apoptosis of hepatocytes, which are associated with human pathologies, such as liver inflammation hepatic steatosis and steatohepatitis. Furthermore, we observed sex-specific responses in the livers of fish through different cell signaling pathways. In female fish, hypoxia causes dysregulation of expression of genes related to impairment in endoplasmic reticulum structure and liver metabolism. In male fish, genes associated with redox homeostasis and fatty acid metabolism were altered by hypoxic stress. The findings of this study support the notion that hypoxia could cause sex-specific changes (hepatic toxicity and changes) in marine fish.
缺氧是全球海洋环境中常见的低氧水平问题。实验室和野外研究都表明，缺氧会破坏海洋生物的内分泌系统。我们之前的研究已经证明了海洋鱼类的神经和生殖系统对缺氧的性别特异性反应。在本报告中，我们旨在研究鱼类肝脏对缺氧应激的转录组水平的性别特异性反应。通过使用比较转录组分析，然后进行系统的生物信息学分析，包括数据库注释、可视化和综合发现 (DAVID) 和 IPA，我们发现缺氧改变了与肝细胞增殖和凋亡相关的基因的表达，这些基因与人类病理学有关，如肝脏炎症、肝脂肪变性和脂肪性肝炎。此外，我们通过不同的细胞信号通路观察到鱼类肝脏的性别特异性反应。在雌性鱼类中，缺氧导致与内质网结构和肝脏代谢损伤相关的基因表达失调。在雄性鱼类中，与氧化还原平衡和脂肪酸代谢相关的基因受到缺氧应激的影响。这项研究的结果支持这样一种观点，即缺氧可能会导致海洋鱼类产生性别特异性的变化（肝毒性和变化）。
