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.

低氧，低环境氧含量，是全球海洋中的普遍问题。在实验室和现场研究中，已知缺氧都会破坏海洋生物的内分泌系统。我们以前的研究已经证明了海水鱼类神经和生殖系统对缺氧的性别特异性反应。在本报告中，我们旨在研究鱼类在转录组水平上对低氧应激的性别特异性肝反应。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，包括注释，可视化和综合发现数据库（DAVID）和创造力途径分析（IPA），我们发现低氧改变了与肝细胞增殖和凋亡相关的基因表达，与人类病理相关的 如肝炎，肝脂肪变性和脂肪性肝炎。此外，我们观察到鱼肝中通过不同细胞信号通路的性别特异性反应。在雌鱼中，缺氧会导致与内质网结构和肝代谢受损相关的基因表达失调。在雄鱼中，缺氧胁迫改变了与氧化还原稳态和脂肪酸代谢相关的基因。这项研究的结果支持以下观点：缺氧会导致海水鱼类的性别特异性变化（肝毒性和变化）。缺氧会导致与内质网结构受损和肝脏代谢相关的基因表达失调。在雄鱼中，缺氧应激改变了与氧化还原稳态和脂肪酸代谢相关的基因。这项研究的结果支持以下观点：缺氧会导致海水鱼类的性别特异性变化（肝毒性和变化）。缺氧会导致与内质网结构受损和肝脏代谢相关的基因表达失调。在雄鱼中，缺氧应激改变了与氧化还原稳态和脂肪酸代谢相关的基因。这项研究的结果支持以下观点：缺氧会导致海水鱼类的性别特异性变化（肝毒性和变化）。