Zou Yongfeng, Cao Panhui, Bao Zhiming, Xu Yu, Xu Zhiqiang, Guo Hui
College of Fisheries, Guangdong Ocean University, Zhanjiang 524088, PR China.
Key Laboratory of Genetic Breeding and Cultivation for Freshwater Crustacean, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Institute of Jiangsu Province, Nanjing 210017, PR China.
Ecotoxicol Environ Saf. 2025 Jan 1;289:117459. doi: 10.1016/j.ecoenv.2024.117459. Epub 2024 Dec 7.
In the context of global warming, heat stress poses a threat to aquatic organisms. In the present study, a comprehensive analysis in hepatopancreas from Procambarus clarkii was conducted to examine the histology, physiological changes, and transcriptome alterations after exposed at 32 and 37 ℃ for 24 and 72 h, respectively, with 26 ℃ as the control group. The results demonstrated that the survival rate of P. clarkii decreased significantly with the stress time and the temperature increased, with a corresponding damage to its hepatopancreas. Significant fluctuations were observed in the malondialdehyde (MDA) content, reactive oxygen species (ROS) production, total antioxidant capacity (T-AOC), and activities of pyruvate kinase (PK), hexokinase (HK), alkaline phosphatase (ALP), lysozyme (LYS), acid phosphatase (ACP), fatty acid synthase (FAS), as well as lipoprotein lipase (LPL) in response to different stress conditions (P < 0.05). Heat stress notably altered the expression of genes related to glucose, lipid, and protein metabolism, as well as oxidative phosphorylation pathways. The expression of genes related to protein processing and degradation pathways in the endoplasmic reticulum was up-regulation. On the contrary, the expression of genes related to ER autophagy was suppressed. Simultaneously, the differentially expressed genes (DEGs) were significantly enriched in lysosomal and phagosomal pathways. In summary, heat stress induced oxidative damage, disrupted metabolic pathways, impacted protein processing, and compromised immune defense mechanisms, ultimately resulting in decreased survival rates of P. clarkii. These findings contribute to a deeper understanding of aquatic organisms respond to heat stress.
在全球变暖的背景下，热应激对水生生物构成威胁。在本研究中，以26℃为对照组，对克氏原螯虾的肝胰腺进行了全面分析，以研究其分别在32℃和37℃暴露24小时和72小时后的组织学、生理变化和转录组改变。结果表明，克氏原螯虾的存活率随应激时间和温度的升高而显著降低，其肝胰腺也相应受损。在不同应激条件下，丙二醛（MDA）含量、活性氧（ROS）产生量、总抗氧化能力（T-AOC）以及丙酮酸激酶（PK）、己糖激酶（HK）、碱性磷酸酶（ALP）、溶菌酶（LYS）、酸性磷酸酶（ACP）、脂肪酸合酶（FAS）和脂蛋白脂肪酶（LPL）的活性均出现显著波动（P<0.05）。热应激显著改变了与葡萄糖、脂质和蛋白质代谢以及氧化磷酸化途径相关的基因表达。内质网中与蛋白质加工和降解途径相关的基因表达上调。相反，与内质网自噬相关的基因表达受到抑制。同时，差异表达基因（DEGs）在溶酶体和吞噬体途径中显著富集。总之，热应激诱导氧化损伤、扰乱代谢途径、影响蛋白质加工并损害免疫防御机制，最终导致克氏原螯虾存活率降低。这些发现有助于更深入地了解水生生物对热应激的反应。
