Gao Jun, Zhu Haojun, Gao Jiancao, Xu Gangchun
Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Antioxidants (Basel). 2025 May 23;14(6):626. doi: 10.3390/antiox14060626.
Transport stress in aquaculture poses significant challenges to fish health by inducing oxidative stress and intestinal damage. This study investigated the effects of transport stress on intestinal microbiota, host gene regulation, and metabolic responses in . The fish were subjected to simulated transport conditions, followed by an analysis of their intestinal antioxidant capacity, inflammatory factors, transcriptome sequencing, metagenomic profiling, and metabolomic assays. The results revealed that transport stress significantly suppressed antioxidant enzyme activities (e.g., catalase, superoxide dismutase, glutathione peroxidase) and elevated oxidative damage (malondialdehyde, lipid peroxidation) alongside upregulating pro-inflammatory cytokines. The transcriptomic analysis identified differentially expressed genes enriched in the lipid metabolism and ferroptosis pathways, with the increased lipid peroxidation and iron overload activating ferroptosis. The metagenomic data showed an altered gut microbiota composition, including increased and reduced beneficial metabolites (e.g., propionic acid, bile acids). Correlation analyses linked the microbial shifts and metabolite changes to ferroptosis and barrier dysfunction. These findings demonstrate that transport stress disrupts intestinal redox balance, induces ferroptosis, and reshapes gut microbiota, collectively compromising intestinal integrity and health in .
水产养殖中的运输应激通过诱导氧化应激和肠道损伤,对鱼类健康构成重大挑战。本研究调查了运输应激对肠道微生物群、宿主基因调控和代谢反应的影响。对鱼进行模拟运输条件处理,随后分析其肠道抗氧化能力、炎症因子、转录组测序、宏基因组分析和代谢组学检测。结果显示,运输应激显著抑制抗氧化酶活性(如过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶),并增加氧化损伤(丙二醛、脂质过氧化),同时上调促炎细胞因子。转录组分析确定了在脂质代谢和铁死亡途径中富集的差异表达基因,脂质过氧化增加和铁过载激活了铁死亡。宏基因组数据显示肠道微生物群组成发生改变,包括有害菌增加和有益代谢物(如丙酸、胆汁酸)减少。相关性分析将微生物变化和代谢物变化与铁死亡和屏障功能障碍联系起来。这些发现表明,运输应激会破坏肠道氧化还原平衡,诱导铁死亡,并重塑肠道微生物群,共同损害肠道完整性和健康。