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绿鳍马面鲀鳃对镉暴露的响应机制:氧化应激、免疫反应和能量代谢

Mechanisms of Gills Response to Cadmium Exposure in Greenfin Horse-Faced Filefish (): Oxidative Stress, Immune Response, and Energy Metabolism.

作者信息

Zhang Xuanxuan, Zhang Wenquan, Zhao Linlin, Zheng Li, Wang Bingshu, Song Chengbing, Liu Shenghao

机构信息

School of Advanced Manufacturing, Fuzhou University, Jinjiang 362200, China.

Key Laboratory of Marine Eco-Environmental Science and Technology, First Institute of Oceanography, Ministry of Natural Resources, Qingdao 266061, China.

出版信息

Animals (Basel). 2024 Feb 7;14(4):561. doi: 10.3390/ani14040561.

Abstract

Cadmium (Cd) pollution has become a global issue due to industrial and agricultural developments. However, the molecular mechanism of Cd-induced detrimental effects and relevant signal transduction/metabolic networks are largely unknown in marine fishes. Here, greenfin horse-faced filefish () were exposed to 5.0 mg/L Cd up to 7 days. We applied both biochemical methods and multi-omics techniques to investigate how the gills respond to Cd exposure. Our findings revealed that Cd exposure caused the formation of reactive oxygen species (ROS), which in turn activated the MAPK and apoptotic pathways to alleviate oxidative stress and cell damage. Glycolysis, protein degradation, as well as fatty acid metabolism might assist to meet the requirements of nutrition and energy under Cd stress. We also found that long-term (7 days, "long-term" means compared to 12 and 48 h) Cd exposure caused the accumulation of succinate, which would in turn trigger an inflammatory response and start an immunological process. Moreover, ferroptosis might induce inflammation. Overall, Cd exposure caused oxidative stress, energy metabolism disturbance, and immune response in greenfin horse-faced filefish. Our conclusions can be used as references for safety risk assessment of Cd to marine economic fishes.

摘要

由于工农业发展,镉(Cd)污染已成为一个全球性问题。然而,在海洋鱼类中,Cd诱导有害效应的分子机制以及相关信号转导/代谢网络在很大程度上尚不清楚。在此,将绿鳍马面鲀暴露于5.0 mg/L Cd中长达7天。我们应用生化方法和多组学技术来研究鳃对Cd暴露的反应。我们的研究结果表明,Cd暴露导致活性氧(ROS)的形成,进而激活丝裂原活化蛋白激酶(MAPK)和凋亡途径以减轻氧化应激和细胞损伤。糖酵解、蛋白质降解以及脂肪酸代谢可能有助于满足Cd胁迫下的营养和能量需求。我们还发现长期(7天,“长期”是与12小时和48小时相比)Cd暴露导致琥珀酸积累,这反过来会引发炎症反应并启动免疫过程。此外,铁死亡可能诱导炎症。总体而言,Cd暴露在绿鳍马面鲀中引起氧化应激、能量代谢紊乱和免疫反应。我们的结论可为Cd对海洋经济鱼类的安全风险评估提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f664/10886137/b45756498d7c/animals-14-00561-g001.jpg

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