Temporal correlations of ferroptosis, inflammation and oxidative stress under acute ammonia exposure in brain tissue of yellow catfish (Pelteobagrus fulvidraco)
文献类型： 外文期刊
作者： Long, Xinran 1 ; He, Kewei 1 ; Zhang, Muzi 1 ; Li, Ming 3 ; Wang, Zhenlu 1 ; Wang, Changan 4 ; Dong, Xianghong 1 ; Shao, Jian 1 ; Gan, Lei 1 ; Hu, Xiaojuan 5 ; Jiang, Haibo 1 ;
作者机构： 1.Guizhou Univ, Breeding & Reprod Plateau Mountainous Reg, Minist Educ, Guiyang 550025, Peoples R China
2.Guizhou Univ, Coll Anim Sci, Guiyang 550025, Peoples R China
3.Ningbo Univ, Sch Marine Sci, Ningbo 315211, Peoples R China
4.Chinese Acad Fishery Sci, Heilongjiang River Fisheries Res Inst, Harbin 150070, Peoples R China
5.Guizhou Educ Univ, Sch Foreign Languages, Guiyang 550018, Peoples R China
关键词： Ammonia toxicity; Ferroptosis; Inflammatory response; Oxidative stress; Pelteobagrus fulvidraco
期刊名称：COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY （ 影响因子：3.9； 五年影响因子：3.8 ）
ISSN： 1532-0456
年卷期： 2023 年 271 卷
页码：
收录情况： SCI
摘要： Ammonia is one of the most serious environmental stressors which severely affect fishery production. Ammonia toxicity to fish has a tight relationship with oxidative stress, inflammation and ferroptosis (a type of programmed cell death characterized by iron-dependent lipid peroxidation), but the temporal response of the above three in brain remains unclear. In the present study, yellow catfish were exposed to three concentrations of ammonia: low concentration (TA-N < 0.01 mg L-1, LA), middle concentration (TA-N 5.70 mg L-1, MA), high concentration (TA-N 28.50 mg L-1, HA) for 96 h. Brain was selected as target tissues for analysis. Results showed that ammonia stress resulted in firstly increased contents of hydroxyl radical at 1 h, total iron at 12 h, malondialdehyde at 48 h, respectively, and decreased contents of GSH at 3 h. The initial high expression levels of ferroptosis (GPX4, system xc- , TFR1) and inflammatory-related factors (NF-ƙB p65, TNF, COX-2, and LOX-15B), antioxidant enzymes genes (SOD and CAT) were observed at first hour upon MA or HA stress. Combining all, it suggested that brain fer-roptosis and inflammation were the first to be activated at the initial stage of ammonia stress, and then that provoked oxidative stress.
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