Feng Wenrong, He Qinghong, Yang Qiqin, Xu Yuanfeng, Jiang Gang, Li Jianlin, Zhou Jun, Jia Rui, Tang Yongkai
Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China.
Antioxidants (Basel). 2025 Jul 22;14(8):897. doi: 10.3390/antiox14080897.
Oxidative stress is a key mediator of physiological dysfunction in aquatic organisms under environmental challenges, yet its comprehensive impacts on gill physiology require further clarification. This study investigated the molecular and cellular responses of gills to hydrogen peroxide (HO)-induced oxidative stress, integrating antioxidant defense, ion transport regulation, and stress-induced cell apoptosis and autophagy. Morphological alterations in the gill filaments were observed, characterized by septum degeneration, accumulation of haemolymph cells, and pronounced swelling. For antioxidant enzymes like catalase (CAT) and glutathione peroxidase (GPx), activities were enhanced, while superoxide dismutase (SOD) activity was reduced following 48 h of exposure. Overall, the total antioxidant capacity (T-AOC) showed a significant increase. The elevated concentrations of malondialdehyde (MDA) and HO indicated oxidative stress. Ion transport genes displayed distinct transcription patterns: Na-K-2Cl co-transporter-1 (), Na/H exchanger 3 (), aquaporin 7 (), and chloride channel protein 2 () were significantly upregulated; the α-subunit of Na/K-ATPase α) and carbonic anhydrase () displayed an initial increase followed by decline; whereas vacuolar-type ATPase () consistently decreased, suggesting compensatory mechanisms to maintain osmotic balance. Concurrently, HO triggered apoptosis (, Caspase-3/8) and autophagy (beclin-1, ), likely mediated by MAPK and AMPK signaling pathways. These findings reveal a coordinated yet adaptive response of crab gills to oxidative stress, providing new insights into the mechanistic basis of environmental stress tolerance in crustaceans.
氧化应激是水生生物在环境挑战下生理功能障碍的关键介质，但其对鳃生理的全面影响仍需进一步阐明。本研究调查了鳃对过氧化氢（H₂O₂）诱导的氧化应激的分子和细胞反应，整合了抗氧化防御、离子转运调节以及应激诱导的细胞凋亡和自噬。观察到鳃丝的形态改变，其特征为隔膜退化、血淋巴细胞积聚和明显肿胀。对于过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）等抗氧化酶，其活性增强，而暴露48小时后超氧化物歧化酶（SOD）活性降低。总体而言，总抗氧化能力（T-AOC）显著增加。丙二醛（MDA）和H₂O₂浓度升高表明存在氧化应激。离子转运基因呈现出不同的转录模式：钠-钾-2氯共转运体-1（NKCC1）、钠/氢交换体3（NHE3）、水通道蛋白7（AQP7）和氯离子通道蛋白2（CLC-2）显著上调；钠/钾-ATP酶α亚基（NKAα）和碳酸酐酶（CA）先升高后下降；而液泡型ATP酶（V-ATPase）持续下降，表明存在维持渗透平衡的补偿机制。同时，H₂O₂触发了凋亡（Caspase-3/8）和自噬（beclin-1），可能由丝裂原活化蛋白激酶（MAPK）和腺苷酸活化蛋白激酶（AMPK）信号通路介导。这些发现揭示了蟹鳃对氧化应激的协调且适应性反应，为甲壳类动物环境应激耐受性的机制基础提供了新的见解。
