Foodborne iron overload induces oxidative stress and causes mitochondrial damage in the liver of grass carp (Ctenopharyngodon idellus)
文献类型： 外文期刊
作者： Huang, Xiaoman 1 ; Yang, Yan 1 ; Bai, Yanhan 1 ; Yang, Shiyi 1 ; Chen, Bing 2 ; Zhang, Linpeng 1 ; Liu, Lihan 1 ; Tao, Junjie 1 ; Tu, Chengming 1 ; Lin, Li 1 ; Qin, Zhendong 1 ;
作者机构： 1.Zhongkai Univ Agr & Engn, Coll Anim Sci & Technol, Guangdong Prov Water Environm & Aquat Prod Secur E, Guangzhou Key Lab Aquat Anim Dis & Waterfowl Breed, Guangzhou 510222, Guangdong, Peoples R China
2.Guangdong Acad Agr Sci, Inst Anim Sci, Guangdong Key Lab Anim Breeding & Nutr, Lab Anim Nutr & Feed Sci South China,Minist Agr &, Guangzhou 510640, Peoples R China
关键词： iron overload; Lipid peroxidation; Oxidative stress; Mitochondrial damage; Cell death
期刊名称：AQUACULTURE （ 影响因子：3.9； 五年影响因子：4.4 ）
ISSN： 0044-8486
年卷期： 2025 年 595 卷
页码：
收录情况： SCI
摘要： Iron is essential to biological processes such as energy metabolism and oxygen transport. However, excessive iron can cause iron overload and ultimately result in tissue damage. To date, the damage mechanism of foodborne iron overload in aquatic animals is still unclear. This study used grass carp (Ctenopharyngodon idellas) as the research subject to establish a chronic iron overload model by feeding diets with different iron levels, and combined in vitro experiments to investigate the mechanisms of iron overload-induced damage. The growth performance and liver HE staining indicated that a high-iron diet led to decreased growth in grass carp, accompanied by hepatic iron deposition. ELISA and qRT-PCR analysis data revealed that a high-iron diet disrupted the antioxidant balance and modulated the expression of genes associated with iron metabolism. CCK-8 determination results revealed that treatment of L8824 cells with ferri ammonii citras (FAC) resulted in iron overload, led to disruption of iron metabolism and enhanced the intracellular production of reactive oxygen species (ROS), and caused lipid peroxidation. Furthermore, qRT-PCR analysis results showed that the treatment of L8824 cells with FAC resulted in a significant up-regulation of genes associated with antioxidant, apoptosis, and necrosis pathways, and increased the rate of apoptosis. In addition, fluorescence microscopy observation and mitochondrial DNA detection data showed that excess iron could increase the iron accumulation in mitochondria and the production of mtROS, reduce the mitochondrial membrane potential, and finally cause mitochondria damage. In conclusion, our research offers invaluable insights that iron overload leads to disrupted intracellular iron pool stability, causing mitochondrial damage and oxidative stress, eventually causing cell death.
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