College of Animal Science and Technology, Northeast Agricultural University, NO. 600 Chang Jiang Road, Xiang Fang District, Harbin, 150030, PR China.
Electrical and Information Engineering College, JiLin Agricultural Science and Technology University, Jilin, 132101, PR China.
Fish Shellfish Immunol. 2023 Jul;138:108853. doi: 10.1016/j.fsi.2023.108853. Epub 2023 May 27.
Cadmium (Cd), a toxic heavy metal pollutant, is a threat to human and eatable fish health. Common carps are widely cultivated and eaten by humans. However, there are no reports about Cd-damaged common carp hearts. Our experiment attempted to investigate the cardiotoxicity of Cd to common carps by establishing a common carp Cd exposure model. Our results showed that Cd injured hearts. Moreover, Cd treatment induced autophagy via miR-9-5p/Sirt1/mTOR/ULK1 pathway. Cd exposure caused oxidant/antioxidant imbalance and oxidative stress; and led to energetic impairment. Energetic impairment partook in oxidative stress-mediated autophagy through AMPK/mTOR/ULK1 pathway. Furthermore, Cd caused mitochondrial division/fusion imbalance and resulted in inflammatory injury via NF-κB-COX-2-PTGEs and NF-κB-COX-2-TNF-α pathways. Oxidative stress mediated mitochondrial division/fusion imbalance, further induced inflammation and autophagy via OPA1/NF-κB-COX-2-TNF-α-Beclin1 and OPA1/NF-κB-COX-2-TNF-α/P62 pathways under Cd treatment. Taken together, miR-9-5p, oxidative stress, energetic impairment, mitochondrial division/fusion imbalance, inflammation, and autophagy participated in the mechanism of Cd-cardiotoxicity to common carps. Our study revealed harmful effect of Cd on hearts, and provided new information for researches of environmental pollutant toxicity.
镉 (Cd) 是一种有毒的重金属污染物，对人类和可食用鱼类的健康构成威胁。鲤鱼是广泛养殖和食用的鱼类，但目前尚无关于 Cd 损伤鲤鱼心脏的报道。本实验通过建立鲤鱼 Cd 暴露模型，试图研究 Cd 对鲤鱼心脏的毒性作用。结果表明，Cd 损伤心脏，通过 miR-9-5p/Sirt1/mTOR/ULK1 通路诱导自噬。Cd 暴露导致氧化应激和能量损伤，氧化应激部分通过 AMPK/mTOR/ULK1 通路参与自噬。此外，Cd 引起线粒体分裂/融合失衡，通过 NF-κB-COX-2-PTGEs 和 NF-κB-COX-2-TNF-α 通路导致炎症损伤。氧化应激介导的线粒体分裂/融合失衡通过 OPA1/NF-κB-COX-2-TNF-α-Beclin1 和 OPA1/NF-κB-COX-2-TNF-α/P62 通路进一步诱导炎症和自噬。综上所述，miR-9-5p、氧化应激、能量损伤、线粒体分裂/融合失衡、炎症和自噬参与了 Cd 致鲤鱼心脏毒性的机制。本研究揭示了 Cd 对心脏的有害作用，为环境污染物毒性研究提供了新信息。
