Melatonin relieves 2,2,4,4-tetrabromodiphenyl ether (BDE-47)-induced apoptosis and mitochondrial dysfunction through the AMPK-Sirt1-PGC-1 alpha axis in fish kidney cells (CIK)
文献类型: 外文期刊
作者: Luan, Peixian 1 ; Zhang, Haoran 2 ; Chen, Xiaoming 2 ; Zhu, Yue 2 ; Hu, Guo 1 ; Cai, Jingzeng 2 ; Zhang, Ziwei 2 ;
作者机构: 1.Chinese Acad Fishery Sci, Heilongjiang River Fisheries Res Inst, Harbin 0150070, Peoples R China
2.Northeast Agr Univ, Coll Vet Med, Harbin 150030, Peoples R China
3.Minist Agr & Rural Affairs, Key Lab Freshwater Aquat Biotechnol & Breeding, Harbin 150070, Peoples R China
关键词: BDE-47; Melatonin; Mitochondrial fusion and fission; Apoptosis; Fish kidney cells
期刊名称:ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY ( 影响因子:7.129; 五年影响因子:7.284 )
ISSN: 0147-6513
年卷期: 2022 年 232 卷
页码:
收录情况: SCI
摘要: Polybrominated diphenyl ethers (PBDEs) exist in aquatic environments with nephrotoxicity to non-target aquatic species. Melatonin (MT) exhibits an inhibitory effect of oxidative stress and apoptosis in various diseases. 2, 2', 4, 4'-tetrabromodiphenyl ether (BDE-47) is the main homolog of PBDE samples. Therefore, we investigated the toxic mechanism of BDE-47 and the alleviation effect of MT, the ctenopharyngodon idellus kidney (CIK) cells were treated with BDE-47 (100 mu M) and/or MT (60 mu M) for 24 h. Firstly, BDE-47 exposure could inhibit oxidative stress-related antioxidant enzymes (T-AOC, SOD, CAT and GPx) and increase the content of malondialdehyde (MDA) to cause oxidative stress. Secondly, BDE-47 enhanced mitochondrial division and inhibited fusion to induce mitochondrial membrane potential in CIK cells. BDE-47 enhanced the mRNA and protein levels of mitochondrial-pathway apoptosis related genes (Cas 3, Cyt-c, and BAX). Thirdly, BDE-47 treatment decreased the expression levels of mitochondrial-related regulatory factors AMPK-Sirt1-PGC-1 alpha signal pathway. Intriguingly, BDE-47-induced oxidative stress, mitochondrial pathway apoptosis and mitochondrial dynamics disorder could be alleviated by MT treatment. Overall, we concluded that MT could relieve BDE-47-induced oxidative stress, mitochondrial dysfunction and apoptosis through the AMPK-Sirt1-PGC-1 alpha axis. These results enrich the mechanisms of BDE-47 poisoning and reveal that MT treatment may be a potential strategy for solving BDE-47 poisoning.
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