铜诱导的线粒体功能障碍是通过原发性鸡胚肝细胞中的氧化应激介导的异常线粒体分裂。
Cu-induced mitochondrial dysfunction is mediated by abnormal mitochondrial fission through oxidative stress in primary chicken embryo hepatocytes.
机构信息
College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 211166, China.
出版信息
J Trace Elem Med Biol. 2021 May;65:126721. doi: 10.1016/j.jtemb.2021.126721. Epub 2021 Jan 23.
BACKGROUND
Excess copper (Cu) is an oxidative stress factor which associates with a variety of diseases. The aim of this study was to evaluate the effect of Cu in primary chicken embryo hepatocytes (CEHs).
METHODS
CEHs were isolated from 13 days old chicken embryos and followed by different concentration Cu (0, 10, 100, 200 μM) and/or ALC treatment (0.3 mg/mL) for 12 or 24 h. The effects of Cu exposure in CEHs were determined by detecting reactive oxygen species (ROS), malondialdehyde (MDA), mitochondrial membrane potential (MMP), and ATP levels. The expression of mitochondrial dynamics-related genes and proteins were also detected.
RESULTS
Results showed that Cu treatment (100 or 200 μM) significantly decreased CEHs viability, MMP and ATP levels, increased ROS and MDA levels in 12 or 24 h. The up-regulated mitochondrial fission genes and protein in 100 and 200 μM Cu groups suggested Cu promoted mitochondrial division but not fusion. However, the co-treatment of ALC and Cu alleviated those changes compared with the 100 or 200 μM Cu groups.
CONCLUSION
In conclusion, we speculated that Cu increased the oxidative stress and induced mitochondria dysfunction via disturbing mitochondrial dynamic balance in CEHs, and this process was not completely reversible.
背景
过量的铜(Cu)是一种氧化应激因素,与多种疾病有关。本研究旨在评估 Cu 对原代鸡胚肝细胞(CEHs)的影响。
方法
从 13 日龄鸡胚中分离 CEHs,并分别用不同浓度的 Cu(0、10、100、200 μM)和/或 ALC(0.3 mg/mL)处理 12 或 24 小时。通过检测活性氧(ROS)、丙二醛(MDA)、线粒体膜电位(MMP)和 ATP 水平来确定 Cu 暴露对 CEHs 的影响。还检测了线粒体动力学相关基因和蛋白的表达。
结果
结果表明,Cu 处理(100 或 200 μM)在 12 或 24 小时内显著降低了 CEHs 的活力、MMP 和 ATP 水平,增加了 ROS 和 MDA 水平。100 和 200 μM Cu 组中上调的线粒体分裂基因和蛋白表明 Cu 促进了线粒体分裂而不是融合。然而,与 100 或 200 μM Cu 组相比,ALC 和 Cu 的共同处理减轻了这些变化。
结论
总之,我们推测 Cu 通过干扰 CEHs 中线粒体动态平衡增加氧化应激并诱导线粒体功能障碍,而这一过程并非完全可逆。