Research Center of Stem Cell and Biotherapy Technology, Xinxiang Medical University, Henan 453003, People's Republic of China.
J Biochem Mol Toxicol. 2013 Jun;27(6):330-6. doi: 10.1002/jbt.21495. Epub 2013 May 20.
This study aims to evaluate the cytotoxicity and responses of the cellular antioxidant system of 1-octyl-3-methylimidazolium chloride ([C8 mim][Cl]) on human hepatocarcinoma QGY-7701 cells. The results show that [C8 mim][Cl] can inhibit QGY-7701 cell growth and decrease their viabilities in a dose-dependent manner. The results also reveal that [C8 mim][Cl] exposure can induce apoptosis in the [C8 mim][Cl]-treated QGY-7701 cells. In addition, the results of biochemical assays show that [C8 mim][Cl] exposure causes overproduction of reactive oxygen species (ROS), inhibits superoxide dismutase (SOD) and catalase (CAT) activities, decreases reduced glutathione (GSH) content, and increases the cellular malondialdehyde (MDA) level. These results suggest that ROS-mediated oxidative stress may be responsible for the apoptosis induced by [C8 mim][Cl] in QGY-7701 cells.
本研究旨在评估 1-辛基-3-甲基咪唑氯盐 ([C8 mim][Cl]) 对人肝癌 QGY-7701 细胞的细胞毒性和细胞抗氧化系统的反应。结果表明，[C8 mim][Cl] 可抑制 QGY-7701 细胞生长并呈剂量依赖性降低其活力。结果还表明，[C8 mim][Cl] 暴露可诱导 [C8 mim][Cl] 处理的 QGY-7701 细胞凋亡。此外，生化分析结果表明，[C8 mim][Cl] 暴露导致活性氧（ROS）过度产生，抑制超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性，降低还原型谷胱甘肽（GSH）含量，并增加细胞丙二醛（MDA）水平。这些结果表明，ROS 介导的氧化应激可能是 [C8 mim][Cl] 诱导 QGY-7701 细胞凋亡的原因。
