College of Life Science, Henan Normal University, Xinxiang, Henan, People's Republic of China.
Environ Toxicol. 2020 Jun;35(6):665-672. doi: 10.1002/tox.22901. Epub 2020 Jan 9.
This study purposes to assess the cytotoxicity of 1-dodecyl-3-methylimidazolium chloride ([C min]Cl) in human hepatocellular carcinoma (HepG2) cells. To this end, HepG2 cells were exposed to a range concentration of [C min]Cl and evaluated cell viability, genotoxicity, oxidative stress, apoptosis, cell cycle, and apoptosis-related gene expression to determine cytotoxicity. The outcomes showed that [C min]Cl curbed HepG2 cell growth and reduced cell viability in a concentration- and time-dependent manner. Moreover, our assay results also revealed that exposure to [C min]Cl prompted DNA damage and apoptosis, reduced SOD and GSH content, enhanced MDA level, and changed the cell cycle of HepG2 cells. In addition, [C min] Cl caused alters in the expression levels of p53, Bax, and Bcl-2, indicating that p53 and Bcl-2 family may be involved in the cytotoxicity and apoptosis of HepG2 cells induced by [C min]C1. In summary, these results indicate that [C min]Cl exerts genotoxicity, physiological toxicity and prompts apoptosis in HepG2 cells, and is not an alleged green solvent.
本研究旨在评估 1-十二烷基-3-甲基咪唑氯化物([C min]Cl)在人肝癌细胞(HepG2)中的细胞毒性。为此，将 HepG2 细胞暴露于一系列浓度的[C min]Cl 中，并评估细胞活力、遗传毒性、氧化应激、细胞凋亡、细胞周期和凋亡相关基因表达，以确定细胞毒性。结果表明，[C min]Cl 以浓度和时间依赖的方式抑制 HepG2 细胞生长并降低细胞活力。此外，我们的测定结果还表明，暴露于[C min]Cl 会引发 DNA 损伤和细胞凋亡，降低 SOD 和 GSH 含量，增加 MDA 水平，并改变 HepG2 细胞的细胞周期。此外，[C min]Cl 还导致 p53、Bax 和 Bcl-2 的表达水平发生变化，表明 p53 和 Bcl-2 家族可能参与了[C min]Cl 诱导的 HepG2 细胞的细胞毒性和细胞凋亡。总之，这些结果表明，[C min]Cl 对 HepG2 细胞具有遗传毒性、生理毒性，并诱导其凋亡，并非所谓的绿色溶剂。
