This study purposes to assess the cytotoxicity of 1‐dodecyl‐3‐methylimidazolium chloride ([C12min]Cl) in human hepatocellular carcinoma (HepG2) cells. To this end, HepG2 cells were exposed to a range concentration of [C12min]Cl and evaluated cell viability, genotoxicity, oxidative stress, apoptosis, cell cycle, and apoptosis‐related gene expression to determine cytotoxicity. The outcomes showed that [C12min]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 [C12min]Cl prompted DNA damage and apoptosis, reduced SOD and GSH content, enhanced MDA level, and changed the cell cycle of HepG2 cells. In addition, [C12min] 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 [C12min]C1. In summary, these results indicate that [C12min]Cl exerts genotoxicity, physiological toxicity and prompts apoptosis in HepG2 cells, and is not an alleged green solvent.

中文翻译：

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咪唑离子液体1-十二烷基-3-甲基咪唑氯化物诱导HepG2细胞的细胞毒性、遗传毒性、氧化应激和细胞凋亡

本研究旨在评估 1-dodecyl-3-methylimidazolium chloride ([C12min]Cl) 在人肝细胞癌 (HepG2) 细胞中的细胞毒性。为此，将 HepG2 细胞暴露于一定浓度的 [C12min]Cl 中，并评估细胞活力、基因毒性、氧化应激、细胞凋亡、细胞周期和细胞凋亡相关基因表达，以确定细胞毒性。结果表明，[C12min]Cl 以浓度和时间依赖性方式抑制 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 [C12min]Cl 会导致 DNA 损伤和细胞凋亡，降低 SOD 和 GSH 含量，提高 MDA 水平，并改变 HepG2 细胞的细胞周期。此外，[C12min] Cl 引起 p53、Bax 和 Bcl-2 表达水平的改变，表明 p53 和 Bcl-2 家族可能参与 [C12min]C1 诱导的 HepG2 细胞的细胞毒性和凋亡。总之，这些结果表明 [C12min]Cl 在 HepG2 细胞中发挥遗传毒性、生理毒性并促进细胞凋亡，而不是所谓的绿色溶剂。