Cytotoxicity, oxidative stress, and apoptosis in HepG2 cells induced by ionic liquid 1-methyl-3-octylimidazolium bromide.

Abstract

The present study aimed to determine the cytotoxicity of 1-methyl-3-octylimidazolium bromide ([C8mim]Br) on the human hepatocellular carcinoma (HepG2) cells in order to elucidate the biochemical and molecular mechanism of [C8mim]Br-cytotoxicity. For this purpose, cell viability, oxidative stress, apoptosis, caspase activity, and apoptosis-related gene expression in HepG2 cells following [C8mim]Br-exposure were evaluated. The results showed that viability of HepG2 cells was decreased by [C8mim]Br-exposure in a concentration-dependent pattern. Moreover, biochemical assays reveal that [C8mim]Br-exposure can induce apoptosis, cause overproduction of reactive oxygen species (ROS), inhibit superoxide dismutase and catalase, reduce glutathione content, and increase the cellular malondialdehyde level of HepG2 cells. The transcriptions of p53 and bax were markedly up-regulated while bcl-2 was significantly down-regulated in HepG2 cells after [C8mim]Br-exposure, suggesting that p53 and bcl-2 family may be involved in the cytotoxicity and apoptosis of HepG2 cells caused by [C8mim]Br. In addition, we also found that caspase-3, caspase-8, and caspase-9 were significantly activated in HepG2 cells following [C8mim]Br-exposure. Our results suggest that ROS may be a key early signal of [C8mim]Br-induced apoptosis and caspases play a key role in the initiation and execution of apoptosis of HepG2 cells.

• Authors: Xiaoyu Li, Junguo Ma, Jianji Wang
• Journal: Ecotoxicology and environmental safety (Ecotoxicol Environ Saf) Vol. 120 Pg. 342-8 (Oct 2015) ISSN: 1090-2414 [Electronic] Netherlands
• PMID: 26099465 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier Inc. All rights reserved.

Chemical References

• 1-methyl-3-octylimidazolium bromide
• BAX protein, human
• Imidazoles
• Reactive Oxygen Species
• Tumor Suppressor Protein p53
• bcl-2-Associated X Protein
• Malondialdehyde
• Catalase
• Superoxide Dismutase
• CASP3 protein, human
• CASP8 protein, human
• CASP9 protein, human
• Caspase 3
• Caspase 8
• Caspase 9
• Glutathione

Topics

• Apoptosis (drug effects)
• Caspase 3 (genetics, metabolism)
• Caspase 8 (genetics, metabolism)
• Caspase 9 (genetics, metabolism)
• Catalase (antagonists & inhibitors, metabolism)
• Cell Survival (drug effects)
• Down-Regulation
• Glutathione (antagonists & inhibitors, metabolism)
• Hep G2 Cells
• Humans
• Imidazoles (toxicity)
• Malondialdehyde (metabolism)
• Oxidative Stress (drug effects)
• Reactive Oxygen Species (metabolism)
• Superoxide Dismutase (antagonists & inhibitors, metabolism)
• Tumor Suppressor Protein p53 (genetics, metabolism)
• Up-Regulation
• bcl-2-Associated X Protein (genetics, metabolism)