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1-辛基-3-甲基咪唑氯盐诱导 PC12 细胞的毒性细胞化学改变和线粒体功能障碍。

Toxic cytological alteration and mitochondrial dysfunction in PC12 cells induced by 1-octyl-3-methylimidazolium chloride.

机构信息

College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.

出版信息

Toxicol In Vitro. 2012 Oct;26(7):1087-92. doi: 10.1016/j.tiv.2012.07.006. Epub 2012 Jul 23.

DOI:10.1016/j.tiv.2012.07.006
PMID:22835898
Abstract

Ionic liquids have recently received considerable attention due to their negligible vapor pressure and substitute for conventional organic solvents. However, their solubility in water and a great deal of literature regarding their toxicity on aquatic organisms have caused much concern in recent years. This study aims to evaluate the cytotoxicity of 1-octyl-3-methylimidazolium chloride ([C(8)mim][Cl]) on the rat pheochromocytoma (PC12) cell line by cell viability assay and to determine the cytological alterations and damages in PC12 cells after 24h of exposure at the concentrations of 0.07, 0.14, and 0.28 mM of [C(8)mim][Cl]. The results show that [C(8)mim][Cl] inhibits PC12 cell growth and decreases their viabilities in a remarkable dose-dependent manner, and the 24h EC(50) of [C(8)mim][Cl] for PC12 cells is calculated to be around 0.56 mM. Our results also reveal that [C(8)mim][Cl]-exposure induces DNA damage, sustained increase of intracellular Ca(2+), overproduction of reactive oxygen species, gradually exhausted cellular ATP, mitochondrial permeability transition, and apoptosis in PC12 cells. We suppose that mitochondrial permeability transition and mitochondrial dysfunction maybe the major cytotoxicity mechanism of [C(8)mim]Cl for PC12 cells.

摘要

离子液体由于其蒸汽压低和可替代传统有机溶剂而受到广泛关注。然而,近年来它们在水中的溶解度以及大量关于其对水生生物毒性的文献引起了人们的极大关注。本研究旨在通过细胞活力测定评估 1-辛基-3-甲基咪唑氯化物([C(8)mim][Cl])对大鼠嗜铬细胞瘤(PC12)细胞系的细胞毒性,并确定在浓度为 0.07、0.14 和 0.28mM 的[C(8)mim][Cl]下,PC12 细胞暴露 24 小时后的细胞形态变化和损伤。结果表明,[C(8)mim][Cl]以显著的剂量依赖性方式抑制 PC12 细胞生长并降低其活力,[C(8)mim][Cl]对 PC12 细胞的 24 小时 EC(50)约为 0.56mM。我们的结果还表明,[C(8)mim][Cl]暴露诱导 DNA 损伤、细胞内 Ca(2+)持续增加、活性氧过度产生、细胞内 ATP 逐渐耗尽、线粒体通透性转换和 PC12 细胞凋亡。我们推测线粒体通透性转换和线粒体功能障碍可能是[C(8)mim]Cl 对 PC12 细胞产生细胞毒性的主要机制。

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