Evaluation of cytotoxicity, apoptosis, and genotoxicity induced by indium chloride in macrophages through mitochondrial dysfunction and reactive oxygen species generation

doi:doi.org/10.1016/j.ecoenv.2020.110348

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/22376

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题名:	Evaluation of cytotoxicity, apoptosis, and genotoxicity induced by indium chloride in macrophages through mitochondrial dysfunction and reactive oxygen species generation
作者:	Tsai, Ping-Kun;Wu, Sheng-Wen;Chiang, Chen-Yu;Lee, Min-Wei;Chen, Hung-Yi;Chen, Wen-Ying;Chen, Chun-Jung;Yang, Shun-Fa;Yeh, Chao-Bin;Kuan, Yu-Hsiang
关键词:	Apoptosis;Genotoxicity;InCl(3);Macrophages;Mitochondrial dysfunction;ROS generation.
日期:	2020-04-15
上传时间:	2022-06-06T02:17:46Z (UTC)
出版者:	Elsevier Inc.
摘要:	Due to rapid advances in the era of electronic technologies, indium has played the important material for the production of liquid crystal display screens in the semiconductor and optoelectronic industries. The present study focuses on evaluating the toxic effects and related mechanisms of indium chloride (InCl3) on RAW264.7 macrophages. Cytotoxicity was induced by InCl3 in a concentration- and time-dependent manner. InCl3 had the ability to induce macrophage death through apoptosis rather than through necrosis. According to the cytokinesis-block micronucleus assay and alkaline single-cell gel electrophoresis assay, InCl3 induced DNA damage, also called genotoxicity, in a concentration-dependent manner. Cysteine-dependent aspartate-directed protease (caspase)-3, -8, and -9 were activated by InCl3 in a concentration-dependent manner. Mitochondria dysfunction and cytochrome c release from the mitochondria were induced by InCl3 in a concentration-dependent manner. Downregulation of BCL2 and upregulation of BAD were induced by InCl3 in a concentration-dependent manner. More, we proposed that InCl3 treatment generated reactive oxygen species (ROS) in a concentration-dependent manner. In conclusion, the current study revealed that InCl3 induced macrophage cytotoxicity, apoptosis, and genotoxicity via a mitochondria-dependent apoptotic pathway and ROS generation.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/22376
關聯:	Ecotoxicol Environ Saf, 193, 110348.
显示于类别:	[醫學系] 期刊論文

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