Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Internal Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.
Division of Nephrology, Chung Shan Medical University Hospital, Taichung, Taiwan; The School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Ecotoxicol Environ Saf. 2020 Apr 15;193:110348. doi: 10.1016/j.ecoenv.2020.110348. Epub 2020 Feb 27.
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 (InCl) on RAW264.7 macrophages. Cytotoxicity was induced by InCl in a concentration- and time-dependent manner. InCl 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, InCl induced DNA damage, also called genotoxicity, in a concentration-dependent manner. Cysteine-dependent aspartate-directed protease (caspase)-3, -8, and -9 were activated by InCl in a concentration-dependent manner. Mitochondria dysfunction and cytochrome c release from the mitochondria were induced by InCl in a concentration-dependent manner. Downregulation of BCL2 and upregulation of BAD were induced by InCl in a concentration-dependent manner. More, we proposed that InCl treatment generated reactive oxygen species (ROS) in a concentration-dependent manner. In conclusion, the current study revealed that InCl induced macrophage cytotoxicity, apoptosis, and genotoxicity via a mitochondria-dependent apoptotic pathway and ROS generation.
由于电子技术时代的快速发展，铟在半导体和光电子行业的液晶显示屏生产中发挥了重要材料的作用。本研究旨在评估氯化铟（InCl）对 RAW264.7 巨噬细胞的毒性作用及相关机制。细胞毒性呈浓度和时间依赖性。InCl 通过细胞凋亡而不是坏死诱导巨噬细胞死亡。根据细胞有丝分裂阻断微核试验和碱性单细胞凝胶电泳试验，InCl 以浓度依赖性方式诱导 DNA 损伤，也称为遗传毒性。胱天蛋白酶-3、-8 和 -9 被 InCl 以浓度依赖性方式激活。InCl 以浓度依赖性方式诱导线粒体功能障碍和细胞色素 c 从线粒体释放。InCl 以浓度依赖性方式下调 BCL2 并上调 BAD。此外，我们提出 InCl 处理以浓度依赖性方式产生活性氧（ROS）。总之，本研究表明 InCl 通过线粒体依赖性凋亡途径和 ROS 生成诱导巨噬细胞细胞毒性、细胞凋亡和遗传毒性。
