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

Author(s) Tsai, P.K.; Wu, S.W.; Chiang, C.Y.; Lee, M.W.; Chen, H.Y.; Chen, W.Y.; Chen, C.J.; Yang, S.F.; Bin Yeh, C.; Kuan, Y.H.
Journal Ecotoxicol Environ Saf
Date Published 2020 Apr 15

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.

DOI 10.1016/j.ecoenv.2020.110348
ISSN 1090-2414
Citation Ecotoxicol Environ Saf. 2020;193:110348.

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