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

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

  • Ecotoxicol Environ Saf. 2020 Apr 15:193:110348. doi: 10.1016/j.ecoenv.2020.110348.
Ping-Kun Tsai 1,  Sheng-Wen Wu 2,  Chen-Yu Chiang 3,  Min-Wei Lee 4,  Hung-Yi Chen 5,  Wen-Ying Chen 6,  Chun-Jung Chen 7,  Shun-Fa Yang 8,  Chao-Bin Yeh 9,  Yu-Hsiang Kuan 10
Affiliations

Affiliations

  • 1 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Internal Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.
  • 2 Division of Nephrology, Chung Shan Medical University Hospital, Taichung, Taiwan; The School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
  • 3 Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan; Department of Veterinary Medicine, National Chung Hsing University, Taichung, Taiwan.
  • 4 Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan; A Graduate Institute of Microbiology and Public Health, National Chung Hsing University, Taichung, Taiwan.
  • 5 School of Pharmacy, China Medical University, Taichung, Taiwan.
  • 6 Department of Veterinary Medicine, National Chung Hsing University, Taichung, Taiwan.
  • 7 Department of Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan.
  • 8 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
  • 9 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; The School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Emergency Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.
  • 10 Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan. Electronic address: kuanyh@csmu.edu.tw.
PMID: 32114240 DOI: 10.1016/j.ecoenv.2020.110348
Abstract

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.

Keywords

Apoptosis; Genotoxicity; InCl(3); Macrophages; Mitochondrial dysfunction; ROS generation.

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