SWCNTs induced autophagic cell death in human bronchial epithelial cells

Eun Jung Park, Nur Elida M. Zahari, Eun Woo Lee, Jaewhan Song, Jae Hyeok Lee, Myung Haing Cho, Jae Ho Kim

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)


Carbon nanotubes are being actively introduced in electronics, computer science, aerospace, and other industries. Thus, the urgent need for toxicological studies on CNTs is mounting. In this study, we investigated the alterations in cellular response with morphological changes induced by single-walled carbon nanotubes (SWCNTs) in BEAS-2B cells, a human bronchial epithelial cell line. At 24. h after exposure, SWCNTs rapidly decreased ATP production and cell viability as well a slight increase in the number of cells in the subG1 and G1 phases. In addition, SWCNTs increased the expression of superoxide dismutase (SOD)-1, but not SOD-2, and the number of cells generating ROS. The concentration of Cu and Zn ions also increased in a dose-dependent manner in cells exposed to SWCNTs. SWCNTs significantly enhanced the release of nitric oxide, interleukin (IL)-6, and IL-8 and up-regulated the expression of chemokine- and cytokine-related genes. Furthermore, the levels of autophagy-related genes, especially the DRAM1 gene, and the autophagosome formation-related proteins, were clearly up-regulated together with an increase of autophagosome-like vacuoles. Based on these results, we suggest that SWCNTs induce autophagic cell death through mitochondrial dysfunction and cytosolic damage in human bronchial epithelial cells.

Original languageEnglish
Pages (from-to)442-450
Number of pages9
JournalToxicology in Vitro
Issue number3
Publication statusPublished - 2014 Apr

Bibliographical note

Funding Information:
This work was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2011-35B-E00011). And this research was supported by National Platform Technology Programs of the Korean Ministry of Knowledge Economy (grant 10034751). M.H.C also acknowledges the support of the Veterinary Research Institute of Seoul National University in Korea.

All Science Journal Classification (ASJC) codes

  • Toxicology


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