Pulmonary toxicity of single-wall carbon nanotubes and its oxidative stress mechanism
10.16781/j.0258-879x.2016.07.0815
- Author:
Gao-Jian LÜ
1
Author Information
1. Key Laboratory for Ultrafine Materials of Ministry of Education, School of Material Science andEngineering, East China University of Science and Technology
- Publication Type:Journal Article
- Keywords:
Oxidative stress;
Pulmonary toxicity;
Redox homeostasis;
Single-wall carbon nano tubes
- From:
Academic Journal of Second Military Medical University
2016;37(7):815-820
- CountryChina
- Language:Chinese
-
Abstract:
Objective To systematically study the pulmonary toxicity of single-wall carbon nanotubes (SWCNTs) and to explore the related cytotoxicity mechanism, so as to provide a theoretical basis for the safe productionandapplication of SWCNTs. Methods A549 cells were cultured in the media containing 0, 25, 50, 100, 150, and 200 μg/mL SWCNTs for 24 h, and then the cell viability and degree of cell membrane damage were assessed by CCK-8 and lactate dehydrogenase (LDH) release assay kit, respectively; the ultrastructural alteration of A549 cells was detected by transmission electron microscope (TEM). The oxidative stress response was evaluated by assessing reactive oxygen species (ROS), glutathione (GSH) and superoxide dismutase (SOD). The rats were exposed to SWCNTs by intratracheal inhalation, and then the animals were sacrificed 3 days later and the pathological sections of lung tissue were examined. Results SWCNTs showed considerable toxicity to A549 cells, decreasing cell viability, causing severe damage of cell membrane and ultrastructure, increasing the intracellular ROS level, and decreasing GSH content and SOD activity. It was found that oxidative stress is the main mechanism of SWCNTs toxicity on A549 cells. In vivo toxicity results showed that SWCNTs accumulated in the lung tissue # causing alveolar wall edema. Conclusion In vitro and in vivo toxicity results have found that SWCNTs possess a significant pulmonary toxicity # with its main toxicity mechanismbeing oxidative stress.
