Document Type
Article
Rights
Available under a Creative Commons Attribution Non-Commercial Share Alike 4.0 International Licence
Abstract
Due to their large specific surface area, the potential of nanoparticles to be highly reactive and to induce oxidative stress is particularly high. In addition, some types of nanoparticles contain transition metals as trace impurities which are known to generate reactive oxygen species (ROS) in biological systems. This study investigates the potential of two types of single-walled carbon nanotube samples, nanoparticulate carbon black and crocidolite asbestos to induce ROS in lung epithelial cells in vitro. Carbon nanotube and carbon black samples were used as produced, without further purification or processing, in order to best mimic occupational exposure by inhalation of airborne dust particles derived from carbon nanoparticle production. Intracellular ROS were measured following short-term exposure of primary bronchial epithelial cells (NHBE) and A549 alveolar epithelial carcinoma cells using the redox sensitive probe carboxydichlorofluorescin (carboxy-DCFDA). The oxidative potential of agglomerated nanoparticle samples was compared following dispersion in cell culture medium with and without foetal calf serum (FCS) supplement. In addition, samples were dispersed in dipalmitoylphosphatidylcholine (DPPC), the major component of lung surfactant. It could be illustrated that in vitro exposure of lung epithelial cells to carbon nanomaterial samples results only in moderate or low oxidative stress under the exposure conditions employed. However, cell responses are strongly dependent on the vehicle used for dispersion. Whereas the presence of DPPC increased intracellular ROS formation, FCS seemed to protect the cells from oxidative insult.
DOI
https://doi.org/10.1016/j.taap.2009.02.007
Recommended Citation
Herzog, Eva et al: Dispersion medium modulates oxidative stress response of human lung epithelial cells upon exposure to carbon nanomaterial samples. Toxicology and Applied Pharmacology, Vol.236, pp.276-281. doi:10.1016/j.taap.2009.02.007
Publication Details
In Toxicology and Applied Pharmacology, Vol.236, pp.276-281, 2009.