A comparative study of effects of singlewall carbon nanotubes and crocidolite asbestos in human BEAS-2B cells.
Pacurari-M; Castranova-A; Friend-S; Robinson-V; Vallyathan-V
Toxicologist 2009 Mar; 108(1):461
Single-wall carbon nanotubes (SWCNT) are of great interest to many aspects of industry including, but not limited to, electronics and pharmaceutics. As SWCNTmanufactured goods are being introduced into market, concerns regarding their potential for producing environmental and human health risks have been raised. In the present study, we investigated SWCNT effects on the human broncho-epithelial cells (BEAS-2B). Exposure of BEAS-2B cells to SWCNT resulted in dose-dependent loss of cell viability and oxidative stress by means of dose-dependent increase in OH radical production and superoxide dismutase activity (SOD). Furthermore, SWCNT induced time- and dose-dependent apoptosis and phosphorylation of histone gamma-H2A.X, a variant of histone H2A that is activated following DNA damage. Whether SWCNT have the potential to induce apoptosis, BEAS-2B cells were exposed for different time points to SWCNT (50 mu g/cm2), and analyzed for PARP activation, as a molecular marker of apoptosis. The level of cleaved PARP increased after 18h of exposure. This level decreased when cells were allowed to recover for 6h in normal growth media. We also examined the ability of SWCNT to induce the transactivation of activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kB), transcription factors that are important members of signal transduction pathways. SWCNT induced greater activation of AP-1 and NF-kB at lower doses as compared to higher doses. These effects were diminished by PD98059, an inhibitor of MAP kinase. Crocidolite asbestos was used as a positive control along with SWCNT, and the effects of crocidolite were far greater as compared to SWCNT. Considering the role of airway epithelium as a barrier and its role in pulmonary functioning, the results of the present study suggest that interaction of SWCNT with airway cells may cause adverse biological responses that may initiate respiratory diseases.
Biological-effects; Biological-factors; Cellular-reactions; Cell-biology; Cell-metabolism; Cell-morphology; Cellular-function; Cytology; Electric-properties; Electrical-conductivity; Exposure-assessment; Exposure-levels; Irritants; Inhalation-studies; Lung-cells; Lung-irritants; Microscopic-analysis; Microscopy; Oxidative-metabolism; Particle-aerodynamics; Particulates; Pharmaceutical-industry; Pulmonary-disorders; Pulmonary-system-disorders; Respiratory-irritants; Respiratory-system-disorders; Statistical-analysis; Toxic-effects; Nanotechnology;
Author Keywords: Apoptosis; asbestos; carbon nano-particles; cell toxicity; oxidative stress
7440-44-0; 12001-28-4; 1332-21-4; 1333-86-4
The Toxicologist. Society of Toxicology 48th Annual Meeting and ToxExpo, March 15-19, 2009, Baltimore, Maryland