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Oxidative stress and apoptosis induced by titanium dioxide nanoparticles in cultured BEAS-2B cells
Cited 413 time in
Web of Science
Cited 445 time in Scopus
- Authors
- Issue Date
- 2008-07-10
- Publisher
- Elsevier
- Citation
- Toxicol. Lett. 180, 222-229
- Keywords
- Titanium dioxide nanoparticles ; Apoptosis ; Oxidative stress ; BEAS-2B cells
- Abstract
- As the applications of industrial nanoparticles are being developed, the concerns on the environmental
health are increasing. Cytotoxicities of titanium dioxide nanoparticles of different concentrations (5,
10, 20 and 40 g/ml) were evaluated in this study using a cultured human bronchial epithelial cell line,
BEAS-2B. Exposure of the cultured cells to nanoparticles led to cell death, reactive oxygen species (ROS)
increase, reduced glutathione (GSH) decrease, and the induction of oxidative stress-related genes such
as heme oxygenase-1, thioredoxin reductase, glutathione-S-transferase, catalase, and a hypoxia inducible
gene. The ROS increase by titanium dioxide nanoparticles triggered the activation of cytosolic caspase-
3 and chromatin condensation, which means that titanium dioxide nanoparticles exert cytotoxicity by
an apoptotic process. Furthermore, the expressions of inflammation-related genes such as interleukin-
1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), TNF-a, and C-X-C motif ligand 2 (CXCL2) were also
elevated. The induction of IL-8 by titanium dioxide nanoparticles was inhibited by the pre-treatment
with SB203580 and PD98059, which means that the IL-8 was induced through p38 mitogen-acitvated
protein kinase (MAPK) pathway and/or extracellular signal (ERK) pathway. Uptake of the nanoparticles
into the cultured cells was observed and titanium dioxide nanoparticles seemed to penetrate
into the cytoplasm and locate in the peri-region of the nucleus as aggregated particles, which may
induce direct interactions between the particles and cellular molecules, to cause adverse biological
responses.
- ISSN
- 0378-4274
- Language
- English
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