Cell Growth Inhibition and Apoptosis by SDS-solubilized Single-walled Carbon Nanotubes in Normal Rat Kidney Epithelial Cells

Title
Cell Growth Inhibition and Apoptosis by SDS-solubilized Single-walled Carbon Nanotubes in Normal Rat Kidney Epithelial Cells
Author(s)
곽미경Chang-Won Nam[Chang-Won Nam]강수진Youn Kyung Kang[Youn Kyung Kang]
Keywords
INDUCE OXIDATIVE STRESS; PULMONARY TOXICITY; HEK293 CELLS; CYTOTOXICITY; EXPOSURE; NANOMATERIALS; TOXICOLOGY; MICE
Issue Date
201104
Publisher
PHARMACEUTICAL SOC KOREA
Citation
ARCHIVES OF PHARMACAL RESEARCH, v.34, no.4, pp.661 - 669
Abstract
Carbon nanotubes (CNTs), promising novel nanomaterials, have been applied to drug delivery and bio-imaging; however, their potential harmful effects on human health and environment have gained much attention recently. In the present study, we investigated cytotoxic effect of solubilized single-walled CNTs (SWCNTs), which were dispersed in water by sodium dodesyl sulfate (SDS), in normal rat kidney epithelial cells (NRK-52E). SDS-SWCNT (0.125-10 mu g/mL)-treated NRK-52E cells showed decreased cell viability and enhanced cytotoxicity marker levels following 24-48 h incubation. In addition, SDS-SWCNT treatment evoked the cell growth inhibition: 8 mu g/mL SDS-SWCNT induced the growth arrest at G(0)/G(1) phase and levels of cell cycle-related proteins such as CDK2, CDK6 and phosphorylated-retinoblastoma (pRB) were significantly reduced by CNT. Whereas, at higher concentration of SDS-SWCNT, the percentage of cell numbers in apoptotic sub-G(1) phase was substantially increased. Along with these changes, SDS-SWCNT treatment elevated protein levels for p53 and p21 with a concomitant increase in the single strand DNA breakage. Taken together, these results suggest that SDS-solubilized SWCNTs exert genotoxic effect in renal epithelial cells, and p53-dependent signaling can be associated with the growth arrest and apoptosis events upon CNT-induced DNA damage.
URI
http://hdl.handle.net/YU.REPOSITORY/25386http://dx.doi.org/10.1007/s12272-011-0417-4
ISSN
0253-6269
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약학대학 > 약학부 > Articles
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