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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/61525
Title: Intracellular nickel accumulation induces apoptosis and cell cycle arrest in human astrocytic cells
Authors: Ruedeemars Yubolphan
Suttinee Phuagkhaopong
Kant Sangpairoj
Nathawut Sibmooh
Christopher Power
Pornpun Vivithanaporn
University of Alberta
Faculty of Medicine Ramathibodi Hospital, Mahidol University
Mahidol University
Thammasat University
Keywords: Biochemistry, Genetics and Molecular Biology;Chemistry;Materials Science
Issue Date: 16-Jan-2021
Citation: Metallomics : integrated biometal science. Vol.13, No.1 (2021)
Abstract: © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. Nickel, a heavy metal found in electronic wastes and fume from electronic cigarettes, induces neuronal cell death and is associated with neurocognitive impairment. Astrocytes are the first line of defense against nickel after entering the brain; however, the effects of nickel on astrocytes remain unknown. Herein, we investigated the effect of nickel exposure on cell survival and proliferation and the underlying mechanisms in U-87 MG human astrocytoma cells and primary human astrocytes. Intracellular nickel levels were elevated in U-87 MG cells in a dose- and time-dependent manner after exposure to nickel chloride. The median toxic concentrations of nickel in astrocytoma cells and primary human astrocytes were 600.60 and >1000 µM at 48 h post-exposure, respectively. Nickel exposure triggered apoptosis in concomitant with the decreased expression of anti-apoptotic B-cell lymphoma protein (Bcl-2) and increased caspase-3/7 activity. Nickel induced reactive oxygen species formation. Additionally, nickel suppressed astrocyte proliferation in a dose- and time-dependent manner by delaying G2 to M phase transition through the upregulation of cyclin B1 and p27 protein expression. These results indicate that nickel-induced cytotoxicity of astrocytes is mediated by the activation of apoptotic pathway and disruption of cell cycle regulation.
URI: http://repository.li.mahidol.ac.th/dspace/handle/123456789/61525
metadata.dc.identifier.url: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85101469556&origin=inward
ISSN: 1756591X
Appears in Collections:Scopus 2021

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