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Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells

It has been reported that overproduction of reactive oxygen species occurs after brain injury and mediates neuronal cells degeneration. In the present study, we examined the role of Ras signaling on hydrogen peroxide-induced neuronal cells degeneration in dopaminergic neuroblastoma SH-SY5Y cells. Hy...

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Detalles Bibliográficos
Autores principales: Chetsawang, Jirapa, Govitrapong, Piyarat, Chetsawang, Banthit
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943129/
https://www.ncbi.nlm.nih.gov/pubmed/20871828
http://dx.doi.org/10.1155/2010/803815
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author Chetsawang, Jirapa
Govitrapong, Piyarat
Chetsawang, Banthit
author_facet Chetsawang, Jirapa
Govitrapong, Piyarat
Chetsawang, Banthit
author_sort Chetsawang, Jirapa
collection PubMed
description It has been reported that overproduction of reactive oxygen species occurs after brain injury and mediates neuronal cells degeneration. In the present study, we examined the role of Ras signaling on hydrogen peroxide-induced neuronal cells degeneration in dopaminergic neuroblastoma SH-SY5Y cells. Hydrogen peroxide significantly reduced cell viability in SH-SY5Y cultured cells. An inhibitor of the enzyme that catalyzes the farnesylation of Ras proteins, FTI-277, and a competitive inhibitor of GTP-binding proteins, GDP-beta-S significantly decreased hydrogen peroxide-induced reduction in cell viability in SH-SY5Y cultured cells. The results of this study might indicate that a Ras-dependent signaling pathway plays a role in hydrogen peroxide-induced toxicity in neuronal cells.
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spelling pubmed-29431292010-09-24 Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells Chetsawang, Jirapa Govitrapong, Piyarat Chetsawang, Banthit J Biomed Biotechnol Research Article It has been reported that overproduction of reactive oxygen species occurs after brain injury and mediates neuronal cells degeneration. In the present study, we examined the role of Ras signaling on hydrogen peroxide-induced neuronal cells degeneration in dopaminergic neuroblastoma SH-SY5Y cells. Hydrogen peroxide significantly reduced cell viability in SH-SY5Y cultured cells. An inhibitor of the enzyme that catalyzes the farnesylation of Ras proteins, FTI-277, and a competitive inhibitor of GTP-binding proteins, GDP-beta-S significantly decreased hydrogen peroxide-induced reduction in cell viability in SH-SY5Y cultured cells. The results of this study might indicate that a Ras-dependent signaling pathway plays a role in hydrogen peroxide-induced toxicity in neuronal cells. Hindawi Publishing Corporation 2010 2010-09-05 /pmc/articles/PMC2943129/ /pubmed/20871828 http://dx.doi.org/10.1155/2010/803815 Text en Copyright © 2010 Jirapa Chetsawang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Chetsawang, Jirapa
Govitrapong, Piyarat
Chetsawang, Banthit
Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells
title Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells
title_full Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells
title_fullStr Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells
title_full_unstemmed Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells
title_short Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells
title_sort hydrogen peroxide toxicity induces ras signaling in human neuroblastoma sh-sy5y cultured cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943129/
https://www.ncbi.nlm.nih.gov/pubmed/20871828
http://dx.doi.org/10.1155/2010/803815
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