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Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects
BACKGROUND: Hydrogen peroxide (H(2)O(2)) is a toxic agent that induces oxidative stress and cell death. Silicon (Si) is a biological element involved in limiting aluminium (Al) absorption with possible preventive effects in Alzheimer’s disease. However, Si has not yet been associated with other neur...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203892/ https://www.ncbi.nlm.nih.gov/pubmed/25293674 http://dx.doi.org/10.1186/1472-6882-14-384 |
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author | Garcimartín, Alba Merino, José J González, Maria Pilar Sánchez-Reus, Maria Isabel Sánchez-Muniz, Francisco J Bastida, Sara Benedí, Juana |
author_facet | Garcimartín, Alba Merino, José J González, Maria Pilar Sánchez-Reus, Maria Isabel Sánchez-Muniz, Francisco J Bastida, Sara Benedí, Juana |
author_sort | Garcimartín, Alba |
collection | PubMed |
description | BACKGROUND: Hydrogen peroxide (H(2)O(2)) is a toxic agent that induces oxidative stress and cell death. Silicon (Si) is a biological element involved in limiting aluminium (Al) absorption with possible preventive effects in Alzheimer’s disease. However, Si has not yet been associated with other neuroprotective mechanisms. METHODS: The present experiments evaluated in the SH-SY5Y human neuroblastoma cell line the possible role of different Si G5 (50-1000 ng/mL) concentrations in preventing cellular death induced by H(2)O(2) (400 μM, 24 hours). RESULTS: Our findings showed that H(2)O(2) promoted cell death in the human SH-SY5Y cell cultures and this could be prevented by Si treatment. The loss in cell viability mediated by H(2)O(2) was due to an apoptotic and necrotic process. Apoptotic death was incurred by regulating caspase-8 activity in the extrinsic pathway. The apoptotic and necrotic cell death induced by H(2)O(2) was almost totally reversed by Si (50-500 ng/mL), indicating that it down-regulates both processes in H(2)O(2) treated cells. CONCLUSIONS: According to our data, Si is able to increase SH-SY5Y cell survival throughout partially blocking cellular damage related to oxidative stress through a mechanism that would affect H(2)O(2)/ROS elimination. |
format | Online Article Text |
id | pubmed-4203892 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-42038922014-10-22 Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects Garcimartín, Alba Merino, José J González, Maria Pilar Sánchez-Reus, Maria Isabel Sánchez-Muniz, Francisco J Bastida, Sara Benedí, Juana BMC Complement Altern Med Research Article BACKGROUND: Hydrogen peroxide (H(2)O(2)) is a toxic agent that induces oxidative stress and cell death. Silicon (Si) is a biological element involved in limiting aluminium (Al) absorption with possible preventive effects in Alzheimer’s disease. However, Si has not yet been associated with other neuroprotective mechanisms. METHODS: The present experiments evaluated in the SH-SY5Y human neuroblastoma cell line the possible role of different Si G5 (50-1000 ng/mL) concentrations in preventing cellular death induced by H(2)O(2) (400 μM, 24 hours). RESULTS: Our findings showed that H(2)O(2) promoted cell death in the human SH-SY5Y cell cultures and this could be prevented by Si treatment. The loss in cell viability mediated by H(2)O(2) was due to an apoptotic and necrotic process. Apoptotic death was incurred by regulating caspase-8 activity in the extrinsic pathway. The apoptotic and necrotic cell death induced by H(2)O(2) was almost totally reversed by Si (50-500 ng/mL), indicating that it down-regulates both processes in H(2)O(2) treated cells. CONCLUSIONS: According to our data, Si is able to increase SH-SY5Y cell survival throughout partially blocking cellular damage related to oxidative stress through a mechanism that would affect H(2)O(2)/ROS elimination. BioMed Central 2014-10-08 /pmc/articles/PMC4203892/ /pubmed/25293674 http://dx.doi.org/10.1186/1472-6882-14-384 Text en © Garcimartín et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Garcimartín, Alba Merino, José J González, Maria Pilar Sánchez-Reus, Maria Isabel Sánchez-Muniz, Francisco J Bastida, Sara Benedí, Juana Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects |
title | Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects |
title_full | Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects |
title_fullStr | Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects |
title_full_unstemmed | Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects |
title_short | Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects |
title_sort | organic silicon protects human neuroblastoma sh-sy5y cells against hydrogen peroxide effects |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203892/ https://www.ncbi.nlm.nih.gov/pubmed/25293674 http://dx.doi.org/10.1186/1472-6882-14-384 |
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