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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...

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Detalles Bibliográficos
Autores principales: Garcimartín, Alba, Merino, José J, González, Maria Pilar, Sánchez-Reus, Maria Isabel, Sánchez-Muniz, Francisco J, Bastida, Sara, Benedí, Juana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
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
Descripción
Sumario: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.