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Pharmacological Characterization of the Mechanisms Involved in Delayed Calcium Deregulation in SH-SY5Y Cells Challenged with Methadone
dc.contributor.author | Perez-Alvarez, Sergio | |
dc.contributor.author | Solesio, Maria E | |
dc.contributor.author | Cuenca-Lopez, Maria D | |
dc.contributor.author | Melero-Fernández de Mera, Raquel Maria | |
dc.contributor.author | Villalobos, Carlos | |
dc.contributor.author | Kmita, Hanna | |
dc.contributor.author | Galindo, Maria F | |
dc.contributor.author | Jordán, Joaquin | |
dc.date.accessioned | 2024-02-05T17:00:34Z | |
dc.date.available | 2024-02-05T17:00:34Z | |
dc.date.issued | 2012 | |
dc.identifier.citation | Perez-Alvarez, S., Solesio, M. E., Cuenca-Lopez, M. D., Melero-Fernández de Mera, R. M., Villalobos, C., Kmita, H., Galindo, M. F., & Jordán, J. (2012). Pharmacological Characterization of the Mechanisms Involved in Delayed Calcium Deregulation in SH-SY5Y Cells Challenged with Methadone. International journal of cell biology, 2012, 642482. https://doi.org/10.1155/2012/642482 | es |
dc.identifier.issn | 16878876 | |
dc.identifier.other | https://www.scopus.com/record/display.uri?eid=2-s2.0-84863689879&origin=inward&txGid=79bd58808df2bee5ec5bb3edd6e00b2b | es |
dc.identifier.uri | http://hdl.handle.net/20.500.12020/1195 | |
dc.description.abstract | Previously, we have shown that SH-SY5Y cells exposed to high concentrations of methadone died due to a necrotic-like cell death mechanism related to delayed calcium deregulation (DCD). In this study, we show that, in terms of their Ca2+ responses to 0.5mM methadone, SH-SY5Y cells can be pooled into four different groups. In a broad pharmacological survey, the relevance of different Ca2+-related mechanisms on methadone-induced DCD was investigated including extracellular calcium, L-type Ca2+ channels, -opioid receptor, mitochondrial inner membrane potential, mitochondrial ATP synthesis, mitochondrial Ca2+/2Na+-exchanger, reactive oxygen species, and mitochondrial permeability transition. Only those compounds targeting mitochondria such as oligomycin, FCCP, CGP 37157, and cyclosporine A were able to amend methadone-induced Ca2+ dyshomeostasis suggesting that methadone induces DCD by modulating the ability of mitochondria to handle Ca2+. Consistently, mitochondria became dramatically shorter and rounder in the presence of methadone. Furthermore, analysis of oxygen uptake by isolated rat liver mitochondria suggested that methadone affected mitochondrial Ca2+ uptake in a respiratory substrate-dependent way. We conclude that methadone causes failure of intracellular Ca2+ homeostasis, and this effect is associated with morphological and functional changes of mitochondria. Likely, this mechanism contributes to degenerative side effects associated with methadone treatment. | es |
dc.language.iso | en | es |
dc.publisher | Hindawi Publishing Corporation | es |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | Pharmacological Characterization of the Mechanisms Involved in Delayed Calcium Deregulation in SH-SY5Y Cells Challenged with Methadone | es |
dc.type | article | es |
dc.identifier.doi | https://doi.org/10.1155/2012/642482 | |
dc.journal.title | International Journal of Cell Biology | es |
dc.page.initial | 1 | es |
dc.page.final | 8 | es |
dc.rights.accessRights | openAccess | es |
dc.subject.area | Biología Celular y Molecular | es |
dc.subject.area | Ciencias Biomédicas | es |
dc.subject.keyword | calcium channel L type | es |
dc.subject.keyword | calcium ion | es |
dc.subject.keyword | cyclosporin A | es |
dc.subject.keyword | calcium homeostasis | es |
dc.subject.keyword | mitochondrion | es |
dc.subject.keyword | mitochondrial membrane potential | es |
dc.subject.unesco | 32 Ciencias Médicas | es |
dc.volume.number | 2012 | es |