Apoptotic effect of ethanol is potentiated by caffeine-induced calcium release in rat astrocytes
dc.contributor.author | Hirata, H. | |
dc.contributor.author | Machado, L. S. | |
dc.contributor.author | Okuno, C. S. | |
dc.contributor.author | Brasolin, A. | |
dc.contributor.author | Lopes, G. S. | |
dc.contributor.author | Smaili, Soraya Soubhi [UNIFESP] | |
dc.contributor.institution | Universidade Federal de São Paulo (UNIFESP) | |
dc.date.accessioned | 2016-01-24T12:40:55Z | |
dc.date.available | 2016-01-24T12:40:55Z | |
dc.date.issued | 2006-01-30 | |
dc.description.abstract | In this study, we investigated agents that increased intracellular calcium levels and their correlation with apoptotic cell death induction. We used rat astrocytes to investigate the increase in cytosolic Ca2+, (Ca-c(2+)) and apoptosis induction by drugs that mobilize Ca2+ from different sources. We observed that thapsigargin (Thap), caffeine (Caff) and FCCP which caused similar increases in Ca-c(2+) levels (30-40%), also induced similar apoptotic rates (30-35%). On the other hand, antimycin (Anti), staurosporine (STS) and ethanol (Eth) promoted higher increases in Ca-c(2+) (55-65 %) and higher apoptotic rates (55-85%). Eth induced cell death in a concentration- and time-dependent manner. After treatment with Eth plus Caff for 6, 12 and 24 h, these effects were strongly potentiated. Results suggest that there might be a correlation between Ca-c(2+) increase and the rate of apoptosis. It is possible that Eth induces cell death by activation of more than one pathway and Ca-c(2+) might be one of the elements involved. the present work indicates that Ca-c(2+) can potentiate death by ethanol in rat astrocytes. (c) 2005 Elsevier Ireland Ltd. All rights reserved. | en |
dc.description.affiliation | Universidade Federal de São Paulo, Dept Pharmacol, Sch Med, BR-04044020 São Paulo, Brazil | |
dc.description.affiliationUnifesp | Universidade Federal de São Paulo, Dept Pharmacol, Sch Med, BR-04044020 São Paulo, Brazil | |
dc.description.source | Web of Science | |
dc.format.extent | 136-140 | |
dc.identifier | http://dx.doi.org/10.1016/j.neulet.2005.09.066 | |
dc.identifier.citation | Neuroscience Letters. Clare: Elsevier B.V., v. 393, n. 2-3, p. 136-140, 2006. | |
dc.identifier.doi | 10.1016/j.neulet.2005.09.066 | |
dc.identifier.issn | 0304-3940 | |
dc.identifier.uri | http://repositorio.unifesp.br/handle/11600/28695 | |
dc.identifier.wos | WOS:000234583000012 | |
dc.language.iso | eng | |
dc.publisher | Elsevier B.V. | |
dc.relation.ispartof | Neuroscience Letters | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.rights.license | http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy | |
dc.subject | ethanol | en |
dc.subject | calcium | en |
dc.subject | mitochondria | en |
dc.subject | apoptosis | en |
dc.subject | astrocytes | en |
dc.subject | endoplasmic reticulum | en |
dc.title | Apoptotic effect of ethanol is potentiated by caffeine-induced calcium release in rat astrocytes | en |
dc.type | info:eu-repo/semantics/article |