Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/46397
DC FieldValueLanguage
dc.contributor.authorPerdomo, Juanen_US
dc.contributor.authorCabrera, Javieren_US
dc.contributor.authorEstevez, Franciscoen_US
dc.contributor.authorLoro, Juanen_US
dc.contributor.authorReiter, Russel J.en_US
dc.contributor.authorQuintana, Joseen_US
dc.contributor.otherEstevez, Francisco-
dc.contributor.otherCabrera, Javier-
dc.contributor.otherQuintana, Jose-
dc.contributor.otherloro, juan-
dc.contributor.otherDiaz, Perdomo-
dc.date.accessioned2018-11-23T04:13:10Z-
dc.date.available2018-11-23T04:13:10Z-
dc.date.issued2013en_US
dc.identifier.issn0742-3098en_US
dc.identifier.urihttp://hdl.handle.net/10553/46397-
dc.description.abstractMelatonin is a naturally occurring indoleamine synthesized in the pineal gland that exhibits an extensive repertoire of biological activities. An increasing number of studies indicate that melatonin protects normal cells, while it reducing cancer cell proliferation. In this study, we investigated the effect of melatonin on the growth of the human leukemia cells and found that it efficiently reduced the number of cells in a concentration-and time-dependent manner. Thus, incubation with the indoleamine increased the percentage of cells with a hypodiploid DNA content, augmented the number of annexin V-positive cells, and also provoked ultrastructural changes that are features of apoptotic cell death. Evaluation of caspases revealed that caspase-3, caspase-6, caspase-7, and caspase-9, but not caspase-8 and caspase-2, were quickly activated (3-6 hr). The increase in the activity of these proteases was associated with up-regulation of the pro-apoptotic factor Bax and also with the release of cytochrome c from mitochondria. Pretreatment of the cells with the general caspase inhibitor z-VAD-fmk, reduced melatonin-induced apoptosis, but it did not block cell death suggesting that melatonin activates an alternative cell death modality in the absence of caspase activity. Thus, the activation of caspases was preceded by a fast (< 30 min) increase in reactive oxygen species (ROS). Rotenone and antimycin A reduced the levels of ROS stimulated by melatonin, indicating that the complex I and the complex III of the mitochondrial electron transport chain are important sources of these chemical species. However, the role of ROS in melatonin-induced cell death remains elusive because anti-oxidants that were shown to decrease ROS levels (glutathione, N-acetyl-L-cysteine and Trolox) were unable to abrogate melatonin-induced cell death.en_US
dc.languagespaen_US
dc.publisher0742-3098-
dc.relationEvaluación de Potenciales Compuestos Antileucémicos.en_US
dc.relationEvaluación de Tdf Como Potencial Fármaco Antitumoral.en_US
dc.relation.ispartofJournal of Pineal Researchen_US
dc.sourceJournal Of Pineal Research[ISSN 0742-3098],v. 55 (2), p. 195-206en_US
dc.subject.otherCancer-Cellsen_US
dc.subject.otherOxidative Stressen_US
dc.subject.otherBreast-Canceren_US
dc.subject.otherCytochrome-Cen_US
dc.subject.otherTumor-Cellsen_US
dc.subject.otherHl-60 Cellsen_US
dc.subject.otherDeathen_US
dc.subject.otherInhibitionen_US
dc.subject.otherReceptoren_US
dc.subject.otherProliferationen_US
dc.titleMelatonin induces apoptosis through a caspase-dependent but reactive oxygen species-independent mechanism in human leukemia Molt-3 cellsen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1111/jpi.12062en_US
dc.identifier.scopus84885189105-
dc.identifier.isi000322744600010-
dcterms.isPartOfJournal Of Pineal Research-
dcterms.sourceJournal Of Pineal Research[ISSN 0742-3098],v. 55 (2), p. 195-206-
dc.contributor.authorscopusid55750901700-
dc.contributor.authorscopusid35598975600-
dc.contributor.authorscopusid7003810011-
dc.contributor.authorscopusid6507389169-
dc.contributor.authorscopusid7402574751-
dc.contributor.authorscopusid8681043500-
dc.description.lastpage206en_US
dc.description.firstpage195en_US
dc.relation.volume55en_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000322744600010-
dc.contributor.daisngid32236859-
dc.contributor.daisngid2333322-
dc.contributor.daisngid240124-
dc.contributor.daisngid384944-
dc.contributor.daisngid3210878-
dc.contributor.daisngid227-
dc.contributor.daisngid128315-
dc.identifier.investigatorRIDK-5125-2014-
dc.identifier.investigatorRIDL-9179-2014-
dc.identifier.investigatorRIDK-5709-2014-
dc.identifier.investigatorRIDL-9319-2014-
dc.identifier.investigatorRIDNo ID-
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Perdomo, J-
dc.contributor.wosstandardWOS:Cabrera, J-
dc.contributor.wosstandardWOS:Estevez, F-
dc.contributor.wosstandardWOS:Loro, J-
dc.contributor.wosstandardWOS:Reiter, RJ-
dc.contributor.wosstandardWOS:Quintana, J-
dc.date.coverdateSeptiembre 2013en_US
dc.identifier.ulpgcen_US
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptBioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptBioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptBioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.orcid0000-0002-0163-393X-
crisitem.author.orcid0000-0002-9728-2774-
crisitem.author.orcid0000-0002-0517-8209-
crisitem.author.orcid0000-0001-8225-4538-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNamePerdomo Díaz, Juan-
crisitem.author.fullNameEstévez Rosas, Francisco Jesús-
crisitem.author.fullNameLoro Ferrer, Juan Francisco-
crisitem.author.fullNameQuintana Aguiar, José Martín-
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