Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/4797
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dc.contributor.authorGil, Joana-
dc.contributor.authorAlmeida, Sandra-
dc.contributor.authorOliveira, Catarina R.-
dc.contributor.authorRego, A. Cristina-
dc.date.accessioned2008-09-01T14:14:38Z-
dc.date.available2008-09-01T14:14:38Z-
dc.date.issued2003en_US
dc.identifier.citationFree Radical Biology and Medicine. 35:11 (2003) 1500-1514en_US
dc.identifier.urihttps://hdl.handle.net/10316/4797-
dc.description.abstractIn this study, we investigated the involvement of reactive oxygen species (ROS) and calcium in staurosporine (STS)-induced apoptosis in cultured retinal neurons, under conditions of maintained membrane integrity. The antioxidants idebenone (IDB), glutathione-ethylester (GSH/EE), trolox, and Mn(III)tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP) significantly reduced STS-induced caspase-3-like activity and intracellular ROS generation. Endogenous sources of ROS production were investigated by testing the effect of the following inhibitors: 7-nitroindazole (7-NI), a specific inhibitor of the neuronal isoform of nitric oxide synthase (nNOS); arachidonyl trifluoromethyl ketone (AACOCF3), a phospholipase A2 (PLA2) inhibitor; allopurinol, a xanthine oxidase inhibitor; and the mitochondrial inhibitors rotenone and oligomycin. All these compounds decreased caspase-3-like activity and ROS generation, showing that both mitochondrial and cytosolic sources of ROS are implicated in this mechanism. STS induced a significant increase in intracellular calcium concentration ([Ca2+]i), which was partially prevented in the presence of IDB and GSH/EE, indicating its dependence on ROS generation. These two antioxidants and the inhibitors allopurinol and 7-NI also reduced the number of TdT-mediated dUTP nick-end labeling-positive cells. Thus, endogenous ROS generation and the rise in intracellular calcium are important inter-players in STS-triggered apoptosis. Furthermore, the antioxidants may help to prolong retinal cell survival upon apoptotic cell death.en_US
dc.description.urihttp://www.sciencedirect.com/science/article/B6T38-4B1Y892-D/1/de8345fb5df912dddbc572b28cc1f4been_US
dc.format.mimetypeaplication/PDFen
dc.language.isoengeng
dc.rightsopenAccesseng
dc.subjectApoptosisen_US
dc.subjectAntioxidantsen_US
dc.subjectCalciumen_US
dc.subjectCaspase-3en_US
dc.subjectMitochondriaen_US
dc.subjectReactive oxygen speciesen_US
dc.subjectRetinal cellsen_US
dc.subjectStaurosporineen_US
dc.subjectFree radicalsen_US
dc.titleCytosolic and mitochondrial ROS in staurosporine-induced retinal cell apoptosisen_US
dc.typearticleen_US
dc.identifier.doi10.1016/j.freeradbiomed.2003.08.022-
item.openairetypearticle-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.fulltextCom Texto completo-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0001-6942-4328-
crisitem.author.orcid0000-0003-0700-3776-
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais
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