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dc.creatorMAZARIEGOS,DORA INÉS
dc.creatorCABANTCHIK,Z. IOAV
dc.creatorCASSELS,BRUCE K
dc.creatorNÚÑEZ,MARCO TULIO
dc.date2006-01-01
dc.date.accessioned2019-05-02T21:21:30Z
dc.date.available2019-05-02T21:21:30Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000100024
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/81636
dc.descriptionThere is increasing evidence that accumulation of redox-active iron in mitochondria leads to oxidative damage and contributes to various neurodegenerative diseases, such as Friedreich's ataxia and Parkinson's disease. In this work, we examined the existence of regulatory mechanisms for mitochondrial iron uptake and storage. To that end, we used rhodamine B- [(1,10-phenanthrolin-5-yl)amino carbonyl ] benzyl ester, a new fluorescent iron-sensitive probe that is targeted specifically to the mitochondrion. We found that extracellular iron was incorporated readily into mitochondria in an apparently saturable process. Moreover, the rate of iron incorporation responded to the Fe status of the cell, an indication that the mitochondrion actively regulates its iron content.
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602006000100024
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.39 n.1 2006
dc.subjectmitochondria
dc.subjectiron homeostasis
dc.subjectRPA
dc.subjectHepG2 cells
dc.titleCharacterization of mitochondrial iron uptake in HepG2 cells


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