The Cratylia Mollis Seed Lectin Induces Membrane Permeability Transition In Isolated Rat Liver Mitochondria And A Cyclosporine A-insensitive Permeability Transition In Trypanosoma Cruzi Mitochondria

dc.creatorFernandes M.P.
dc.creatorLeite A.C.R.
dc.creatorAraujo F.F.B.
dc.creatorSaad S.T.O.
dc.creatorBaratti M.O.
dc.creatorCorreia M.T.S.
dc.creatorCoelho L.C.B.B.
dc.creatorGadelha F.R.
dc.creatorVercesi A.E.
dc.date2014
dc.date2015-06-25T17:51:03Z
dc.date2015-11-26T15:39:38Z
dc.date2015-06-25T17:51:03Z
dc.date2015-11-26T15:39:38Z
dc.date.accessioned2018-03-28T22:48:07Z
dc.date.available2018-03-28T22:48:07Z
dc.identifier
dc.identifierJournal Of Eukaryotic Microbiology. Blackwell Publishing Inc., v. 61, n. 4, p. 381 - 388, 2014.
dc.identifier10665234
dc.identifier10.1111/jeu.12118
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84896531390&partnerID=40&md5=33e3031314c30a529f7c4b0172b56fb4
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/85969
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/85969
dc.identifier2-s2.0-84896531390
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1264184
dc.descriptionPrevious results provided evidence that Cratylia mollis seed lectin (Cramoll 1,4) promotes Trypanosoma cruzi epimastigotes death by necrosis via a mechanism involving plasma membrane permeabilization to Ca2+ and mitochondrial dysfunction due to matrix Ca2+ overload. In order to investigate the mechanism of Ca2+-induced mitochondrial impairment, experiments were performed analyzing the effects of this lectin on T. cruzi mitochondrial fraction and in isolated rat liver mitochondria (RLM), as a control. Confocal microscopy of T. cruzi whole cell revealed that Cramoll 1,4 binding to the plasma membrane glycoconjugates is followed by its internalization and binding to the mitochondrion. Electrical membrane potential (ΔΨm) of T. cruzi mitochondrial fraction suspended in a reaction medium containing 10 μM Ca2+ was significantly decreased by 50 μg/ml Cramoll 1,4 via a mechanism insensitive to cyclosporine A (CsA, membrane permeability transition (MPT) inhibitor), but sensitive to catalase or 125 mM glucose. In RLM suspended in a medium containing 10 μM Ca2+ this lectin, at 50 μg/ml, induced increase in the rate of hydrogen peroxide release, mitochondrial swelling, and ΔΨm disruption. All these mitochondrial alterations were sensitive to CsA, catalase, and EGTA. These results indicate that Cramoll 1, 4 leads to inner mitochondrial membrane permeabilization through Ca2+ dependent mechanisms in both mitochondria. The sensitivity to CsA in RLM characterizes this lectin as a MPT inducer and the lack of CsA effect identifies a CsA-insensitive MPT in T. cruzi mitochondria. © 2014 The Author(s) Journal of Eukaryotic Microbiology © 2014 International Society of Protistologists.
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dc.languageen
dc.publisherBlackwell Publishing Inc.
dc.relationJournal of Eukaryotic Microbiology
dc.rightsfechado
dc.sourceScopus
dc.titleThe Cratylia Mollis Seed Lectin Induces Membrane Permeability Transition In Isolated Rat Liver Mitochondria And A Cyclosporine A-insensitive Permeability Transition In Trypanosoma Cruzi Mitochondria
dc.typeArtículos de revistas


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