dc.creatorVERCESI, AE
dc.creatorHOFFMANN, ME
dc.creatorBERNARDES, CF
dc.creatorDOCAMPO, R
dc.date1991
dc.dateMAY
dc.date2014-12-16T11:37:01Z
dc.date2015-11-26T17:27:20Z
dc.date2014-12-16T11:37:01Z
dc.date2015-11-26T17:27:20Z
dc.date.accessioned2018-03-29T00:14:28Z
dc.date.available2018-03-29T00:14:28Z
dc.identifierCell Calcium. Churchill Livingstone, v. 12, n. 5, n. 361, n. 369, 1991.
dc.identifier0143-4160
dc.identifierWOS:A1991FW65200005
dc.identifier10.1016/0143-4160(91)90052-G
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80059
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/80059
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80059
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1284769
dc.descriptionTrypanosoma cruzi epimastigotes maintained an intracellular free calcium concentration of about 0.15-mu-M, as measured with the fluorescent indicator Fura-2. The maintenance of low [Ca2+]i is energy-dependent since it is disrupted by KCN and FCCP. When the cells were permeabilized with digitonin, the steady-state free Ca2+ concentration in the absence of ATP was about 0.7-mu-M. The additional presence of ATP resulted in a steady-state level close to 0.1-0.2-mu-M which compares favorably with the concentration detected in intact cells. Intracellular Ca2+ uptake at high levels of free Ca2+(> 1-mu-M) was due to energy-dependent mitochondrial uptake as indicated by its FCCP-sensitivity. However, as the free Ca2+ concentration was lowered from 1-mu-M, essentially all uptake was due to the ATP-dependent Ca2+ sequestration by the endoplasmic reticulum as indicated by its stimulation by ATP, and its inhibition by sodium vanadate. High concentrations of the calmodulin antagonist trifluoperazine, inhibited both the Ca2+ uptake by the endoplasmic reticulum and by the mitochondria, while calmidazolium released Ca2+ from both compartments. In addition, trifluoperazine and calmidazolium inhibited respiration and collapsed the mitochondrial membrane potential of T. cruzi, thus indicating non-specific effects unrelated to calmodulin.
dc.description12
dc.description5
dc.description361
dc.description369
dc.languageen
dc.publisherChurchill Livingstone
dc.publisherEdinburgh
dc.publisherEscócia
dc.relationCell Calcium
dc.relationCell Calcium
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectFree-radical Metabolites
dc.subjectIndicators Arsenazo-iii
dc.subjectBlood-stream Forms
dc.subjectCa-2+ Transport
dc.subjectMitochondria Insitu
dc.subjectSuperoxide Anion
dc.subjectAntipyrylazo-iii
dc.subjectCalmodulin
dc.subjectBrucei
dc.subjectGeneration
dc.titleREGULATION OF INTRACELLULAR CALCIUM HOMEOSTASIS IN TRYPANOSOMA-CRUZI - EFFECTS OF CALMIDAZOLIUM AND TRIFLUOPERAZINE
dc.typeArtículos de revistas


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