dc.creator | VERCESI, AE | |
dc.creator | HOFFMANN, ME | |
dc.creator | BERNARDES, CF | |
dc.creator | DOCAMPO, R | |
dc.date | 1991 | |
dc.date | MAY | |
dc.date | 2014-12-16T11:37:01Z | |
dc.date | 2015-11-26T17:27:20Z | |
dc.date | 2014-12-16T11:37:01Z | |
dc.date | 2015-11-26T17:27:20Z | |
dc.date.accessioned | 2018-03-29T00:14:28Z | |
dc.date.available | 2018-03-29T00:14:28Z | |
dc.identifier | Cell Calcium. Churchill Livingstone, v. 12, n. 5, n. 361, n. 369, 1991. | |
dc.identifier | 0143-4160 | |
dc.identifier | WOS:A1991FW65200005 | |
dc.identifier | 10.1016/0143-4160(91)90052-G | |
dc.identifier | http://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80059 | |
dc.identifier | http://www.repositorio.unicamp.br/handle/REPOSIP/80059 | |
dc.identifier | http://repositorio.unicamp.br/jspui/handle/REPOSIP/80059 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1284769 | |
dc.description | Trypanosoma 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.description | 12 | |
dc.description | 5 | |
dc.description | 361 | |
dc.description | 369 | |
dc.language | en | |
dc.publisher | Churchill Livingstone | |
dc.publisher | Edinburgh | |
dc.publisher | Escócia | |
dc.relation | Cell Calcium | |
dc.relation | Cell Calcium | |
dc.rights | fechado | |
dc.source | Web of Science | |
dc.subject | Free-radical Metabolites | |
dc.subject | Indicators Arsenazo-iii | |
dc.subject | Blood-stream Forms | |
dc.subject | Ca-2+ Transport | |
dc.subject | Mitochondria Insitu | |
dc.subject | Superoxide Anion | |
dc.subject | Antipyrylazo-iii | |
dc.subject | Calmodulin | |
dc.subject | Brucei | |
dc.subject | Generation | |
dc.title | REGULATION OF INTRACELLULAR CALCIUM HOMEOSTASIS IN TRYPANOSOMA-CRUZI - EFFECTS OF CALMIDAZOLIUM AND TRIFLUOPERAZINE | |
dc.type | Artículos de revistas | |