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|Type:||Artigo de periódico|
|Title:||CA2+/H+ EXCHANGE IN ACIDIC VACUOLES OF TRYPANOSOMA-BRUCEI|
|Abstract:||The use of digitonin to permeabilize the plasma membrane of Trypanosoma brucei procyclic and bloodstream trypomastigotes allowed the identification of a non-mitochondrial nigericin-sensitive Ca2+ compartment. The proton ionophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) was able to cause Ca2+ release from this compartment, which was also sensitive to sodium orthovanadate. Preincubation of the cells with the vacuolar H+-ATPase inhibitor bafilomycin A(1) greatly reduced the nigericin-sensitive Ca2+ compartment. Bafilomycin A(1) inhibited the initial rate of ATP-dependent non-mitochondrial Ca2+ uptake and stimulated the initial rate of nigericin-induced Ca2+ release by permeabilized procyclic trypomastigotes. ATP-dependent and bafilomycin A(1)- and 7-chloro-4-nitrobenz-2-oxa-1,3-diazole (NBD-Cl)-sensitive Acridine Orange uptake was demonstrated in permeabilized cells. Under these conditions Acridine Orange was concentrated in abundant cytoplasmic round vacuoles by a process inhibited by bafilomycin A(1), NBD-Cl, nigericin, and Ca2+. Vanadate or EGTA significantly increased Acridine Orange uptake, while Ca2+ released Acridine Orange from these preparations, thus suggesting that the dye and Ca2+ were being accumulated in the same acidic vacuole. Acridine Orange uptake was reversed by nigericin, bafilomycin A(1) and NH4Cl. The results are consistent with the presence of a Ca2+/H+-ATPase system pumping Ca2+ into an acidic vacuole, that we tentatively named the acidocalcisome.|
|Citation:||Biochemical Journal. Portland Press, v. 304, n. 227, n. 233, 1994.|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
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