Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Bcl-2 Expression And Apoptosis Induction In Human Hl60 Leukaemic Cells Treated With A Novel Organotellurium(iv) Compound Rt-04
Author: Abondanza T.S.
Oliveira C.R.
Barbosa C.M.V.
Pereira F.E.G.
Cunha R.L.O.R.
Caires A.C.F.
Comasseto J.V.
Queiroz M.L.S.
Valadares M.C.
Bincoletto C.
Abstract: Organotellurium(IV) compounds have been reported to have multiple biological activities including cysteine protease-inhibitory activity, mainly cathepsin B. As cathepsin B is a highly predictive indicator for prognosis and diagnosis of cancer, a possible antitumor potential for these new compounds is expected. In this work, it was investigated the effectiveness of organotellurium(IV) RT-04 to produce lethal effects in the human promyelocytic leukaemia cell line HL60. Using the MTT tetrazolium reduction test, and trypan blue exclusion assay, the IC50 for the compound after 24 h incubation was 6.8 and 0.35 μM, respectively. Moreover, the compound was found to trigger apoptosis in HL60 cells, inducing DNA fragmentation and caspase-3, -6, and -9 activations. The apoptsosis-induced by RT-04 is probably related to the diminished Bcl-2 expression, observed by RT-PCR, in HL60-treated cells. In vivo studies demonstrated that the RT-04 treatment (2.76 mg/kg given for three consecutive days) produces no significant toxic effects for bone marrow and spleen CFU-GM. However, higher doses (5.0 and 10 mg/kg) produced a dose-dependent reduction in the number of CFU-GM of RT-04-treated mice. These results suggest that RT-04 is able to induce apoptosis in HL60 cells by Bcl-2 expression down-modulation. Further studies are necessary to better clarify the effects of this compound on bone marrow normal cells. © 2008 Elsevier Ltd. All rights reserved.
Rights: fechado
Identifier DOI: 10.1016/j.fct.2008.04.010
Date Issue: 2008
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.