Please use this identifier to cite or link to this item:
Title: 6′-Benzyloxy-4-bromo-2′-hydroxychalcone is cytotoxic against human leukaemia cells and induces caspase-8- and reactive oxygen species-dependent apoptosis
Authors: Saavedra Díaz, Ester Gloria 
Del Rosario, Henoc
Brouard, Ignacio
Quintana, José 
Estévez, Francisco 
Keywords: Activated Protein-Kinase
Mitochondrial Dysfunction
Induction, et al
Issue Date: 2019
Publisher: 0009-2797
Journal: Chemico-biological interactions (Print) 
Abstract: In this study, we investigated the effects of synthetic 6'-benzyloxy-4-bromo-2'-hydroxychalcone on viabilities of seven human leukaemia cells. It was cytotoxic against U-937, HL-60, K-562, NALM-6, MOLT-3 cells, and also against Bcl-2-overexpressing U-937/Bcl-2 cells and P-glycoprotein-overexpressing K-562/ADR, but had no significant cytotoxic effects against quiescent or proliferating human peripheral blood mononuclear cells. This chalcone is a potent apoptotic inducer in human leukaemia U-937 cells. Cell death was (i) mediated by the activation and the cleavage of initiator and executioner caspases and poly(ADP-ribose) polymerase; (ii) prevented by the pan-caspase inhibitor z-VAD-fmk, and by the selective caspase-3/7, -6 and -8 inhibitors, and by a cathepsins B/L inhibitor; (iii) associated with the release of mitochondrial proteins, including cytochrome c and Smac/DIABLO; (iv) accompanied by dissipation of the mitochondrial membrane potential, (v) partially blocked by the inhibition of p38(MAPK) and (vi) mostly abrogated by catalase. In conclusion, the synthetic chalcone is cytotoxic against several types of human leukaemia cell with apoptosis being induced by activation of the extrinsic pathway and the generation of reactive oxygen species.
ISSN: 0009-2797
DOI: 10.1016/j.cbi.2018.12.010
Source: Chemico-Biological Interactions[ISSN 0009-2797],v. 298, p. 137-145
Appears in Collections:Artículos
Show full item record

Page view(s)

checked on Sep 17, 2022

Google ScholarTM




Export metadata

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