Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Growth inhibitory effects of 3 '-nitro-3-phenylamino nor-beta-lapachone against HL-60: A redox-dependent mechanism
Author: Araujo, AJ
de Souza, AA
da Silva, EN
Marinho, JDB
de Moura, MABF
Rocha, DD
Vasconcellos, MC
Costa, CO
Pessoa, C
de Moraes, MO
Ferreira, VF
de Abreu, FC
Pinto, AV
Montenegro, RC
Costa-Lotufo, LV
Goulart, MOF
Abstract: In this study, the cytotoxicity, genotoxicity and early ROS generation of 2,2-dimethyl-(3H)-3-(N-3'-nitrophenylamino)naphtho[1,2-b]furan-4,5-dione (QPhNO(2)) were investigated and compared with those of its precursor, nor-beta-lapachone (nor-beta), with the main goal of proposing a mechanism of antitumor action. The results were correlated with those obtained from electrochemical experiments held in protic (acetate buffer pH 4.5) and aprotic (DMF/TBABF(4)) media in the presence and absence of oxygen and with those from dsDNA biosensors and ssDNA in solution, which provided evidence of a positive interaction with DNA in the case of QPhNO(2). QPhNO(2) caused DNA fragmentation and mitochondrial depolarization and induced apoptosis/necrosis in HL-60 cells. Pre-treatment with N-acetyl-L-cysteine partially abolished the observed effects related to the QPhNO(2) treatment, including those involving apoptosis induction, indicating a partially redox-dependent mechanism. These findings point to the potential use of the combination of pharmacology and electrochemistry in medicinal chemistry. (C) 2012 Elsevier Ltd. All rights reserved.
Subject: Apoptosis
DNA sensors
Country: Inglaterra
Editor: Pergamon-elsevier Science Ltd
Citation: Toxicology In Vitro. Pergamon-elsevier Science Ltd, v. 26, n. 4, n. 585, n. 594, 2012.
Rights: fechado
Identifier DOI: 10.1016/j.tiv.2012.02.003
Date Issue: 2012
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
WOS000303702900006.pdf1.01 MBAdobe PDFView/Open

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