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Synthesis, Structure Characterization and Antitumor Activity Study of a New Iron(III) Complex of 5-Nitro-8-hydroxylquinoline (HNOQ)
Journal article   Open access   Peer reviewed

Synthesis, Structure Characterization and Antitumor Activity Study of a New Iron(III) Complex of 5-Nitro-8-hydroxylquinoline (HNOQ)

Hai-Rong Zhang, Ting Meng, Yan-Cheng Liu, Qi-Pin Qin, Zhen-Feng Chen, You-Nian Liu, Hong Liang and aCollege of Chemistry and Chemical Engineering
Chemical & pharmaceutical bulletin, v 64(8), pp 1208-1217
01 Aug 2016
PMID: 27238362
url
https://www.jstage.jst.go.jp/article/cpb/64/8/64_c16-00330/_pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1248/bpb.c16-00330View
Published, Version of Record (VoR) Open

Abstract

Chemistry Chemistry, Medicinal Chemistry, Multidisciplinary Life Sciences & Biomedicine Pharmacology & Pharmacy Physical Sciences Science & Technology
A new iron(III) complex (1) of 5-nitro-8-hydroxylquinoline (HNOQ) was synthesized and structurally characterized in its solid state and solution state by IR, UV-Vis, electrospray ionization (ESI)-MS, elemental analysis, conductivity and X-ray single crystal diffraction analysis. The DNA binding study suggested that complex 1 interacted with calf thymus (ct)-DNA mainly via an intercalative binding mode. By 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide (MTT) assay, the in vitro cytotoxicity of complex 1, comparing with HNOQ and cisplatin, was screened towards a series of tumor cell lines as well as the normal liver cell line HL-7702. Complex 1 showed higher cytotoxicity towards the tested tumor cell lines but lower cytotoxicity towards HL-7702 than HNOQ, in which the T-24 was the most sensitive cell line for 1. Complex 1 caused G2 phase cell cycle arrest and induced cell apoptosis in T-24 cells in a dose-dependent mode, evidenced by changes in cell morphology. Targeting the mitochondrial pathway due to the redox potential of Fe(III)/Fe(II), the apoptotic mechanism in T-24 cells treated by 1 was investigated by reactive oxygen species (ROS) detection, intracellular [Ca2+] measurement and caspase-9 and caspase-3 activity assay. It suggested that complex 1 induced cell apoptosis by triggering the caspase-9 and caspase-3 activation via a mitochondrion -mediated pathway.

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Collaboration types
Domestic collaboration
Web of Science research areas
Chemistry, Medicinal
Chemistry, Multidisciplinary
Pharmacology & Pharmacy
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