NDLI: A novel 7-azaisoindigo derivative-induced cancer cell apoptosis and mitochondrial dysfunction mediated by oxidative stress

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A novel 7-azaisoindigo derivative-induced cancer cell apoptosis and mitochondrial dysfunction mediated by oxidative stress

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A novel 7-azaisoindigo derivative-induced cancer cell apoptosis and mitochondrial dysfunction mediated by oxidative stress

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Xu, Jing-jing Dai, Xiao-min Liu, Hai-liang Guo, Wen-jie Gao, Jing Wang, Chao-hui Li, Wen-bin Yao, Qi-zheng
Description	Author Affiliation: Xu JJ ( School of Pharmacy, Jiangsu University, Zhenjiang, People's Republic of China.)
Abstract	This research focused on a novel 7-azaisoindigo derivative [namely $N^{1}-(n-butyl)-7-azaisoindigo,$ 7-AI-b], and investigated its molecular antitumor mechanism by exploring the means of cell death and the effects on mitochondrial function. 7-AI-b inhibited cancer cell proliferation in a dose- and time-dependent way. The morphological and nuclei changes in $H_{2}B-GFP-labeled$ HeLa cells were observed using a live cell system. The results suggested that cell death induced by 7-AI-b is closely related to apoptosis. 7-AI-b induced release of cytochrome C from mitochondria to cytosol and activation of caspase-3, showing that the apoptosis is mediated by the mitochondrial pathway. Furthermore, our data indicated that 7-AI-b triggers apoptosis through reactive oxygen species (ROS): cellular ROS levels were increased after 3 h exposure of 7-AI-b, which was reversed by the ROS scavenger N-acetyl-l-cysteine. As a consequence, 7-AI-b-mediated cell death, mitochondrial transmembrane potential collapse and ATP level were partly blocked by N-acetyl-l-cysteine. Further study showed that 7-AI-b could induce mitochondrial dysfunction: collapse of the mitochondrial transmembrane potential and reduction of intracellular ATP level. In summary, the novel synthesized 7-AI-b was demonstrated to be effective in killing cancer cells via an ROS-promoted and mitochondria- and caspase-dependent apoptotic pathway. Copyright © 2010 John Wiley & Sons, Ltd.
File Format	HTM / HTML
ISSN	0260437X
Issue Number	2
Volume Number	31
e-ISSN	10991263
Journal	Journal of Applied Toxicology
Language	English
Publisher	Wiley
Publisher Date	2011-03-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Toxicology Antineoplastic Agents, Phytogenic Pharmacology Apoptosis Drug Effects Indoles Mitochondria Neoplasms Drug Therapy Oxidative Stress Acetylcysteine Adenosine Triphosphate Metabolism Caspase 3 Cell Line, Tumor Cell Proliferation Cell Survival Enzyme Activation Free Radical Scavengers Humans Membrane Potential, Mitochondrial Pathology Osmolar Concentration Reactive Oxygen Species Time Factors Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Toxicology

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