Ornithine decarboxylase prevents dibenzoylmethane-induced apoptosis through repressing reactive oxygen species generation.

doi:10.1002/jbt.20391

中山醫學大學機構典藏 CSMUIR > 醫學院 > 免疫學研究所 > 期刊論文 > Item 310902500/11705

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11705

Title:	Ornithine decarboxylase prevents dibenzoylmethane-induced apoptosis through repressing reactive oxygen species generation.
Authors:	Wu, CL Liao, YF Hung, YC Lu, KH Hung, HC Liu, GY
Contributors:	中山醫學大學
Keywords:	Dibenzoylmethane;Apoptosis;Ornithine decarboxylase;Reactive oxygen species
Date:	2011
Issue Date:	2015-07-28T04:29:36Z (UTC)
ISSN:	1095-6670
Abstract:	Dibenzoylmethane (DBM) belongs to the flavonoid family and is a minor constituent of the root extract of licorice and the β-diketone analogue of curcumin. It exhibits antimutagenic, anticancer, and chemopreventive effects. Ornithine decarboxylase (ODC), the rate-limiting enzyme of the polyamine biosynthetic pathway, plays an important role in growth, proliferation, and transformation. Our previous studies showed ODC overexpression prevented etoposide-, paclitaxel-, and cisplatin-induced apoptosis. Here, we investigated one mechanism of DBM-induced apoptosis and the antiapoptotic effects of ODC during DBM treatment. We found that DBM induced apoptosis, promoted reactive oxygen species (ROS) generation, and disrupted the mitochondrial membrane potential (Δψ(m). N-acetylcysteine, a ROS scavenger, reduced DBM-induced apoptosis, which led to the loss of Δψ(m) due to reduced ROS. Overexpression of ODC in parental cells had the same effects as the ROS scavenger. The results demonstrated that DBM-induced apoptosis was a ROS-dependent pathway and ODC overexpression blocked DBM-induced apoptosis by inhibiting intracellular ROS production. Copyright © 2011 Wiley Periodicals, Inc.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11705 http://dx.doi.org/10.1002/jbt.20391
Relation:	J Biochem Mol Toxicol. 2011 Sep-Oct;25(5):312-9.
Appears in Collections:	[免疫學研究所] 期刊論文

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