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

✍ Scribed by Chih-Lung Wu; Ya-Fan Liao; Ying-Cheng Hung; Ko-Hsiu Lu; Hui-Chih Hung; Guang-Yaw Liu

Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
348 KB
Volume
25
Category
Article
ISSN
1095-6670

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✦ Synopsis

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 (Δ ψ~m~. N‐acetylcysteine, a ROS scavenger, reduced DBM‐induced apoptosis, which led to the loss of Δ ψ~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. © 2011 Wiley Periodicals, Inc. J Biochem Mol Toxicol 25:312–319, 2011; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.20391

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