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|標題:||Ornithine Decarboxylase Prevents Dibenzoylmethane-Induced Apoptosis through Repressing Reactive Oxygen Species Generation||作者:||Wu, C.L.
|關鍵字:||Dibenzoylmethane;Apoptosis;Ornithine decarboxylase;Reactive oxygen;species;mammary epithelial-cells;bcl-x-l;alpha-difluoromethylornithine;carcinoma-cells;dna-adducts;sencar mice;hl-60 cells;inhibition;cancer;polyamines||Project:||Journal of Biochemical and Molecular Toxicology||期刊/報告no：:||Journal of Biochemical and Molecular Toxicology, Volume 25, Issue 5, Page(s) 312-319.||摘要:||
Dibenzoylmethane (DBM) belongs to the flavonoid family and is a minor constituent of the root extract of licorice and the beta-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 (Delta psi(m)). N-acetylcysteine, a ROS scavenger, reduced DBM-induced apoptosis, which led to the loss of Delta psi(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. (C) 2011 Wiley Periodicals, Inc. J Biochem Mol Toxicol 25:312-319, 2011; View this article online at wileyonlinelibrary.com. DOI 10:1002/jbt.20391
|Appears in Collections:||生命科學系所|
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