The coinitiator DMABEE induces death by apoptosis and necrosis in human monoblastoid cells

• Published in: Clinical oral investigations 2005-09, Vol.9 (3), p.168-172
• Main Authors: Cimpan, Mihaela Roxana, Matre, Roald, Skaug, Nils, Lie, Stein Atle, Lygre, Henning
• Format: Article
• Language: English
• Subjects: 4-Aminobenzoic Acid - toxicity; Analysis of Variance; Annexin A5 - metabolism; Apoptosis - drug effects; Cell Membrane - drug effects; Cell Survival - drug effects; Composite Resins - metabolism; Composite Resins - toxicity; Dose-Response Relationship, Drug; Humans; Membrane Lipids - metabolism; Monocytes - drug effects; Necrosis - chemically induced; para-Aminobenzoates; Phase Transition; U937 Cells - drug effects
• ISSN: 1432-6981; 1436-3771
• DOI: 10.1007/s00784-004-0289-9

4-N,N-Dimethyl amino benzoic acid ethylester (DMABEE), a leachable lipophilic component of polymer-based dental-filling materials, has been shown to interact with cell membrane phospholipids, such as phosphatidylcholine and phosphatidylserine (PS). One marker of cellular death by apoptosis is the change in architecture of the plasma membrane involving the translocation of the negatively charged PS from the inner to the outer leaflet of the cell membrane. We therefore hypothesized that DMABEE has the potential to induce apoptosis. The necrosis inducing potential was also investigated. To test our hypothesis human monoblastoid U-937 cells were exposed to 10, 20, 40, 80, 120, 160, and 200 microM of DMABEE for 24, 48, and 72 h. At the culture end-points apoptotic and necrotic cells were detected by flow cytometry. DMABEE enhanced cell death by apoptosis and necrosis in U-937 cells in a dose-dependent fashion. The data support our hypothesis that DMABEE triggers death-signaling pathways.