Selective apoptotic effects of piceatannol and myricetin in human cancer cells
Article first published online: 20 SEP 2011
Copyright © 2011 John Wiley & Sons, Ltd.
Journal of Applied Toxicology
Volume 32, Issue 12, pages 986–993, December 2012
How to Cite
Morales, P. and Haza, A. I. (2012), Selective apoptotic effects of piceatannol and myricetin in human cancer cells. J. Appl. Toxicol., 32: 986–993. doi: 10.1002/jat.1725
- Issue published online: 24 OCT 2012
- Article first published online: 20 SEP 2011
- Manuscript Revised: 15 JUL 2011
- Manuscript Accepted: 15 JUL 2011
- Manuscript Received: 17 MAY 2011
- reactive oxygen species
Numerous studies have shown the potential of dietary polyphenols as anticarcinogenic agents. The aim of the present study was to evaluate the apoptotic effects of piceatannol and myricetin, naturally occurring polyphenols in red wine, alone or in combination, in two human cell lines: HL-60 (leukemia) and HepG2 (hepatoma). Apoptotic cells were identified by chromatin condensation, poly(ADP-ribose) polymerase cleavage and flow cytometry analysis. Results from TUNEL assay showed that piceatannol or myricetin alone induced apoptotic cell death in a concentration- and time-dependent manners in HL-60 cells. Furthermore, in combined treatment the percentage of apoptotic HL-60 cells was significantly higher. Nevertheless, the percentage of TUNEL positive HepG2 cells only was significant after piceatannol treatment and in combined treatment was even lower than in cells treated with piceatannol alone. Moreover, we also studied the relative reactive oxygen species (ROS) production. Our results indicate that apoptosis induced by piceatannol or myricetin occurs through an ROS-independent cell death pathway. In conclusion, piceatannol and myricetin synergistically induced apoptosis in HL-60 cells but not in HepG2 cells. These findings suggest that the potential anticarcinogenic properties of dietary polyphenols depend largely on the cell line used. The relevance of these data needs to be verified in human epidemiological studies. Copyright © 2011 John Wiley & Sons, Ltd.