The authors declare that no competing interests exist.
The Influence of Lentinan on the Capacity of Repair of DNA Damage and Apoptosis Induced by Paclitaxel in Mouse Bone Marrow Cells
Article first published online: 24 MAY 2013
© 2013 Wiley Periodicals, Inc.
Journal of Biochemical and Molecular Toxicology
Volume 27, Issue 7, pages 370–377, July 2013
How to Cite
Attia, S. M., Harisa, G. I., Abd-Allah, A. R., Ahmad, S. F. and Bakheet, S. A. (2013), The Influence of Lentinan on the Capacity of Repair of DNA Damage and Apoptosis Induced by Paclitaxel in Mouse Bone Marrow Cells. J. Biochem. Mol. Toxicol., 27: 370–377. doi: 10.1002/jbt.21499
Contract Grant Sponsor: Deanship of Scientific Research at King Saud University.
Contract Grant Number: RGP-VPP-120.
- Issue published online: 2 JUL 2013
- Article first published online: 24 MAY 2013
- Manuscript Accepted: 3 MAY 2013
- Manuscript Revised: 24 APR 2013
- Manuscript Received: 14 MAR 2013
- Deanship of Scientific Research at King Saud University. Grant Number: RGP-VPP-120
- DNA Damage and Repair;
- Bone Marrow Suppression;
- Oxidative Stress;
- Secondary Malignancies
The ability of the flavonoid lentinan (LAN) to enhance the repair of paclitaxel (PAC)-induced DNA damage and apoptosis in mouse bone marrow cells was investigated. Moreover, the possible mechanism underlying this modulation was determined. LAN was neither genotoxic nor apoptogenic at doses equivalent to 1 or 2 mg/kg/day. Pretreatment of mice with LAN significantly enhances the repair of PAC-induced DNA damage and bone marrow suppression in a dose dependent manner. Moreover, LAN affords significant protection against PAC-induced apoptosis. A significant increase of reactive oxygen species and a decrease in reduced glutathione levels were observed after PAC treatment and prior administration of LAN before PAC challenge ameliorated these oxidative stress markers. Conclusively, our study provides, for the first time, that LAN enhances the repair of PAC-induced DNA damage and apoptosis that resides, at least in part, on its ability to modulate the cellular antioxidant levels and consequently protect bone marrow cells from PAC genotoxicity. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:370-377, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21499