Abstract |
Ionizing radiation (IR) therapy has been widely employed in the treatment of cancer. However, certain issues, including toxicity, have been raised in conjunction with IR therapy for cancer. Recently, selenomethionine (SeMet) as an antioxidant has been the subject of a great deal of attention for its chemopreventive effects. In this study, we found that DNA repair activity has been enhanced in response to SeMet against IR. In addition, our data showed that p53 functional activity was significantly reduced against IR in the cells expressing a mutant form of redox factor 1 (Ref-1) contrast with Ref-1 wild-type cells treated with SeMet, suggesting that p53 activation under the modulation of Ref-1 might play an important role in IR-treated cells in the presence of SeMet. Furthermore, IR-induced micronuclei numbers were also reduced after treatment with SeMet, strongly implicating protection by SeMet in genomic stability against IR-induced genotoxicity. From this study, we suggest that the p53-mediated protective mechanism of SeMet might provide clues for reducing side effects of IR therapy.
|
Authors | Seok Won Jeong, Hwa Jin Jung, Md Mujibur Rahman, Jee Na Hwang, Young R Seo |
Journal | Journal of medicinal food
(J Med Food)
Vol. 12
Issue 2
Pg. 389-93
(Apr 2009)
ISSN: 1557-7600 [Electronic] United States |
PMID | 19459742
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Antioxidants
- Tumor Suppressor Protein p53
- DNA
- Selenomethionine
- APEX1 protein, human
- DNA-(Apurinic or Apyrimidinic Site) Lyase
|
Topics |
- Antioxidants
(pharmacology)
- Cell Line
- Cell Line, Tumor
- DNA
(drug effects, radiation effects)
- DNA Repair
(drug effects)
- DNA-(Apurinic or Apyrimidinic Site) Lyase
(genetics, metabolism)
- Fibroblasts
(drug effects, radiation effects)
- Gene Expression
- Humans
- Micronuclei, Chromosome-Defective
(drug effects, radiation effects)
- Mutation
- Radiation, Ionizing
- Selenomethionine
(pharmacology)
- Tumor Suppressor Protein p53
(metabolism)
|