Dose selenomethionine have radio-protective effect on cell lines with wild type p53?
- 1. Minami-Wakayama National Hospital, (Japan)
- 2. Nara Medical University, (Japan)
- 3. Fukui Medical University, (Japan)
Description
Full text: Selenium compounds are known to have cancer preventive effects. It is reported recently that selenium in the form of selenomethionine (SeMet) can protect cells with wild type p53 from UV-induced cell killing by activating the DNA repair mechanism of p53 tumor suppressor protein via redox factor Ref1 by reducing p53 cysteine residue 275 and 277. In contrast, SeMet has no protective effect on UV-induced cell killing in p53-null cells. If SeMet also has protective effect in cells with wild type p53 on cell killing by photon irradiation, SeMet can be used as normal tissue radio-protector. We examined the effect of SeMet on cell killing by X-ray irradiation in several cell lines with different p53 status at exponentially growing phase. Cell lines used in this experiment were as follows: H1299/neo; human lung cancer cell line of p53 null type tranfected with control vector with no p53, H1299/wp53; wild type p53 transfected counterpart. A172/neo; human glioblastoma cell line with wild type p53, A172/mp53-248; mp53-248 (248-mutant, ARG >TRP) transfected counterpart. SAS/neo; human tongue cancer cell line with wild type p53, and SAS/mp53-248; mp53-248 transfected counterpart. Cells were subcultured at monolayer in D-MEM containing 10% FBS. Survivals of the cells were determined by colony forming ability. Ten-MV linac X-ray was used to irradiate the cells. Exponentially growing cells were incubated with 20μM of SeMet for 15 hours before irradiation. After 24 hours exposure of SeMet, cells were incubated up to two weeks in growth medium for colony formation. Twenty-four hours exposure of 20μM of SeMet had no cytotoxicity on these cell lines. SeMet had no modification effect on cell killing by photon irradiation in H1299/neo, H1299/wp53, SAS/neo, SAS/mp53-248, and A172/mp53-248. On the other hand, SeMet sensitized A172/neo in radiation cell killing. The effects of p53 on interaction of SeMet and photon irradiation differ according to cell lines
Additional details
Publishing Information
- Publisher
- AINSE
- Imprint Title
- 12th Quadrennial Congress of the International Association for Radiation Research incorporating the 50th Annual Meeting of Radiation Research Society, RANZCR Radiation Oncology Annual Scientific Meeting and AINSE Radiation Science Conference
- Imprint Pagination
- 414 p.
- Journal Page Range
- p. 361
Conference
- Title
- 12. Quadrennial Congress of the International Association for Radiation Research
- Acronym
- ICRR 2003
- Dates
- 17-22 Aug 2003
- Place
- Brisbane, QLD (Australia)
INIS
- Country of Publication
- Australia
- Country of Input or Organization
- Australia
- INIS RN
- 36019560
- Subject category
- S63: RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS;
- Resource subtype / Literary indicator
- Conference, Non-conventional Literature
- Descriptors DEI
- BIOLOGICAL RADIATION EFFECTS; CELL CULTURES; CELL KILLING; COLONY FORMATION; CYSTEINE; DNA REPAIR; LUNGS; MICROSTRUCTURE; MUTANTS; NEOPLASMS; PHOTON BEAMS; PROTEINS; RADIOPROTECTIVE SUBSTANCES; SELENIUM COMPOUNDS; TONGUE; TOXICITY; TUMOR CELLS; ULTRAVIOLET RADIATION; X RADIATION
- Descriptors DEC
- AMINO ACIDS; ANIMAL CELLS; BEAMS; BIOLOGICAL EFFECTS; BIOLOGICAL RECOVERY; BIOLOGICAL REPAIR; BODY; CARBOXYLIC ACIDS; DIGESTIVE SYSTEM; DISEASES; DRUGS; ELECTROMAGNETIC RADIATION; IONIZING RADIATIONS; ORAL CAVITY; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC SULFUR COMPOUNDS; ORGANS; RADIATION EFFECTS; RADIATIONS; REPAIR; RESPIRATORY SYSTEM; RESPONSE MODIFYING FACTORS; THIOLS