الفهرس | Only 14 pages are availabe for public view |
Abstract from the benefits-versus-risks point of view, the use of ionizing radiation in the treatment of cancer is greatly beneficial. Radiation damages cellular DNA thus blocking the cells’ ability for divisions and eventually leads to apoptosis and/or nonapoptotic cell death. Radiotherapy promotes tumor control, reduces the risk of recurrence, and improves overall survival. However, the therapeutic gain can be compromised by numerous undesirable side effects that are often induced in nearby healthy tissues as a response to radiation injury (Guha & Kavanagh, 2011). Administration of chemical radioprotectors prior to or shortly after irradiation can be effective in reducing radiation-induced toxicities. Ectoines, produced by many halophilic bacteria, are natural compounds characterized by being effective stabilizers of biomolecules including proteins, nucleic acids, and biological membranes (Rieckmann et al., 2019). Therefore, ectoines are widely utilized in many over-the-counter products for their cytoprotective properties and is under review in this study as a potential radioprotector. In the present study, we reviewed the possible radioprotective effect of ectoine on radiation-induced intrinsic apoptosis in irradiated mice by evaluating the levels of expression of Apaf-1, Bcl-xL, COXIII, and COAI on days 1, 3, 7, 16, and 30 following irradiation. Mice included in this study were divided into 4 main groups: 1. Control group (group C): 30 mice injected intraperitoneally with 0.2 ml saline each. 2. group E: 25 mice injected with ectoine at a concentration of 200 g/kg body weight. 3. group R: 36 mice received a single whole-body radiation dose of 6 Gy externally and an injection of 0.2 ml saline as well. 4. group ER: 36 mice were injected intraperitoneally with 200 g/kg ectoine and irradiated after 24 hours with a single whole-body dose of 6 Gy. Our results showed that: The number of mice that died prior to the time of dissection was significantly higher in the irradiated groups (R and ER) when compared to the control group. The number of deaths in mice of group ER was also notably lower than that in group R and no mice died in group E before dissection. In the first three days following irradiation, Apaf-1 and Bcl-xL levels decreased in group R and, to a lesser extent, group ER. COXIII levels, on another hand, significantly increased in group ER during the first 24 hours after irradiation. On day 7, Apaf-1, Bcl-xL, and COXIII levels significantly increased in group R. Group ER also demonstrated a prominent increase of the same genes but in a lesser magnitude. Bcl- xL levels were found to be persistently high in groups R and ER on day 16, however, a much clearer difference was observed between the two groups at this stage with group R showing higher levels of Bcl-xL than group ER. Apaf-1 and COXIII levels in all treated groups were notably lower on day 16 than they were on day 7. Summary, Conclusion and Recommendations 39 Apaf-1 levels decreased in all treated groups on day 30 to values lower than those in the control group. However, Bcl-xL levels in all treated groups were still higher than control with group ER also showing a lesser elevation in Bcl-xL than group R. COXIII levels on day 30 were restored to nearly control levels in all treated groups except group ER in which they were still elevated. |