الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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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
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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.