Background:
In this study, we aimed to detect the changes in the level of interleukin
(IL)-4 and IL-13 cytokines and their downstream genes including interleukin-13 receptor subunit
alpha-2 (IL13Ra2), interleukin-4 receptor subunit alpha-1 (IL4Ra1), dual oxidase 1 (DUOX1) and
dual oxidase 2 (DUOX2). The protective effects of Selenium-L-methionine on radiation-induced
histopathological damages and changes in the level of these cytokines and genes were detected.
Methods:
Four groups of 20 rats (5 rats in each) namely, control; Selenium-L-methionine, radiation
and radiation plus Selenium-L-methionine were used in this study. 4 mg/kg of Selenium-Lmethionine
was administered 1 day before irradiation and five consecutive days after irradiation.
Irradiation was done using a dose of 15 Gy 60Co gamma rays at 109 cGy/min. All rats were sacrificed
10 weeks after irradiation for detecting changes in IL-4 and IL-13 cytokines, the expressions
of IL13Ra2, IL4Ra1, Duox1 and Duox2 and histopathological changes.
Results:
The level of IL-4 but not IL-13 increased after irradiation. This was associated with increased
expression of IL4Ra1, Duox1 and Duox2, in addition to changes in morphological properties.
Selenium-L-methionine could attenuate all injury markers following lung irradiation.
Conclusion:
Selenium-L-methionine can protect lung tissues against toxic effects of ionizing radiation.
It is possible that the modulation of immune responses and redox interactions are involved in
the radioprotective effect of this agent.
Introduction: Redox interactions play a key role in radiation injury including heart diseases. In present study, we aimed to detect the possible protective role of selenium-L-methionine on infiltration of immune cells and Duox1&2 upregulation in rat’s heart tissues. Methods: In this study, 20 rats were divided into 4 groups (5 rats in each) namely: irradiation; irradiation plus Selenium-L-methionine; control; and Selenium-L-methionine treatment. Irradiation (15 Gy to chest) was performed using a cobalt-60 gamma ray source while 4 mg/kg of selenium-L-methionine was administered intraperitoneally. Ten weeks after irradiation, rats were sacrificed for detection of IL-4 and IL-13 cytokines, infiltration of macrophages and lymphocytes as well as the expressions of IL4Ra1, Duox1, IL13Ra2 and Duox2. Results: Results showed an increase in the level of IL-4 as well as the expressions of IL4Ra1, Duox1 and Duox2. Similarly, there was an increase in the infiltration of lymphocytes and macrophages. There was significant attenuation of all these changes following treatment with selenium-L-methionine. Conclusion: Selenium-L-methionine has the potential to protect heart tissues against radiation injury. Downregulation of pro-oxidant genes and modulation of some cytokines such as IL-4 are involved in the radioprotective effect of selenium-L-methionine on heart tissues.
These results suggest that MET can protect mononuclear cells against apoptosis induced by IR through induction of cellular anti-apoptotic signaling.Key words: ionizing radiation - metformin - apoptosis - genes - proteins - blood cells.
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