Effect of Low-Dose Selenium Supplementation on the Genotoxicity, Tissue Injury and Survival of Mice Exposed to Acute Whole-Body Irradiation

Effect of Low-Dose Selenium Supplementation on the Genotoxicity, Tissue Injury and Survival of... The aim of the present study is to evaluate the radioprotective effect of low-dose selenium supplementation (multiple administrations) on radiation toxicities and mortality induced by lethal dose of whole-body irradiation (WBI). For this, BALB/c mice received sodium selenite (4 μg/kg body wt) intraperitoneally for five consecutive days and subjected to WBI at an absorbed dose of 8 Gy (60Co, 1 Gy/min). Administration of sodium selenite was continued even during the post irradiation days three times a week till the end of the experiment. The radioprotective effect was evaluated in terms of the improvement in 30 days post irradiation survival, protection from DNA damage, and biochemical and histological changes in radiosensitive organs. The results indicated that low-dose sodium selenite administration did not protect the mice from radiation-induced hematopoietic and gastrointestinal injuries and subsequent mortality. However, it significantly prevented the radiation-induced genotoxicity or DNA damage in peripheral leukocytes. Further sodium selenite administration modulated the messenger RNA (mRNA) expression of GPx1, GPx2, and GPx4 in the spleen and intestine differentially and led to a significant increase in GPx activity (∼1.5 to 2-folds) in these organs. In line with this observation, sodium selenite administration reduced the level of lipid peroxidation in the intestine. In conclusion, our study shows that low-dose sodium selenite supplementation can be an effective strategy to prevent WBI-induced genotoxicity but may not have an advantage against mortality sustained during nuclear emergencies. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biological Trace Element Research Springer Journals

Effect of Low-Dose Selenium Supplementation on the Genotoxicity, Tissue Injury and Survival of Mice Exposed to Acute Whole-Body Irradiation

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Life Sciences; Biochemistry, general; Biotechnology; Nutrition; Oncology
ISSN
0163-4984
eISSN
1559-0720
D.O.I.
10.1007/s12011-017-0955-9
Publisher site
See Article on Publisher Site

Abstract

The aim of the present study is to evaluate the radioprotective effect of low-dose selenium supplementation (multiple administrations) on radiation toxicities and mortality induced by lethal dose of whole-body irradiation (WBI). For this, BALB/c mice received sodium selenite (4 μg/kg body wt) intraperitoneally for five consecutive days and subjected to WBI at an absorbed dose of 8 Gy (60Co, 1 Gy/min). Administration of sodium selenite was continued even during the post irradiation days three times a week till the end of the experiment. The radioprotective effect was evaluated in terms of the improvement in 30 days post irradiation survival, protection from DNA damage, and biochemical and histological changes in radiosensitive organs. The results indicated that low-dose sodium selenite administration did not protect the mice from radiation-induced hematopoietic and gastrointestinal injuries and subsequent mortality. However, it significantly prevented the radiation-induced genotoxicity or DNA damage in peripheral leukocytes. Further sodium selenite administration modulated the messenger RNA (mRNA) expression of GPx1, GPx2, and GPx4 in the spleen and intestine differentially and led to a significant increase in GPx activity (∼1.5 to 2-folds) in these organs. In line with this observation, sodium selenite administration reduced the level of lipid peroxidation in the intestine. In conclusion, our study shows that low-dose sodium selenite supplementation can be an effective strategy to prevent WBI-induced genotoxicity but may not have an advantage against mortality sustained during nuclear emergencies.

Journal

Biological Trace Element ResearchSpringer Journals

Published: Feb 11, 2017

References

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