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Magnesium Supplementation Diminishes Peripheral Blood Lymphocyte DNA Oxidative Damage in Athletes and Sedentary Young Man

Authors :
Petrović, Jelena
Petrović, Jelena
Stanić, Dušanka
Dmitrašinović, Gordana
Plećaš-Solarović, Bosiljka
Ignjatović, Svetlana
Batinić, Bojan
Popović, Dejana
Pešić, Vesna
Petrović, Jelena
Petrović, Jelena
Stanić, Dušanka
Dmitrašinović, Gordana
Plećaš-Solarović, Bosiljka
Ignjatović, Svetlana
Batinić, Bojan
Popović, Dejana
Pešić, Vesna
Source :
Oxidative Medicine and Cellular Longevity
Publication Year :
2016

Abstract

Sedentary lifestyle is highly associated with increased risk of cardiovascular disease, obesity, and type 2 diabetes. It is known that regular physical activity has positive effects on health; however several studies have shown that acute and strenuous exercise can induce oxidative stress and lead to DNA damage. As magnesium is essential in maintaining DNA integrity, the aim of this study was to determine whether four-week-long magnesium supplementation in students with sedentary lifestyle and rugby players could prevent or diminish impairment of DNA. By using the comet assay, our study demonstrated that the number of peripheral blood lymphocytes (PBL) with basal endogenous DNA damage is significantly higher in rugby players compared to students with sedentary lifestyle. On the other hand, magnesium supplementation significantly decreased the number of cells with high DNA damage, in the presence of exogenous H2O2, in PBL from both students and rugby players, and markedly reduced the number of cells with medium DNA damage in rugby players compared to corresponding control nonsupplemented group. Accordingly, the results of our study suggest that four-week-long magnesium supplementation has marked effects in protecting the DNA from oxidative damage in both rugby players and in young men with sedentary lifestyle.

Details

Database :
OAIster
Journal :
Oxidative Medicine and Cellular Longevity
Notes :
Oxidative Medicine and Cellular Longevity
Publication Type :
Electronic Resource
Accession number :
edsoai.on1120686275
Document Type :
Electronic Resource