Epidemiological studies have demonstrated an inverse relationship between selenium (Se) intake and cancer incidence and/or mortality.
However, the molecular mechanisms underlying the cancer chemopreventive activity of Se compounds remain largely unknown. The objective of this study was to investigate the effect of low doses of Se on the stimulation of DNA repair systems in response to 4 different qualities of DNA damage. P53-proficient LNCaP human prostate adenocarcinoma cells were grown either untreated or in the presence of low concentrations of two Se compounds (30 nM sodium selenite, or 10 μM selenomethionine) and exposed to UVA, H(2)O(2), methylmethane sulfonate (MMS) or UVC. Cell viability as well as DNA damage induction and repair were evaluated by the alkaline Comet assay. Overall, Se was shown to be a very potent protector against cell toxicity and genotoxicity induced by oxidative stress (UVA or H(2)O(2)) but not from agents that induce other types of deleterious lesions (MMS or UVC). Furthermore, Se-treated cells exhibited increased oxidative DNA repair activity, indicating a novel mechanism of Se action. Therefore, the benefits of Se could be explained by a combination of antioxidant activity, the reduction in DNA damage and the enhancement of oxidative DNA repair capacity.
Written by:
de Rosa V, Erkekoğlu P, Forestier A, Favier A, Hincal F, Diamond AM, Douki T, Rachidi W. Are you the author?
Reference: Free Radic Res. 2011 Dec 7. [Epub ahead of print]
PubMed Abstract
PMID: 22145923
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