Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 2 • March-April 2012


Selenium Shown to Specifically Stimulate
Repair of Oxidative DNA Damage in
LNCaP Prostate Cancer Cells

Some epidemiological studies have found an inverse relationship between selenium intake and incidence/mortality of certain cancers, including prostate cancer. In an effort to identify possible mechanisms for these protective effects, researchers investigated the effect of low doses of selenium on the stimulation of DNA repair systems in LNCaP human prostate adenocarcinoma cells in response to four different sources of DNA damage.1 They examined DNA damage caused by UVA (ultraviolet light A), hydrogen peroxide, methylmethane sulfonate (MMS), or UVC (ultraviolet light C). Overall, their results showed that selenium was a very potent protector against cell toxicity and genotoxicity induced by oxidative stress (UVA or hydrogen peroxide) but not from the agents that induce other types of deleterious DNA lesions (MMS or UVC). In addition, they found that selenium treatment resulted in increased DNA repair capacity in oxidative DNA damaged cells.

The researchers noted that “the most robust results of the Nutritional Prevention of Cancer Trial (NPC Trial) came from the analyses of the complete data for prostate cancer incidence, which showed that dietary supplementation with 200 µg/day of yeast-enriched selenium resulted in a 63% reduction in prostate cancer risk.” Another study of the effects of selenium on the incidence of prostate cancer was performed by a different group, which used aged beagle dogs because dogs and humans are said to be the only two species in which prostate cancer occurs spontaneously with appreciable frequency;2 they reported efficient protection against DNA damage.

The researchers used two types of selenium in their study: sodium selenite or selenomethionine. Cells were cultured in medium either with or without selenium supplementation (30 nM sodium selenite or 10 µM selenomethionine) for 72 hours. The LNCaP human prostate cell line they used are wild type for both p53 and Rb genes (not mutated), although both genes are mutated in the vast majority of human prostate cancers.1 It may be, therefore, that the beneficial effects of selenium reported in this paper1 — reduced carcinogenesis and increased DNA repair — might apply to prostate cells without mutations in these genes but not apply once prostate cells had become cancerous in conjunction with mutations in these genes. As reported in another paper.3 however, sodium selenite redox cycling can kill cancer cells.

References

  1. de Rosa et al. Low doses of selenium specifically stimulate the repair of oxidative DNA damage in LNCaP prostate cancer cells. Free Radic Res 46(2):105-15 (2012).
  2. Waters et al. Effects of dietary selenium supplementation on DNA damage and apoptosis in canine prostate. J Natl Cancer Inst 95(3):237-41 (2003).
  3. Olm et al. Extracellular thiol-assisted selenium uptake dependent on the x(c)- cystine transporter explains the cancer-specific cytotoxicity of selenite. Proc Natl Acad Sci USA 106(27):11400-5 (2009).

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