Cancer Letters

Cancer Letters

Volume 27, Issue 2, June 1985, Pages 163-170
Cancer Letters

Research letter
Selenium inhibits UV-light-induced skin carcinogenesis in hairless mice

https://doi.org/10.1016/0304-3835(85)90105-3Get rights and content

Abstract

Female hairless inbred hrhr mice were exposed to UV-B irradiation from Philips TL 40W12 fluorescent tubes. Fractionated irradiation, given as single daily doses 5 days a week, was gradually increased from 0.04 to 0.4 J/cm2 over 2 weeks. Irradiation at 0.4 J/cm2 was continued for 20 weeks. Selenium supplementation given as sodium selenite in the drinking water at 2, 4 and 8 mg/l began 3 weeks before UV-irradiation and continued thereafter. Development of skin tumors was followed by weekly examinations. Statistical analyses revealed significant dose-dependent selenium-mediated protection against UV-light-induced skin cancer. Leukemia developed in 5 of 150 UV-irradiated mice as opposed to none in a group of 60 unirradiated mice.

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    A 2018 review concluded with high certainty that there was no significant benefit of selenium supplements in reducing cancer risk; however, NMSC did have vastly heterogeneous results, and therefore the authors did not report the same level of certainty regarding the lack of antineoplastic benefit selenium may or may not have on NMSC.162 Animal studies have demonstrated a dose-dependent protection against UV light and the development of skin tumors in mice with selenium supplemented diets.163 Selenium-deficient mice had lower levels of glutathione peroxidase resulting in elevated levels of superoxide dismutase and catalase in response to UV light treatment.164

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    DNA damage measured by comet assay show a nonlinear dose response with increased damage induced by both low and high Se levels [62]. In further support of possible anti-cancer activity, Se protects against DNA damage from ionizing radiation [63] and UV light [64]. Selenite and SeMet are the most widely used compounds with extensive evidence for inhibition of mutagenesis, increase in excision capacity, increase in activity of DNA repair enzymes like glycosylases and reduction in DNA oxidation [65–67].

  • Diet in dermatology: Part I. Atopic dermatitis, acne, and nonmelanoma skin cancer

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    In addition, 3 case control studies83-85 and 5 cohort studies74,77,79,81,98 failed to identify a significant association between vitamin C and NMSC. Selenium protects against UVB-induced cytotoxicity in human keratinocytes and carcinogenesis in mice.133-135 Studies have found a potentially protective role of selenium for NMSC.

  • Nutrition: The future of melanoma prevention?

    2014, Journal of the American Academy of Dermatology
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    This may complicate use of selenium as a nutritional supplement in patients with melanoma, but may suggest that selenium is a better candidate as an oral adjuvant agent where higher doses can be administrated. Many studies have shown an inverse relationship between overall mortality from various forms of cancer (including skin cancers)27-32 and both selenium dietary intake and topical application. Mouse studies have shown a decrease in melanoma lung metastases with increased dietary amounts of selenium,33,34 although the relationship between selenium exposure and human melanoma incidence remains unclear.34,35

  • Nutrition and nonmelanoma skin cancers

    2010, Clinics in Dermatology
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    Selenium is incorporated into selenoproteins as a covalently bound selenocysteine residue.110,111 Selenium has been shown to protect against UVB112,113 and chemically induced skin cancer in mice,114 as well as prostate, lung, breast, and colon cancer in humans.115 The mechanism by which selenium exerts its protective effect is likely through reduction of reactive hydroxyl free radicals, which are thought to attack DNA and cause mutations.116

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    A number of epidemiologic studies have found an inverse relationship between selenium in the diet and overall cancer death rates.19-22 Oral and topical selenium both provide protection against UV-induced sunburn, tanning, and skin cancer.23,24 In vitro studies have demonstrated that selenium causes dose-dependent apoptosis in human A375 melanoma cell lines through inducing mitochondria-mediated oxidative stress.25,26

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Sponsored by the Danish Cancer Society, grant No. 14/83.

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