gms | German Medical Science

27th German Cancer Congress Berlin 2006

German Cancer Society (Frankfurt/M.)

22. - 26.03.2006, Berlin

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Vitamin D analogues modulate DNA repair following UV- and ionizing radiation

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  • corresponding author presenting/speaker Lea Tremezaygues - Universitätsklinik des Saarlandes, Homburg, Deutschland
  • Markus Seifert - Universitätsklinik des Saarlandes, Homburg
  • Viktor Meineke - Sanitätsakademie der Bundeswehr, München
  • Markus Löbrich - Universität des Saarlandes, Homburg
  • Wolfgang Tilgen - Universitätsklinik des Saarlandes, Homburg
  • Jörg Reichrath - Universitätsklinik des Saarlandes, Homburg

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocPE513

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dkk2006/06dkk623.shtml

Published: March 20, 2006

© 2006 Tremezaygues et al.
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Outline

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Both UV- and ionizing radiation have been characterized as carcinogens that may induce malignant epithelial skin tumors, with UV-light being the most important environmental risk factor. Increase in phosphorylated histone H2AX (gH2AX) foci has been shown to signal the presence of DNA damage following ionizing radiation, in particular double strand breaks. UV-light does not directly produce DNA double-strand breaks but rather produces pyrimidine dimers and other photoproducts, that must be removed or bypassed to prevent arrest of the replication fork. We have now analyzed effects of the biologically active vitamin D metabolite 1,25-dihydroxyvitamin D3 on presence of pyrimidine dimers and phosphorylated gH2AX in non-malignant and malignant human Keratinocytes (HaCaT, SCL-1) following UV(100 J/m2 – 1000 J/m2)- and ionizing irradiation (IR, 1Gy – 5Gy).), respectively. Additionally, we analyzed cell proliferation, cell viability and the expression of key components of the vitamin D system (vitamin D receptor, 1OHase, 25OHase, 24OHase).

Our findings indicate that pretreatment with 1,25(OH)2D3 time- and dose-dependently: (I) results in increased cell viability following UV-B or IR, (II) modulates expression of key components of the vitamin D system, and (III) reduces the presence of pyrimidine dimers and gH2AX foci following UV-B and ionizing irradiation, respectively. Our data support the hypothesis that the local cutaneous production of 1,25-dihydroxyvitamin D3 may represent an evolutionary highly conserved endocrine system to prevent mutagenic damage induced by UV- or ionizing irradiation.