Vitamin D and Death by Sunshine

International Journal of Molecular Sciences

Katie M. Dixon¹  Wannit Tongkao-On¹  Vanessa B. Sequeira¹  Sally E. Carter¹  Eric J. Song¹  Mark S. Rybchyn¹  Clare Gordon-Thomson¹ 

[1] Discipline of Physiology, Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia; E-Mails:

关键词: vitamin D;    1;    25-dihydroxyvitamin D3;    ultraviolet radiation;    sunburn cells;    cyclobutane pyrimidine dimers;    p53;    nitric oxide;    MAPK;    AKT;   

DOI  :  10.3390/ijms14011964

来源: mdpi

【 摘 要 】

Exposure to sunlight is the major cause of skin cancer. Ultraviolet radiation (UV) from the sun causes damage to DNA by direct absorption and can cause skin cell death. UV also causes production of reactive oxygen species that may interact with DNA to indirectly cause oxidative DNA damage. UV increases accumulation of p53 in skin cells, which upregulates repair genes but promotes death of irreparably damaged cells. A benefit of sunlight is vitamin D, which is formed following exposure of 7-dehydrocholesterol in skin cells to UV. The relatively inert vitamin D is metabolized to various biologically active compounds, including 1,25-dihydroxyvitamin D3. Therapeutic use of vitamin D compounds has proven beneficial in several cancer types, but more recently these compounds have been shown to prevent UV-induced cell death and DNA damage in human skin cells. Here, we discuss the effects of vitamin D compounds in skin cells that have been exposed to UV. Specifically, we examine the various signaling pathways involved in the vitamin D-induced protection of skin cells from UV.

【 授权许可】

CC BY   
© 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.