Vitamin D and death by sunshine.

Abstract

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.

• Authors: Katie M Dixon, Wannit Tongkao-On, Vanessa B Sequeira, Sally E Carter, Eric J Song, Mark S Rybchyn, Clare Gordon-Thomson, Rebecca S Mason
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 14 Issue 1 Pg. 1964-77 (Jan 18 2013) ISSN: 1422-0067 [Print] Switzerland
• PMID: 23334476 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Dehydrocholesterols
• TP53 protein, human
• Tumor Suppressor Protein p53
• Vitamins
• 7-dehydrocholesterol
• Calcitriol

Topics

• Calcitriol (metabolism, therapeutic use)
• Cell Death (drug effects, radiation effects)
• DNA Damage
• Dehydrocholesterols (metabolism)
• Humans
• Skin Neoplasms (metabolism, pathology, prevention & control)
• Sunlight (adverse effects)
• Tumor Suppressor Protein p53 (metabolism)
• Ultraviolet Rays (adverse effects)
• Vitamins (metabolism, therapeutic use)