Selenium protects primary human keratinocytes from apoptosis induced by exposure to ultraviolet radiation

• Published in: Clinical and experimental dermatology Vol. 28; no. 3; pp. 294 - 300
• Main Authors: Rafferty, T. S., Beckett, G. J., Walker, C., Bisset, Y. C., McKenzie, R. C.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.05.2003; Blackwell; Oxford University Press
• Subjects: Acridine Orange; Apoptosis - drug effects; Biological and medical sciences; Blotting, Western; Cells, Cultured; Dermatology; Dose-Response Relationship, Drug; Humans; Investigative techniques, diagnostic techniques (general aspects); Keratinocytes - drug effects; Keratinocytes - metabolism; Keratinocytes - radiation effects; Medical sciences; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Selenium - pharmacology; Selenomethionine - pharmacology; Sodium Selenite - pharmacology; Tumor Suppressor Protein p53 - metabolism; Ultraviolet Rays - adverse effects; Human; Cell culture; Ultraviolet radiation; Keratinocyte; Exposure; Selenium; Photoprotection; Protection; Biological activity; Apoptosis
• ISSN: 0307-6938; 1365-2230
• DOI: 10.1046/j.1365-2230.2003.01254.x

Summary The generation of reactive oxygen species has been implicated in ultraviolet radiation (UVR)‐induced skin damage. In mice, increasing dietary selenium intake protects skin from UVR‐induced DNA damage and photocarcinogenesis. We sought to determine whether selenium supplementation could protect keratinocytes from apoptosis resulting from exposure to broadband (TL20W/12) UVR. Unirradiated cultures contained 6.5 ± 1% apoptotic cells; the maximum percentage of apoptotic cells (34 ± 5%) was seen 16 h after UVR of 600 J/m2. Under these conditions cell death from necrosis was 15 ± 2.5% of the total cells. A 24‐h preincubation with sodium selenite (10 nm−1 µm) or selenomethionine (50 nm−1 µm) protected cultured human keratinocytes from UVR‐induced apoptosis. In primary keratinocytes the greatest reduction in apoptosis was found with 100 nm of either selenium compound (71% reduction in the numbers of total apoptotic cells; P < 0.01). Supplementation with 100–200 nm selenite or selenomethionine prevented UVR‐induced apoptosis, but did not decrease the levels of UVR‐induced p53, as measured by Western blotting. Collectively, this data suggests that selenium prevents UVR‐induced cell death by inhibiting p53‐independent cell death pathways.