Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death

T S Rafferty, R C McKenzie, J A A Hunter, A F Howie, J R Arthur, F Nicol, G J Beckett

Research output: Contribution to journalArticle

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Abstract

The generation of reactive oxygen species has been implicated as part of the mechanism responsible for UVB-radiation-induced skin damage. In mice, evidence suggests that increased dietary selenium intake may protect skin from many of the harmful effects of WE radiation. We sought to determine the selenoprotein profile of cultured human skin cells and whether selenium supplementation could protect keratinocytes and melanocytes from the lethal effects of UVB radiation. Labelling experiments using [Se-75]selenite showed qualitative and quantitative differences in selenoprotein expression by human fibroblasts, keratinocytes and melanocytes. This was most noticeable for thioredoxin reductase (60 kDa) and phospholipid glutathione peroxidase (21 kDa); these proteins were identified by Western blotting. Despite these differences, we found that a 24 h preincubation with sodium selenite or selenomethionine protected both cultured human keratinocytes and melanocytes from WE-induced cell death. With primary keratinocytes, the greatest reduction in cell death was found with 10 nM sodium selenite (79% cell death reduced to 21.7%; P < 0.01) and with 50 nM selenomethionine (79% cell death reduced to 13.2%; P < 0.01). Protection could be obtained with concentrations as low as 1 nM with sodium selenite and 10 nM with selenomethionine. When selenium was added after UVB radiation, little protection could be achieved, with cell death only being reduced from 88.5% to about 50% with both compounds. In all of the experiments sodium selenite was more potent than selenomethionine at providing protection from UVB radiation.

Original languageEnglish
Pages (from-to)231-236
Number of pages6
JournalBiochemical Journal
Volume332
Issue number1
Publication statusPublished - 15 May 1998

Keywords

  • glutathione-peroxidase
  • thioredoxin reductase
  • lipid hydroperoxides
  • gene-expression
  • metabolism
  • carcinogenesis
  • selenocysteine
  • keratinocytes
  • cytokines
  • component

Cite this

Rafferty, T. S., McKenzie, R. C., Hunter, J. A. A., Howie, A. F., Arthur, J. R., Nicol, F., & Beckett, G. J. (1998). Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death. Biochemical Journal, 332(1), 231-236.

Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death. / Rafferty, T S ; McKenzie, R C ; Hunter, J A A ; Howie, A F ; Arthur, J R; Nicol, F; Beckett, G J .

In: Biochemical Journal, Vol. 332, No. 1, 15.05.1998, p. 231-236.

Research output: Contribution to journalArticle

Rafferty, TS, McKenzie, RC, Hunter, JAA, Howie, AF, Arthur, JR, Nicol, F & Beckett, GJ 1998, 'Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death', Biochemical Journal, vol. 332, no. 1, pp. 231-236.
Rafferty TS, McKenzie RC, Hunter JAA, Howie AF, Arthur JR, Nicol F et al. Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death. Biochemical Journal. 1998 May 15;332(1):231-236.
Rafferty, T S ; McKenzie, R C ; Hunter, J A A ; Howie, A F ; Arthur, J R ; Nicol, F ; Beckett, G J . / Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death. In: Biochemical Journal. 1998 ; Vol. 332, No. 1. pp. 231-236.
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abstract = "The generation of reactive oxygen species has been implicated as part of the mechanism responsible for UVB-radiation-induced skin damage. In mice, evidence suggests that increased dietary selenium intake may protect skin from many of the harmful effects of WE radiation. We sought to determine the selenoprotein profile of cultured human skin cells and whether selenium supplementation could protect keratinocytes and melanocytes from the lethal effects of UVB radiation. Labelling experiments using [Se-75]selenite showed qualitative and quantitative differences in selenoprotein expression by human fibroblasts, keratinocytes and melanocytes. This was most noticeable for thioredoxin reductase (60 kDa) and phospholipid glutathione peroxidase (21 kDa); these proteins were identified by Western blotting. Despite these differences, we found that a 24 h preincubation with sodium selenite or selenomethionine protected both cultured human keratinocytes and melanocytes from WE-induced cell death. With primary keratinocytes, the greatest reduction in cell death was found with 10 nM sodium selenite (79{\%} cell death reduced to 21.7{\%}; P < 0.01) and with 50 nM selenomethionine (79{\%} cell death reduced to 13.2{\%}; P < 0.01). Protection could be obtained with concentrations as low as 1 nM with sodium selenite and 10 nM with selenomethionine. When selenium was added after UVB radiation, little protection could be achieved, with cell death only being reduced from 88.5{\%} to about 50{\%} with both compounds. In all of the experiments sodium selenite was more potent than selenomethionine at providing protection from UVB radiation.",
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N2 - The generation of reactive oxygen species has been implicated as part of the mechanism responsible for UVB-radiation-induced skin damage. In mice, evidence suggests that increased dietary selenium intake may protect skin from many of the harmful effects of WE radiation. We sought to determine the selenoprotein profile of cultured human skin cells and whether selenium supplementation could protect keratinocytes and melanocytes from the lethal effects of UVB radiation. Labelling experiments using [Se-75]selenite showed qualitative and quantitative differences in selenoprotein expression by human fibroblasts, keratinocytes and melanocytes. This was most noticeable for thioredoxin reductase (60 kDa) and phospholipid glutathione peroxidase (21 kDa); these proteins were identified by Western blotting. Despite these differences, we found that a 24 h preincubation with sodium selenite or selenomethionine protected both cultured human keratinocytes and melanocytes from WE-induced cell death. With primary keratinocytes, the greatest reduction in cell death was found with 10 nM sodium selenite (79% cell death reduced to 21.7%; P < 0.01) and with 50 nM selenomethionine (79% cell death reduced to 13.2%; P < 0.01). Protection could be obtained with concentrations as low as 1 nM with sodium selenite and 10 nM with selenomethionine. When selenium was added after UVB radiation, little protection could be achieved, with cell death only being reduced from 88.5% to about 50% with both compounds. In all of the experiments sodium selenite was more potent than selenomethionine at providing protection from UVB radiation.

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