DIFFERENTIAL EXPRESSION OF SELENOPROTEINS BY HUMAN SKIN CELLS AND PROTECTION BY SELENIUM FROM UVB-RADIATION-INDUCED CELL-DEATH

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 pr otect skin from many of the harmful effects of WE radiation. We sought to determine the selenoprotein profile of cultured human skin cells a nd whether selenium supplementation could protect keratinocytes and me lanocytes from the lethal effects of UVB radiation. Labelling experime nts using [Se-75]selenite showed qualitative and quantitative differen ces in selenoprotein expression by human fibroblasts, keratinocytes an d 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 fou nd that a 24 h preincubation with sodium selenite or selenomethionine protected both cultured human keratinocytes and melanocytes from WE-in duced cell death. With primary keratinocytes, the greatest reduction i n cell death was found with 10 nM sodium selenite (79% cell death redu ced to 21.7%; P < 0.01) and with 50 nM selenomethionine (79% cell deat h reduced to 13.2%; P < 0.01). Protection could be obtained with conce ntrations as low as 1 nM with sodium selenite and 10 nM with selenomet hionine. When selenium was added after UVB radiation, little protectio n could be achieved, with cell death only being reduced from 88.5% to about 50% with both compounds. In all of the experiments sodium seleni te was more potent than selenomethionine at providing protection from UVB radiation.