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J Invest Dermatol. 2009 May;129(5):1271-9. doi: 10.1038/jid.2008.362. Epub 2008 Nov 27.

Infrared radiation confers resistance to UV-induced apoptosis via reduction of DNA damage and upregulation of antiapoptotic proteins.

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1
Department of Dermatology, University Kiel, Kiel, Germany.

Abstract

Infrared radiation (IR) is increasingly used for wellness purposes. In this setting, it is frequently combined with UV radiation, primarily for tanning purposes. The impact of IR on UV-induced carcinogenesis is still unclear. Hence, we investigated the interplay between IR and UV with regard to UV-induced apoptosis. Pretreatment of murine keratinocytes with IR before UV reduced the apoptotic rate. Likewise, the number of sunburn cells was reduced in mice preexposed to IR before UV. The amounts of UV-induced DNA damage were reduced by IR both in vitro and in vivo. This was not observed in DNA repair-deficient mice. UV-induced downregulation of the antiapoptotic proteins FLIP(L) and BCL-X(L) was prevented by IR, whereas the proapoptotic protein BAX was downregulated. These data indicate that IR reduces UV-induced apoptosis that may be mediated by several pathways, including reduction of DNA damage and induction of antiapoptotic proteins. The antiapoptotic effects of IR may support the survival of UV-damaged cells and thus carcinogenesis. As, however, IR reduces UV-induced DNA damage, the balance between these two effects may be important. Thus, in vivo carcinogenesis studies are required to define the role of IR and its interaction with UV in photocarcinogenesis.

PMID:
19037232
DOI:
10.1038/jid.2008.362
[Indexed for MEDLINE]
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