Send to:

Choose Destination
See comment in PubMed Commons below
Exp Mol Med. 2003 Aug 31;35(4):263-8.

Melatonin reduces ultraviolet-B induced cell damages and polyamine levels in human skin fibroblasts in culture.

Author information

  • 1Institute of Medical Science, School of Medicine, Keimyung University, Daegu 700-120, Korea.


UV radiation is known to cause photoaging of the skin and is considered one of the leading cause of developing skin carcinogenesis. Melatonin which has a highly lipophilic molecular structure facilitating penetration of cell membranes and serving as an extra- and intracellular free radical scavenger has been demonstrated to protect photodamage of skin affected by UV exposure. In this study, we have examined the role of melatonin in response to UVB induced photodamaging process, using human skin fibroblasts in vitro. Cell survival curves after UVB irradiation showed dose-dependent decrease. Only 60% of fibroblasts were survived at 140 mJ/cm(2) UVB irradiation. By pre-cultivation of cells with melatonin (100 nM), a significant number of cells remained unaffected. After UVB irradiation with 70 mJ/cm(2), the level of putrescine was 1.7+/-0.3 fold increased compared to melatonin pre-treated group. In Northern analyses, the transcriptional level of ornithine decarboxylase (ODC) gene expression was increased by UVB irradiation and prohibited by melatonin. These results indicated that melatonin was effectively able to neutralize membrane peroxidation when present in relevant concentration during UVB irradiation and diminishes the UVB-induced increase of polyamine synthesis and ODC gene expression. Collectively, ODC response to UVB induced changes are possibly involves a melatonin or antioxidant sensitive regulatory pathway in normal human skin fibroblast.

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group Icon for Korean Society for Biochemistry and Molecular Biology
    Loading ...
    Write to the Help Desk