Document Detail


Melatonin increases survival of HaCaT keratinocytes by suppressing UV-induced apoptosis.
MedLine Citation:
PMID:  16313494     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Melatonin is a potent antioxidant and direct radical scavenger. As keratinocytes represent the major population in the skin and UV light causes damage to these cells, the possible protective effects of melatonin against UV-induced cell damage in HaCaT keratinocytes were investigated in vitro. Cells were preincubated with melatonin at graded concentrations from 10(-9) to 10(-3) m for 30 min prior to UV irradiation at doses of 25 and 50 mJ/cm2. Biological markers of cellular viability such as DNA synthesis and colony-forming efficiency as well as molecular markers of apoptosis were measured. DNA synthesis was determined by [3H]-thymidine incorporation into insoluble cellular fraction, clonogenicity through plating efficiency experiments and apoptosis by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. DNA synthesis experiments showed a strong protective effect by preincubation with melatonin at concentrations of 10(-4) m (P < 0.01) and 10(-3) m (P < 0.001). Additional postirradiation treatment with melatonin showed no increase in the pre-UV incubation protective effect. These results indicate that preincubation is a requirement for melatonin to exert its protective effects. The mechanism of melatonin's protective effect (10(-6) to 10(-3) m) includes inhibition of apoptosis as measured by TUNEL assay. Moreover, the biological significance of these effects is supported by clonogenic studies showing a significantly higher number of colonies in cultures treated with melatonin compared to controls. Thus, pretreatment with melatonin led to strong protection against UVB-induced damage in keratinocytes.
Authors:
T W Fischer; B Zbytek; R M Sayre; E O Apostolov; A G Basnakian; T W Sweatman; J Wortsman; P Elsner; A Slominski
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of pineal research     Volume:  40     ISSN:  0742-3098     ISO Abbreviation:  J. Pineal Res.     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2005-11-29     Completed Date:  2006-03-14     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8504412     Medline TA:  J Pineal Res     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  18-26     Citation Subset:  IM    
Affiliation:
Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Cells, Cultured
Dose-Response Relationship, Radiation
Humans
In Situ Nick-End Labeling
Keratinocytes / drug effects*,  metabolism,  radiation effects*
Melatonin / pharmacology*
Thymidine / metabolism
Ultraviolet Rays
Grant Support
ID/Acronym/Agency:
P01 DK58324-01A1/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
50-89-5/Thymidine; 73-31-4/Melatonin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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