Document Detail


Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca(2+) signaling molecular pathways in breast cancer.
MedLine Citation:
PMID:  23194197     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Aims: Exposure to electromagnetic radiation (EMR) may increase breast cancer risk by inducing oxidative stress and suppressing the production of melatonin. Aim of the present review is to discuss the mechanisms and risk factors of EMR and oxidative stress-induced breast cancer, to summarize the controlled studies evaluating measures for prevention, and to conclude with evidence-based strategies for prevention. Materials: Review of the relevant literature and results from our recent basic studies, as well as critical analyses of published systematic reviews were obtained from the Pubmed and the Science Citation Index. Results: It has been proposed that chronic exposure to EMR may increase the risk of breast cancer by suppressing the production of melatonin; this suppression may affect the development of breast cancer either by increasing levels of circulation of estrogen or through over production of free oxygen radicals. Most epidemiological studies have also indicated overall effect of EMR exposure in premenopausal women, particularly for estrogen receptor positive breast tumors. Enhanced voltage-dependent Ca(2+) current and impaired inhibitory G-protein function, and derangement of intracellular organelles with a Ca(2+) buffering effect, such as endoplasmic reticulum and mitochondria have been also shown to contribute to disturbed Ca(2+) signaling in breast cancer. Conclusion: Melatonin may modulate breast cancer through modulation of enhanced oxidative stress and Ca(2+) influx in cell lines. However, there is not enough evidence on increased risk of breast cancer related to EMR exposure.
Authors:
Mustafa Nazıroğlu; Sümeyye Tokat; Seda Demirci
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of receptor and signal transduction research     Volume:  32     ISSN:  1532-4281     ISO Abbreviation:  J. Recept. Signal Transduct. Res.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9509432     Medline TA:  J Recept Signal Transduct Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  290-7     Citation Subset:  IM    
Affiliation:
Department of Biophysics, Medical Faculty, Süleyman Demirel University , Isparta , Turkey.
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