Document Detail

Hyperglycemia-related pathophysiologic mechanisms and potential beneficial actions of melatonin.
MedLine Citation:
PMID:  18855729     Owner:  NLM     Status:  MEDLINE    
Chronically-elevated blood glucose initiates a harmful series of processes in which toxic reactive species play crucial roles. Oxidative as well as nitro-oxidative stress is harmful for virtually all biomolecules including lipids, proteins and DNA. Such pathophysiologic mechanisms eventually results in cellular dysfunction, apoptosis or necrosis. Melatonin is a multifunctional indolamine which counteracts several pathophysiologic steps and displays significant beneficial effects against hyperglycemia-induced cellular toxicity. These are related to melatonin's antioxidative, anti-inflammatory and possibly epigenetic regulatory properties. Current knowledge encourages using this non-toxic indolamine either as a sole treatment or in conjunction with other treatments for inhibition of the biohazards of hyperglycemia.
Ahmet Korkmaz; Turgut Topal; Sukru Oter; Dun-Xian Tan; Russel J Reiter
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Mini reviews in medicinal chemistry     Volume:  8     ISSN:  1389-5575     ISO Abbreviation:  Mini Rev Med Chem     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-10-15     Completed Date:  2008-11-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101094212     Medline TA:  Mini Rev Med Chem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1144-53     Citation Subset:  IM    
Gulhane Askeri Tip Akademisi, Fizyoloji Anabilim Dali, 06018 Ankara, Turkey.
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MeSH Terms
Hyperglycemia / metabolism*,  physiopathology*
Melatonin / metabolism*
Oxidative Stress
Poly(ADP-ribose) Polymerases / metabolism
Reactive Nitrogen Species / metabolism
Reactive Oxygen Species / metabolism
Reg. No./Substance:
0/Reactive Nitrogen Species; 0/Reactive Oxygen Species; 73-31-4/Melatonin; EC Polymerases

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

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