Document Detail


Cytotoxicity of advanced glycation endproducts in human micro- and astroglial cell lines depends on the degree of protein glycation.
MedLine Citation:
PMID:  18825304     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Advanced glycation endproducts (AGEs) arise from the reaction of sugars with side chains and the N-terminus of proteins and are thought to be involved in the pathogenesis of several diseases by inducing oxidative stress, inflammation and cell death presumably mediated through activation of the receptor of AGE (RAGE). To address the question whether the cell damaging effect of AGE depends on the degree of its protein glycation, differential modified AGEs derived from incubating human serum albumin with increasing concentrations of methyl glyoxal were tested on cell viability, reactive oxygen species (ROS) formation, intracellular ATP levels, and activation of caspases 3/7 in two human glial cell lines, which were used as a model for human glia cells. All AGEs tested, regardless of their degree of modification, were found to induce ROS formation in both microglial (CHME-5) and astroglial cells (U373 MG), while only highly modified AGEs were able to decrease the cell viability and to induce apoptosis. This indicates that apoptotic events may be involved in the change of physiological parameters.
Authors:
Katrin Bigl; Frank Gaunitz; Annett Schmitt; Sven Rothemund; Reinhard Schliebs; Gerald Münch; Thomas Arendt
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-09-30
Journal Detail:
Title:  Journal of neural transmission (Vienna, Austria : 1996)     Volume:  115     ISSN:  0300-9564     ISO Abbreviation:  J Neural Transm     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-10-30     Completed Date:  2009-01-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9702341     Medline TA:  J Neural Transm     Country:  Austria    
Other Details:
Languages:  eng     Pagination:  1545-56     Citation Subset:  IM    
Affiliation:
Interdisciplinary Centre of Clinical Research (IZKF), Faculty of Medicine, University of Leipzig, Inselstr. 22, 04103, Leipzig, Germany. katrin.bigl@yahoo.de
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Apoptosis / drug effects
Astrocytes / drug effects*,  metabolism
Caspase 3 / metabolism
Caspase 7 / metabolism
Cell Line
Cell Survival / drug effects
Cells, Cultured
Glycosylation End Products, Advanced / chemistry*,  toxicity*
Humans
Microglia / drug effects*,  metabolism
Proteins / chemistry,  metabolism
Reactive Oxygen Species / metabolism
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Chemical
Reg. No./Substance:
0/Glycosylation End Products, Advanced; 0/Proteins; 0/Reactive Oxygen Species; 56-65-5/Adenosine Triphosphate; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 7

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