J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


A more recent version of this article appeared on May 1, 2006

Papers In Press, published online ahead of print February 9, 2006
J. Lipid Res., doi:10.1194/jlr.M500348-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
M500348-JLR200v1
47/5/964    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Higuchi, O.
Right arrow Articles by Miyazawa, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Higuchi, O.
Right arrow Articles by Miyazawa, T.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Submitted on August 5, 2005
Revised on February 7, 2006
Accepted on February 8, 2006

Aminophospholipid glycation and its inhibitor screening system: A new role of pyridoxal 5'-phosphate and pyridoxal as lipid glycation inhibitor

Ohki Higuchi, Kiyotaka Nakagawa, Tsuyoshi Tsuzuki, Toshihide Suzuki, Shinichi Oikawa, and Teruo Miyazawa

Tohoku University, Sendai

Corresponding Author: miyazawa{at}biochem.tohoku.ac.jp

Peroxidized phospolipid-mediated cytotoxity involves in the pathophysiology of diseases (i.e., an abnormal increase of phosphatidylcholine hydroperoxide, PCOOH, found in plasma of type 2 diabetic patients). The PCOOH accumulation may relate to Amadori-glycated phosphatidylethanolamine (deoxy-D-fructosyl PE, namely Amadori-PE), since Amadori-PE causes oxidative stress. However, lipid glycation inhibitor has not been discovered yet due to lack of a lipid glycation model study useful for inhibitor screening. Consequently, we optimized and developed a lipid glycation model considering various reaction conditions (glucose concentration, temperature, buffer type and pH) between phosphatidylethanolamine (PE) and glucose. Using the developed model, various protein glycation inhibitors (aminoguanidine, pyridoxamine, aspirin and carnosine), antioxidants (ascorbic acid, alpha -tocopherol, quercetin and rutin) and other food compounds (L-lysine, L-cysteine, pyridoxine, pyridoxal and pyridoxal 5'-phosphate) were evaluated for their anti-glycative property. As results, pyridoxal 5'-phosphate and pyridoxal (vitamin B6 derivatives) were the most effective anti-glycative compounds. These pyridoxals could easily be condensed with PE before glucose/PE reaction occurred. Since we found that PE-pyridoxal 5'-phosphate adduct was detectable in human red blood cells and that elevated plasma Amadori-PE concentration in streptozotocin-induced diabetic rats was decreased by dietary supplementation of pyridoxal 5'-phosphate, it is likely that pyridoxal 5'-phosphate acts as lipid glycation inhibitor in vivo, which possibly contributes to diabetes prevention.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.