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Hemodialysis and Protein Oxidation Products

Authors :
Alper Gümüş
Cihan Coskun
Yasemin Erdogan Doventas
Humeyra Ozturk
Macit Koldas
Berrin Bercik Inal
Alev Kural
Source :
Annals of the New York Academy of Sciences. 1100:404-408
Publication Year :
2007
Publisher :
Wiley, 2007.

Abstract

The presence of a chronic inflammatory state has also been widely documented in end-stage renal disease patients receiving maintenance hemodialysis (HD). It is commonly attributed to the constantly renewed activation of circulating neutrophils and monocytes following blood passage through dialysis circuits and subsequent generation of activated complement components due to contact of plasma with bioincompatible membranes and/or transfer of endotoxins from the dialyzate to the blood compartment. This conjunction leads to a massive generation of reactive oxygen species (ROS), for example, superoxide anion, hydrogen peroxide, hydroxyl radical, and chlorinated oxidants, such as hypochlorous acid by activated neutrophils. The exquisite vulnerability of proteins to ROS is now well documented. Oxidation of amino acid residues, such as tyrosine, leads to the formation of dityrosine, protein aggregation, cross-linking, and fragmentation. Dityrosine-containing protein cross-linking products in the plasma of dialysis patients are named as advanced oxidation protein products (AOPP). In addition, advanced glycation end-products (AGE) is a protein carbonyl compound and produced by protein–ROS interaction. We investigated both the effect of the renewed activation of the immune cells, due to blood–dialyzer interaction over protein oxidation products like AOPP and AGE, among chronic renal failure (CRF) patients receiving maintenance HD, and choice of dialyzers like high flux or the other group on protein oxidation product levels.

Details

ISSN :
00778923
Volume :
1100
Database :
OpenAIRE
Journal :
Annals of the New York Academy of Sciences
Accession number :
edsair.doi.dedup.....6be69a96f2df5e54102be197876106f3
Full Text :
https://doi.org/10.1196/annals.1395.045