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• W4233614380 abstract "We wish to thank Dr. Lipinski for his most pertinent remarks. We agree that the species isolated from the blood of diabetic patients, macromolecular complex protein complex (MPC), described in the laboratory of Dr. Lipinski could, most likely, be included in the group of oxidatively-modified proteins including advanced oxidation protein products (AOPP) [1.Witko-Sarsat V. Friedlander M. Nguyen K.T. et al.Advanced oxidation protein products (AOPP) as novel mediators of inflammation and monocyte activation in chronic renal failure.J Immunol. 1998; 161: 2524-2532PubMed Google Scholar]. We have recently obtained information on the biochemical and molecular characteristics of AOPP. The use of various analytical techniques enabled localizing and identifying the main oxidized proteins in hemodialysis (HD) plasma with human serurm albumin (HAS). To interpret the spectral modifications detected in HD plasma fractions we described in detail some structural modifications that occur as a result of plasma or HSA treatment with HOCl. Our results indicate that HOCl, and not NO2 generated by myeloperoxidase (MPO), represents a pathway for AOPP production in plasma proteins exposed to activated phagocytes (manuscript submitted for publication). However, this pathway is not exclusive and other oxido-reduction reactions may occur. The fact that MPC did not react in an enzyme-linked immunosorbent assay (ELISA) specific for the detection of oxidized proteins might be due to restricted epitopes, which might not be apparent on MPC. Therefore, the presence of oxidatively modified protein features in MPC could not be ruled out. Interestingly, MPC contained fibrinogen A alpha chain and triglyceride-rich lipoprotein, the latter also being present in plasma AOPP. In our opinion, the evidence that MPC could be obtained by exposing plasma to hydroxyl radical confirmed that MPC could be generated by oxidants, even if this hydroxyl radical–generating system involved reducing systems such as ascorbic acid and transition metals. Indeed, protein reduction would prevent disulfide bridges and decreased protein cross-linking. The report of the group of Dr. Lipinski extends the concept of the biologic and pathophysiologic relevance of oxidatively modified proteins. We have recently reported that AOPP could induce interleukin (IL)-8 synthesis by neutrophils and by monocytes, thus corroborating our previous results that demonstrate that AOPP are inflammatory mediators [2.Witko-Sarsat V. Gausson V. Descamps-Latscha B. Are advanced oxidation protein products potential uremic toxins?.Kidney Int. 2003; 63: S11-S14Abstract Full Text Full Text PDF Scopus (87) Google Scholar]. Therefore, further investigation on the involvement of AOPP and/or MPC should be performed, especially in diabetic or in uremic patients." @default.
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• W4233614380 date "2004-01-01" @default.
• W4233614380 modified "2023-09-25" @default.
• W4233614380 title "Markers of oxidative stress in uremia" @default.
• W4233614380 doi "https://doi.org/10.1111/j.1523-1755.2004.414_7.x" @default.
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