LEVELS OF LIPID-PEROXIDATION PRODUCT AND GLYCATED HEMOGLOBIN A(1)C INTHE ERYTHROCYTES OF DIABETIC-PATIENTS

Citation
M. Inouye et al., LEVELS OF LIPID-PEROXIDATION PRODUCT AND GLYCATED HEMOGLOBIN A(1)C INTHE ERYTHROCYTES OF DIABETIC-PATIENTS, Clinica chimica acta, 276(2), 1998, pp. 163-172
Citations number
35
Categorie Soggetti
Medical Laboratory Technology",Biology
Journal title
ISSN journal
00098981
Volume
276
Issue
2
Year of publication
1998
Pages
163 - 172
Database
ISI
SICI code
0009-8981(1998)276:2<163:LOLPAG>2.0.ZU;2-Z
Abstract
In diabetes, the glycation and subsequent browning (or glycoxidation) reactions are enhanced by elevated glucose concentrations. It is uncle ar whether or not the diabetic state per se also induces an increase i n the generation of oxygen-derived free radicals (QFRs). There is some evidence, however, that glycation itself may induce the formation of OFRs. OFRs could cause oxidative damage to endogenous molecules. We ex amined the relationship between the levels of lipid peroxidation and t he levels of glycated hemoglobin A(1)c (GHbA(1)c) in erythrocytes of d iabetic and healthy subjects. Lipid peroxidation was assessed in eryth rocyte membrane lipids by monitoring peak height ratios of conjugated linoleic acid (CLA), one of the products of lipid peroxidation, to lin oleic acid (LA) using gas chromatography-mass spectrometry (GC/MS). CL A is a collective term used to designate a mixture of positional and g eometric isomers of LA in which the double bonds are conjugated. The p eak height ratio of CLA to LA was used asa biomarker of lipid peroxida tion. GHbA(1)c, an index of glycemic stress, was measured by high-perf ormance liquid chromatography. There were significantly increased rati os of CLA to LA in diabetic erythrocytes compared with control erythro cytes. These ratios of CLA to LA were also significantly correlated wi th GHbA(1)c values. This suggests that glycation via chronic hyperglyc emia links lipid peroxidation in the erythrocytes of both diabetic and healthy subjects. (C) 1998 Elsevier Science B.V. All rights reserved.