Glycated hemoglobin and lipid peroxidation in erythrocytes of diabetic patients

被引:43
作者
Inouye, M
Mio, T
Sumino, K
机构
[1] Hyogo Rehabil Ctr Hosp, Dept Internal Med, Nishi Ku, Kobe, Hyogo 6512181, Japan
[2] Kobe Univ, Sch Med, Dept Publ Hlth, Kobe, Hyogo 650, Japan
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1999年 / 48卷 / 02期
关键词
D O I
10.1016/S0026-0495(99)90035-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In diabetes, glycation and subsequent browning (or glycoxidation) reactions are enhanced by elevated glucose concentrations. It is unclear whether the diabetic state per se also induces an increase in the generation of oxygen-derived free radicals (OFRs), However, there is some evidence that glycation itself may induce the formation of OFRs, OFRs cause oxidative damage to endogenous molecules, including cholesterol, 7-Oxocholesterol is known to be one of the major products of cholesterol oxidation, The level of cholesterol peroxidation products was assessed in erythrocyte membrane lipid by monitoring the peak height ratio of 7-oxocholesterol, one of the products of cholesterol peroxidation, to cholesterol with gas chromatography/mass spectrometry (GC/MS), The peak height ratio of 7-oxocholesterol to cholesterol was used as a biomarker of lipid peroxidation. The hemoglobin Ale (HbA1c) value, an index of glycemic stress, was measured by high-performance liquid chromatography, We examined the relationship between the levels of cholesterol peroxidation products and HbA1c in erythrocytes of diabetic and healthy subjects. There was a significantly increased ratio of 7-oxocholesterol to cholesterol in diabetic erythrocytes compared with control erythrocytes. The ratio of 7-oxocholesterol to cholesterol was significantly correlated with the level of HbA1c, This suggests that glycation of hemoglobin via chronic hyperglycemia is linked to cholesterol peroxidation in erythrocytes of both diabetic and healthy subjects. Copyright (C) 1999 by W.B. Saunders Company.
引用
收藏
页码:205 / 209
页数:5
相关论文
共 38 条
[1]   ROLE OF OXIDATIVE STRESS IN DEVELOPMENT OF COMPLICATIONS IN DIABETES [J].
BAYNES, JW .
DIABETES, 1991, 40 (04) :405-412
[2]   EFFECTS OF OXYGEN-CENTERED FREE-RADICALS ON LOW-DENSITY-LIPOPROTEIN STRUCTURE AND METABOLISM [J].
BEDWELL, S ;
JESSUP, W .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1987, 15 (02) :259-260
[3]   OXIDATION OF CHOLESTEROL MOIETY OF LOW-DENSITY-LIPOPROTEIN IN THE PRESENCE OF HUMAN ENDOTHELIAL-CELLS OR CU+2 IONS - IDENTIFICATION OF MAJOR PRODUCTS AND THEIR EFFECTS [J].
BHADRA, S ;
ARSHAD, MAQ ;
RYMASZEWSKI, Z ;
NORMAN, E ;
WHERLEY, R ;
SUBBIAH, MTR .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1991, 176 (01) :431-440
[4]  
BRUCKDORFER KR, 1990, CURR OPIN LIPIDOL, V1, P529
[5]  
CAMERON NE, 1977, DIABETES S2, V46, pS3
[6]   FREE-RADICAL ACTIVITY IN TYPE-2 DIABETES [J].
COLLIER, A ;
WILSON, R ;
BRADLEY, H ;
THOMSON, JA ;
SMALL, M .
DIABETIC MEDICINE, 1990, 7 (01) :27-30
[7]   HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY METHOD FOR HEMOGLOBIN A1C [J].
DAVIS, JE ;
MCDONALD, JM ;
JARETT, L .
DIABETES, 1978, 27 (02) :102-107
[8]  
DRAZNIN B, 1993, DIABETES ATHEROSCLER, P203
[9]   GLYCOSYLATED HEMOGLOBIN AND DIABETIC CONTROL [J].
GABBAY, KH .
NEW ENGLAND JOURNAL OF MEDICINE, 1976, 295 (08) :443-444
[10]  
GILLERY P, 1988, DIABETES METAB, V14, P25