Oxidative damage, plasma antioxidant capacity, and glucemic control in elderly NIDDM patients

被引:55
|
作者
Aguirre, F
Martin, I
Grinspon, D
Ruiz, M
Hager, A
De Paoli, T
Ihlo, J
Farach, HA
Poole, CP
机构
[1] Univ Buenos Aires, Hosp Clin Jose de San Martin, RA-1053 Buenos Aires, DF, Argentina
[2] Univ Buenos Aires, Fac Farm & Bioquim, Catedra Fis, RA-1053 Buenos Aires, DF, Argentina
[3] Univ Buenos Aires, RLBM, LANAIS, RA-1053 Buenos Aires, DF, Argentina
[4] Univ S Carolina, Dept Phys & Astron, Columbia, SC 29208 USA
关键词
free radical; lipid peroxidation; diabetes mellitus; erythrocyte; low-density lipoproteins;
D O I
10.1016/S0891-5849(97)00293-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A study of oxidative damage was made in elderly noninsulin-dependent diabetes mellitus (NIDDM) patients. A statistically significant increase in glucose and fructosamine was found in fasting NIDDM patients, as well as an increase in the oxidation induced by tert-butyl hydroperoxide. The Total Reactive Antioxidant Potential (TRAP) of the plasma was much reduced (p < .02) and the uricemia was unchanged. The erythrocytes of diabetic patients show greater basal oxidation products (p < .05), and the susceptibility of the diabetic erythrocytes to oxidation injury was also shown to increase in the oxidation induced by t-BOOH (p < .05). Linear regression studies showed that TRAP was associated directly with uric acid (p < .05) and inversely with fructosamine and with glucose (p < .03 and p < .05 respectively) in patients with NIDDM, but not in the controls, The levels of fructosamine were found to be related to the basal damage of the red blood cells (direct correlation, p < .001). This study suggest an useful approach to diabetic oxidative stress for clinical settings. (C) 1998 Elsevier Science Inc.
引用
收藏
页码:580 / 585
页数:6
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