Aguirre F, Martin I, Grinspon D, Ruiz M, Hager A, De Paoli T, Ihlo J, Farach H A, Poole C P
Hospital de Clínicas José de San Martin, Universidad de Buenos Aires, Argentina.
Free Radic Biol Med. 1998 Mar 1;24(4):580-5. doi: 10.1016/s0891-5849(97)00293-1.
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.
对老年非胰岛素依赖型糖尿病（NIDDM）患者进行了氧化损伤研究。在空腹NIDDM患者中发现葡萄糖和果糖胺有统计学显著增加，以及叔丁基过氧化氢诱导的氧化增加。血浆的总反应抗氧化能力（TRAP）大幅降低（p < 0.02），而尿酸血症未改变。糖尿病患者的红细胞显示出更高的基础氧化产物（p < 0.05），并且在叔丁基过氧化氢诱导的氧化中，糖尿病红细胞对氧化损伤的易感性也增加（p < 0.05）。线性回归研究表明，在NIDDM患者中，TRAP与尿酸直接相关（p < 0.05），与果糖胺和葡萄糖呈负相关（分别为p < 0.03和p < 0.05），但在对照组中并非如此。发现果糖胺水平与红细胞的基础损伤有关（直接相关，p < 0.001）。这项研究为临床环境中糖尿病氧化应激提供了一种有用的方法。
