OBJECTIVE -Diabetes increases the risk of coronary heart disease (CHD) to a greater extent in women than in men. We investigated whether type 1 diabetic patients with short duration of disease and without complications have an altered oxidative status and whether there are differences between men and women.RESEARCH DESIGN AND METHODS -We investigated oxidative status in 29 control subjects and 37 patients with uncomplicated type 1 diabetes with duration of 6 Ϯ 3 years.RESULTS -Compared with control subjects, type 1 diabetic patients had lower total plasma antioxidant capacity (TRAP) (720.3 Ϯ 111.2 vs. 972.5 Ϯ 97.7 mol/l in men, P Ͻ 0.001; 579.8 Ϯ 95.4 vs. 930.1 Ϯ 84.2 in women, P Ͻ 0.001), higher lipid hydroperoxide (ROOH) levels (6.4 Ϯ 2.2 vs. 2.0 Ϯ 0.7 mol/l in men, P Ͻ 0.001; 8.1 Ϯ 1.9 vs. 2.2 Ϯ 0.6 in women, P Ͻ 0.001), higher total conjugated diene (CD) levels (0.037 Ϯ 0.003 vs. 0.033 Ϯ 0.002 A.U. in men, P Ͻ 0.001), lower 246-nm CD levels (0.0032.Ϯ 0.0010 vs. 0.0070 Ϯ 0.0012 A.U. in men, P Ͻ 0.001; 0.0022 Ϯ 0.0011 vs. 0.0072 Ϯ 0.0014 A.U. in women, P Ͻ 0.001), and higher 232-nm CD levels (0.0348 Ϯ 0.0041 vs. 0.0257 Ϯ 0.0022 A.U. in men, P Ͻ 0.001; 0.0346 Ϯ 0.0031 vs. 0.0246 Ϯ 0.0074 A.U. in women, P Ͻ 0.001). Compared with diabetic men, diabetic women had lower TRAP (P Ͻ 0.01), higher ROOH levels (P Ͻ 0.01), and lower 246-nm CD levels (P Ͻ 0.05). Plasma concentration of uric acid was significantly lower in patients with type 1 diabetes than in control subjects (3.3 Ϯ 0.3 vs. 4.3 Ϯ 0.2 mg/dl; P ϭ 0.009) with a significant difference between women and men with type 1 diabetes (2.6 Ϯ 0.3 vs. 3.9 Ϯ 0.3, respectively; P ϭ 0.009).CONCLUSIONS -Our findings suggest that reduced antioxidant activity and increased oxidative stress occur early after the diagnosis of type 1 diabetes, especially in women, and this might explain, at least in part, the increased susceptibility of diabetic women to cardiovascular complications.
Oxidative stress is postulated to be increased in patients with IDDM. Accumulating evidence suggests that oxidative cell injury caused by free radicals contributes to the development of IDDM complications. On the other side, a decreased efficiency of antioxidant defenses (both enzymatic and nonenzymatic) seems to correlate with the severity of pathological tissue changes in IDDM. Thus, we determined plasma antioxidant defenses, measuring the total radical-trapping antioxidant capacity (TRAP) and the two markers of oxidative stress, lipid hydroperoxides (ROOHs) and conjugated dienes, in 72 patients with well-controlled IDDM and without evident complications, compared with 45 nondiabetic subjects. Compared with control subjects, IDDM patients showed significantly reduced plasma TRAP (669 +/- 131 vs. 955 +/- 104 micromol/l, P < 0.001) and significantly increased levels of ROOHs (7.13 +/- 2.11 vs. 2.10 +/- 0.71 micromol/l, P < 0.001) and conjugated dienes (0.0368 +/- 0.0027 vs. 0.0328 +/- 0.0023 arbitrary units [AU], P < 0.01), especially in the trans-trans conformation (0.0340 +/- 0.0028 vs. 0.0259 +/- 0.0022 AU, P < 0.001), with a concurrent reduction of conjugated dienes in the cis-trans conformation (0.0028 +/- 0.0011 vs. 0.0069 +/- 0.0012 AU, P < 0.001). The oxidative parameters studied did not appear to be correlated with metabolic control (HbA1c levels) and lipid profile (cholesterol or triglyceride levels). The reduced TRAP and the increased ROOH and conjugated diene plasma levels, together with the decreased ratio of cis-trans/trans-trans conjugated dienes, which reflects an altered redox status of plasma, indicate that in IDDM patients, oxidative stress is enhanced and antioxidant defenses are defective, regardless of diabetes duration, metabolic control, or presence of complications.
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