Figures & data
Table 1. Subject characteristics*
Figure 1. Oxidative stress and total antioxidant status of plasma increases in early type 2 diabetes patients. Plasma from type 2 diabetes patients at first clinical onset and from non-diabetes age-matched subjects was evaluated for Trolox equivalent antioxidant capacity (TEAC) (A) and malondialdehyde–thiobarbituric acid (MDA–TBA) adducts (B). Values are mean ± SE. *P < 0.01, #P < 0.001 vs. controls (analysis of variance Kruskal–Wallis test).
![Figure 1. Oxidative stress and total antioxidant status of plasma increases in early type 2 diabetes patients. Plasma from type 2 diabetes patients at first clinical onset and from non-diabetes age-matched subjects was evaluated for Trolox equivalent antioxidant capacity (TEAC) (A) and malondialdehyde–thiobarbituric acid (MDA–TBA) adducts (B). Values are mean ± SE. *P < 0.01, #P < 0.001 vs. controls (analysis of variance Kruskal–Wallis test).](/cms/asset/4c0063f6-22bb-49a4-965f-09c29ecc1bae/yrer_a_11700308_f0001_b.jpg)
Figure 2. Oxidative stress and total antioxidant status of RBCs is increased in type 2 diabetes patients at first clinical onset. Red blood cells (RBCs) from early type 2 diabetes patients and from non-diabetes age-matched subjects were evaluated for TEAC (A) and MDA–TBA adducts (B). Values are mean ± SE. *P < 0.01, #P < 0.001 vs. controls (analysis of variance Kruskal–Wallis test). Hg, hemoglobin.
![Figure 2. Oxidative stress and total antioxidant status of RBCs is increased in type 2 diabetes patients at first clinical onset. Red blood cells (RBCs) from early type 2 diabetes patients and from non-diabetes age-matched subjects were evaluated for TEAC (A) and MDA–TBA adducts (B). Values are mean ± SE. *P < 0.01, #P < 0.001 vs. controls (analysis of variance Kruskal–Wallis test). Hg, hemoglobin.](/cms/asset/f42db672-c286-4eac-8887-c5c8808ae70a/yrer_a_11700308_f0002_b.jpg)
Figure 3. Antioxidant enzymatic activity is upregulated early in erythrocytes from type 2 diabetes patients. Superoxide dismutase (SOD) (A), catalase (CAT) (B), and glutathione peroxidase (GPX) (C) activity was measured in erythrocytes from type 2 diabetes patients at first clinical onset and from non-diabetes age-matched individuals. Values are mean ± SE. *P < 0.05, #P < 0.01 vs. controls (analysis of variance, one-way Tukey test).
![Figure 3. Antioxidant enzymatic activity is upregulated early in erythrocytes from type 2 diabetes patients. Superoxide dismutase (SOD) (A), catalase (CAT) (B), and glutathione peroxidase (GPX) (C) activity was measured in erythrocytes from type 2 diabetes patients at first clinical onset and from non-diabetes age-matched individuals. Values are mean ± SE. *P < 0.05, #P < 0.01 vs. controls (analysis of variance, one-way Tukey test).](/cms/asset/0dd20dd2-05c5-40a6-81ea-a417dd49736e/yrer_a_11700308_f0003_b.jpg)
Figure 4. Caspase-3 is activated in RBCs of type 2 diabetes patients from first clinical onset. Caspase-3 activity was measured in RBCs from early type 2 diabetes patients and from non-diabetes age-matched subjects. Values are mean ± SE. #P < 0.05 vs. controls (analysis of variance Kruskal–Wallis test).
![Figure 4. Caspase-3 is activated in RBCs of type 2 diabetes patients from first clinical onset. Caspase-3 activity was measured in RBCs from early type 2 diabetes patients and from non-diabetes age-matched subjects. Values are mean ± SE. #P < 0.05 vs. controls (analysis of variance Kruskal–Wallis test).](/cms/asset/11e28063-4bd7-4b2c-9e28-bde3050e2914/yrer_a_11700308_f0004_b.jpg)