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Oxidants, antioxidants and mitochondrial function in non-proliferative diabetic retinopathy.

Rodríguez-Carrizalez AD, Castellanos-González JA, Martínez-Romero EC, Miller-Arrevillaga G, Villa-Hernández D, Hernández-Godínez PP, Ortiz GG, Pacheco-Moisés FP, Cardona-Muñoz EG, Miranda-Díaz AG - J Diabetes (2013)

Bottom Line: TAC had significant decrease levels with minimum peak in severe retinopathy with 7.98 ± 0.48 mEq/mL (P < 0.0001).The fluidity of membrane submitochondrial particles decreased significantly in T2DM patients with mild, moderate, or severe NPDR compared with that in healthy volunteers (P < 0.0001 for all).Patients with NPDR exhibit oxidative deregulation with decreased membrane fluidity of submitochondrial particles and increased systemic catabolism (mitochondrial dysfunction) with the potential for generalized systemic damage in T2DM.

View Article: PubMed Central - PubMed

Affiliation: University Health Sciences Centre, University of Guadalajara, Guadalajara, México.

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Oxidants (a,b) and antioxidants (c–e) in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) Products of lipid peroxidation (LPO), given as malondialdehyde (MDA) and 4-hydroxyalkenals (4HDA), were highest in patients with severe NPDR (3.29 ± 0.05 μmol/L; P < 0.017 compared with control), as were levels of (b) nitric oxide (NO) catabolites (45.62 ± 1.27 pmol/mL; P < 0.0001 compared with control). (c) Total antioxidant capacity (TAC) was significantly decreased in all three groups of NPDR, with the greatest decrease seen in patients with severe NPDR (7.98 ± 0.48 mEq/mL; P < 0.0001 compared with control). (d,e) Erythrocyte catalase and glutathione peroxidase (GPx) activity was higher in patients with NPDR, with maximum catalase activity seen in patients with mild retinopathy (142 ± 6 U/mg protein; P < 0.0001 compared with control), whereas GPx activity was highest in those with severe retinopathy (117 ± 15 U/min/mg protein; P < 0.0001 compared with control). Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.
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fig01: Oxidants (a,b) and antioxidants (c–e) in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) Products of lipid peroxidation (LPO), given as malondialdehyde (MDA) and 4-hydroxyalkenals (4HDA), were highest in patients with severe NPDR (3.29 ± 0.05 μmol/L; P < 0.017 compared with control), as were levels of (b) nitric oxide (NO) catabolites (45.62 ± 1.27 pmol/mL; P < 0.0001 compared with control). (c) Total antioxidant capacity (TAC) was significantly decreased in all three groups of NPDR, with the greatest decrease seen in patients with severe NPDR (7.98 ± 0.48 mEq/mL; P < 0.0001 compared with control). (d,e) Erythrocyte catalase and glutathione peroxidase (GPx) activity was higher in patients with NPDR, with maximum catalase activity seen in patients with mild retinopathy (142 ± 6 U/mg protein; P < 0.0001 compared with control), whereas GPx activity was highest in those with severe retinopathy (117 ± 15 U/min/mg protein; P < 0.0001 compared with control). Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.

Mentions: Levels of LPO products in healthy controls were 0.98 ± 0.13 μmol/L. These increased significantly with the severity of retinopathy from 1.42 ± 0.08 to 2.49 ± 0.05, and 3.29 ± 0.05 μmol/L (mild, moderate, and severe NPDR, respectively; P < 0.017; Fig. 1a), suggesting the presence of oxidative stress in NPDR. Because LPO is a well-established mechanism of cellular lesions, these findings suggest cellular and systemic oxidative stress.


Oxidants, antioxidants and mitochondrial function in non-proliferative diabetic retinopathy.

Rodríguez-Carrizalez AD, Castellanos-González JA, Martínez-Romero EC, Miller-Arrevillaga G, Villa-Hernández D, Hernández-Godínez PP, Ortiz GG, Pacheco-Moisés FP, Cardona-Muñoz EG, Miranda-Díaz AG - J Diabetes (2013)

Oxidants (a,b) and antioxidants (c–e) in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) Products of lipid peroxidation (LPO), given as malondialdehyde (MDA) and 4-hydroxyalkenals (4HDA), were highest in patients with severe NPDR (3.29 ± 0.05 μmol/L; P < 0.017 compared with control), as were levels of (b) nitric oxide (NO) catabolites (45.62 ± 1.27 pmol/mL; P < 0.0001 compared with control). (c) Total antioxidant capacity (TAC) was significantly decreased in all three groups of NPDR, with the greatest decrease seen in patients with severe NPDR (7.98 ± 0.48 mEq/mL; P < 0.0001 compared with control). (d,e) Erythrocyte catalase and glutathione peroxidase (GPx) activity was higher in patients with NPDR, with maximum catalase activity seen in patients with mild retinopathy (142 ± 6 U/mg protein; P < 0.0001 compared with control), whereas GPx activity was highest in those with severe retinopathy (117 ± 15 U/min/mg protein; P < 0.0001 compared with control). Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig01: Oxidants (a,b) and antioxidants (c–e) in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) Products of lipid peroxidation (LPO), given as malondialdehyde (MDA) and 4-hydroxyalkenals (4HDA), were highest in patients with severe NPDR (3.29 ± 0.05 μmol/L; P < 0.017 compared with control), as were levels of (b) nitric oxide (NO) catabolites (45.62 ± 1.27 pmol/mL; P < 0.0001 compared with control). (c) Total antioxidant capacity (TAC) was significantly decreased in all three groups of NPDR, with the greatest decrease seen in patients with severe NPDR (7.98 ± 0.48 mEq/mL; P < 0.0001 compared with control). (d,e) Erythrocyte catalase and glutathione peroxidase (GPx) activity was higher in patients with NPDR, with maximum catalase activity seen in patients with mild retinopathy (142 ± 6 U/mg protein; P < 0.0001 compared with control), whereas GPx activity was highest in those with severe retinopathy (117 ± 15 U/min/mg protein; P < 0.0001 compared with control). Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.
Mentions: Levels of LPO products in healthy controls were 0.98 ± 0.13 μmol/L. These increased significantly with the severity of retinopathy from 1.42 ± 0.08 to 2.49 ± 0.05, and 3.29 ± 0.05 μmol/L (mild, moderate, and severe NPDR, respectively; P < 0.017; Fig. 1a), suggesting the presence of oxidative stress in NPDR. Because LPO is a well-established mechanism of cellular lesions, these findings suggest cellular and systemic oxidative stress.

Bottom Line: TAC had significant decrease levels with minimum peak in severe retinopathy with 7.98 ± 0.48 mEq/mL (P < 0.0001).The fluidity of membrane submitochondrial particles decreased significantly in T2DM patients with mild, moderate, or severe NPDR compared with that in healthy volunteers (P < 0.0001 for all).Patients with NPDR exhibit oxidative deregulation with decreased membrane fluidity of submitochondrial particles and increased systemic catabolism (mitochondrial dysfunction) with the potential for generalized systemic damage in T2DM.

View Article: PubMed Central - PubMed

Affiliation: University Health Sciences Centre, University of Guadalajara, Guadalajara, México.

Show MeSH
Related in: MedlinePlus