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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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Mitochondrial function in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) The fluorescence ratio of the excimer (Ie) to monomer (Im) decreased significantly in patients with NPDR, with the greatest decrease seen in patients with mild retinopathy (Ie/Im 0.12 ± 0.01; P < 0.0001 compared with control). (b) Significant increases were seen in the hydrolytic activity of F0/F1-ATPase in all three groups of NPDR, with the greatest increase seen in patients with mild retinopathy (300 ± 38 nmol PO4; P < 0.0001 compared with control). This could mean lower ATP synthesis with excessive production of cellular catabolism. Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.
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fig02: Mitochondrial function in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) The fluorescence ratio of the excimer (Ie) to monomer (Im) decreased significantly in patients with NPDR, with the greatest decrease seen in patients with mild retinopathy (Ie/Im 0.12 ± 0.01; P < 0.0001 compared with control). (b) Significant increases were seen in the hydrolytic activity of F0/F1-ATPase in all three groups of NPDR, with the greatest increase seen in patients with mild retinopathy (300 ± 38 nmol PO4; P < 0.0001 compared with control). This could mean lower ATP synthesis with excessive production of cellular catabolism. Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.

Mentions: The Ie/Im ratio in the healthy control group was 0.24 ± 0.01. The Ie/Im ratio decreased significantly in T2DM patients with mild, moderate, and severe NPDR (0.12 ± 0.01, 0.16 ± 0.02, and 0.13 ± 0.01, respectively; P < 0.0001). The decrease in fluidity compared with the control group could be related to the effect that the fluidity of the membrane has on membrane potential induced by the increase in HbA1c, dyslipidemia, oxidative stress or their combination (Fig. 2a).


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)

Mitochondrial function in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) The fluorescence ratio of the excimer (Ie) to monomer (Im) decreased significantly in patients with NPDR, with the greatest decrease seen in patients with mild retinopathy (Ie/Im 0.12 ± 0.01; P < 0.0001 compared with control). (b) Significant increases were seen in the hydrolytic activity of F0/F1-ATPase in all three groups of NPDR, with the greatest increase seen in patients with mild retinopathy (300 ± 38 nmol PO4; P < 0.0001 compared with control). This could mean lower ATP synthesis with excessive production of cellular catabolism. Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4232896&req=5

fig02: Mitochondrial function in type 2 diabetes mellitus patients with mild, moderate, or severe non-proliferative diabetic retinopathy (NPDR). (a) The fluorescence ratio of the excimer (Ie) to monomer (Im) decreased significantly in patients with NPDR, with the greatest decrease seen in patients with mild retinopathy (Ie/Im 0.12 ± 0.01; P < 0.0001 compared with control). (b) Significant increases were seen in the hydrolytic activity of F0/F1-ATPase in all three groups of NPDR, with the greatest increase seen in patients with mild retinopathy (300 ± 38 nmol PO4; P < 0.0001 compared with control). This could mean lower ATP synthesis with excessive production of cellular catabolism. Data are the mean ± SE. *P < 0.05 compared with healthy volunteers.
Mentions: The Ie/Im ratio in the healthy control group was 0.24 ± 0.01. The Ie/Im ratio decreased significantly in T2DM patients with mild, moderate, and severe NPDR (0.12 ± 0.01, 0.16 ± 0.02, and 0.13 ± 0.01, respectively; P < 0.0001). The decrease in fluidity compared with the control group could be related to the effect that the fluidity of the membrane has on membrane potential induced by the increase in HbA1c, dyslipidemia, oxidative stress or their combination (Fig. 2a).

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