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Journal of Global Diabetes & Clinical Metabolism

Aabstract


Research Article

The Effect of Coenzyme Q10 Administration on DNA Damage in Diabetic Polyneuropathy. A Randomized Double-Blind Placebo-Controlled Phase IIa Clinical Trial

Sandra Carrillo-Ibarra, Sonia Sifuentes-Franco, Luis Miguel Roman-Pintos, Adolfo Daniel Rodriguez-Carrizalez, Fermin Paul Pacheco-Moises and Alejandra Guillermina Miranda-Diaz

Correspondence Address :

Alejandra Guillermina Miranda-Diaz MD PhD
Jalisco
Mexico
Tel: +52- 333- 630-1355
Email: kindalex1@outlook.com

Received on: March 30, 2017 , Accepted on: April 26, 2017 , Published on: May 08, 2017

Citation: Sandra Carrillo-Ibarra, Sonia Sifuentes-Franco, Luis Miguel Roman-Pintos, Adolfo Daniel Rodriguez-Carrizalez, Fermin Paul Pacheco-Moises, Alejandra Guillermina Miranda-Diaz(2017). The Effect of Coenzyme Q10 Administration on DNA Damage in Diabetic Polyneuropathy. A Randomized Double-Blind Placebo-Controlled Phase IIa Clinical Trial

Copyright: 2017 Alejandra Guillermina Miranda-Diaz, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

  • Abstract

Abstract
Aim: To evaluate the effect of Coenzyme Q10 (CoQ10) administration on DNA damage in diabetic polyneuropathy (DPN). 
Methods: We performed a randomized double-blind placebo-controlled clinical trial. A single daily dose of Placebo or CoQ10 (400 mg) was given for 16 weeks in patients with DPN. Serum levels of 8-hydroxy-2deoxyguanosine (8-OHdG), 8-oxoguanine-DNA-N-glycosylase (hOGG1), endogenous CoQ10, and superoxide dismutase (SOD) were analyzed. We included 9 healthy control subjects (HC) to compare baseline - final levels for each group. 
Results: Baseline levels of 8-OHdG in Placebo patients were 5.15 +/- 0.59, and final levels, 5.95 +/- 1.21 ng/mL (p=0.715). Baseline levels of 8-OHdG in the CoQ10 patients had 6.60 +/- 0.80 ng/mL, and final, 7.10 +/- 0.74 ng/mL (p=0.768). Baseline levels of hOGG1 in HC were 0.39 +/- 0.01 ng/mL, while in the Placebo patients was 0.42 +/- 0.01 ng/mL (p=0.027 vs. HC) and final 0.41 +/- 0.00 ng/mL (p=0.353 baseline-final). The CoQ10 patients had baseline levels of hOGG1, 0.43 +/- 0.01 ng/mL (p=0.01 vs. HC), and final of 0.43 +/- 0.01 ng/mL. A significant reduction of SOD activity was found in both groups. Superoxide dismutase baseline in Placebo patients was 6.29 +/- 0.74 (p=0.025 vs. HC) and the CoQ10 patients had 5.37 +/- 0.58 U/L (p=0.006 vs. HC). At the end of the study, tendency for SOD to increase was noted in the CoQ10 patients to 6.07 +/- 0.68 U/L (p=0.15). Baseline levels of CoQ10 in HC were 1380.12 +/- 135.51 ng/mL and the Placebo patients had 579.56 +/- 67.91 ng/mL (p<0.001 vs. HC). The CoQ10 patients had tendency to improve levels from baseline from 999.09 +/- 108.49 ng/mL to 1062.39 +/- 152.10 ng/mL at the final result. 
Conclusion: The administration of CoQ10 offering antioxidant benefits with tendency to augment the SOD activity and improve endogenous CoQ10 concentrations. No effect of supplementation with CoQ10 on oxidative DNA damage in DPN patients was observed. 
Keywords: DNA damage, Oxidative stress, Coenzyme Q10, Antioxidants, Diabetic polyneuropathy