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The effect of Ubiquinone administration on oxidative DNA damage and repair in plasma levels in non-proliferative diabetic retinopathy

Sonia Sifuentes-Franco, Adolfo Daniel Rodriguez-Carrizalez, Sandra Carrillo- Ibarra, Jose Alberto Castellanos Gonzalez, Esau Cesar Martinez-Romero, Guillermo Miller-Arrevillaga & Alejandra Guillermina Miranda-Diaz*

Background: Diabetic retinopathy (DR) initially is denominate non-proliferative DR (NPDR), and has the possibility to develop to proliferative DR (PDR). Aim: To determine the effect of Ubiquinone on the oxidative DNA damage and DNA repair in plasma levels in NPDR. Methods: Through a double-blinded, placebo- controlled, clinical trial, 20 patients were treated with Placebo and 20 patients with 400 mg/day of Ubiquinone (Coenzime Q10) for 6 months. Inclusion criteria were male or female, with type 2 diabetes mellitus and NPDR. The informed consent was signed. The DNA oxidative damage was determinate by the plasma levels of 8-hydroxy-2’-deoxyguanosine (8-OHdG) and DNA repair by the 8-oxoguanine-DNA-N-glycosylase-1 (hOGG1). Superoxide Dismutase (SOD) activity and CoQ10 were assessed as antioxidants. Results: Levels of the 8-OHdG were significantly increased in baseline measurements in Ubiquinone and Placebo group, with significant decrease (p=0.05) in the Ubiquinone group at the end of the study. Levels of DNA repair enzyme hOGG1 were increased in baseline 0.42 ± 0.03 ng/mL–final results 0.43 ± 0.05 ng/mL in Ubiquinone group. The SOD activity were diminished in Ubiquinone and Placebo groups at baseline (p=0.006, p=0.01 respectively), even in Placebo group, the SOD decreased even more (p=0.02). The endogenous antioxidant (CoQ10) was consumed at baseline in both groups and improved to normal levels at the end only in the Ubiquinone group (p<0.001). Conclusion: We observed an increase of 8-OHdG in the baseline determination to patients with NPDR suggesting DNA damage with the repairing enzyme trying to compensate for oxidative damage. The CoQ10 supplementation could diminish the oxidative DNA damage in NPDR.