The Scavenging Activity of Coenzyme Q Plus a Nutritional Complex on Human Retinal Pigment Epithelial Cells

Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are common retinal diseases responsible for most blindness in working-age and elderly populations. Oxidative stress and mitochondrial dysfunction play roles in these pathogenesis, and new therapies counteracting these contributors could be of great interest. Some molecules, like coenzyme Q (CoQ), are considered beneficial to maintain mitochondrial homeostasis and contribute to the prevention of cellular apoptosis. We investigated the impact of adding CoQ (Q) to a nutritional antioxidant complex (Nutrof Total; N) on the mitochondrial status and apoptosis in an in vitro hydrogen peroxide (HO)-induced oxidative stress model in human retinal pigment epithelium (RPE) cells. HO significantly increased 8-OHdG levels ( < 0.05), caspase-3 ( < 0.0001) and TUNEL intensity ( < 0.01), and RANTES ( < 0.05), caspase-1 ( < 0.05), superoxide ( < 0.05), and DRP-1 ( < 0.05) levels, and also decreased , , and gene expression ( < 0.05) vs. control. Remarkably, Q showed a significant recovery in gene expression, TUNEL, TNFα, caspase-1, and JC-1 ( < 0.05) vs. HO and NQ showed a synergist effect in caspase-3 ( < 0.01), TUNEL ( < 0.0001), mtDNA, and DRP-1 ( < 0.05). Our results showed that CoQ supplementation is effective in restoring/preventing apoptosis and mitochondrial stress-related damage, suggesting that it could be a valid strategy in degenerative processes such as AMD or DR.