The Scavenging Activity of Coenzyme Q 10 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 10 (CoQ 10 ), are considered beneficial to maintain mitochondrial homeostasis and contribute to the prevention of cellular apoptosis. We investigated the impact of adding CoQ 10 (Q) to a nutritional antioxidant complex (Nutrof Total ® ; N) on the mitochondrial status and apoptosis in an in vitro hydrogen peroxide (H 2 O 2 )-induced oxidative stress model in human retinal pigment epithelium (RPE) cells. H 2 O 2 significantly increased 8-OHdG levels ( p < 0.05), caspase-3 ( p < 0.0001) and TUNEL intensity ( p < 0.01), and RANTES ( p < 0.05), caspase-1 ( p < 0.05), superoxide ( p < 0.05), and DRP-1 ( p < 0.05) levels, and also decreased IL1β , SOD2 , and CAT gene expression ( p < 0.05) vs. control. Remarkably, Q showed a significant recovery in IL1β gene expression, TUNEL, TNFα, caspase-1, and JC-1 ( p < 0.05) vs. H 2 O 2, and NQ showed a synergist effect in caspase-3 ( p < 0.01), TUNEL ( p < 0.0001), mtDNA, and DRP-1 ( p < 0.05). Our results showed that CoQ 10 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.