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Laura Fernandez-Sanchez, Cristina Pedrero-Prieto, Oksana Kutsyr, Yoana Rabanal-Ruiz, Natalia Martínez-Gil, Xavier Sánchez-Sáez, Agustina Noailles, Pedro Lax, Francisco J Alcain, Nicolas Cuenca; Dietary intake of Coenzyme Q10 is able to slow down retinal degeneration in a model of retinitis pigmentosa.. Invest. Ophthalmol. Vis. Sci. 2019;60(9):4883.
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© ARVO (1962-2015); The Authors (2016-present)
It has been demonstrated that photoreceptor cell death in retinitis pigmentosa (RP) triggers an imbalance of reactive oxygen species (ROS) and it is widely accepted that oxidative stress is a major enhancer of retinal degeneration. Ubiquinone, also known as Coenzyme Q10 (CoQ10) is a component of mitochondrial electron transport chain and plays a critical role decreasing the superoxide anion level generated by mitochondrial complex I. The aim of this study was to assess the neuroprotective effects of CoQ10 treatment in a model of RP.
Rd10 mice were divided in two groups. Rd10 pups from one group were fed with CoQ10-supplemented diet from P14 to P25. The other group was fed with normal diet for the same age range. At the end of the treatment, retinal function was evaluated by electroretinography (ERG), and optical coherence tomography (OCT) images were acquired. After that, animals were sacrificed and retinal structure was assessed by immunohistochemistry.
Scotopic light-induced retinal responses showed significantly higher a-waves in CoQ10-treated animals compared to untreated-animals. Maximal differences were observed at the highest light stimuli. Scotopic b-wave presented similar results in both experimental groups. In rd10 mice, CoQ10 slows down synaptic contact loss between photoreceptors and bipolar and horizontal cells. Double immunolabeling for rod bipolar cells (PKCa) and synaptic ribbons (Bassoon) revealed a higher density of synaptic contacts between photoreceptor and rod bipolar cells in CoQ10-treated animals. The immunolabeling using specific antibodies for synaptic ribbons (CtBP2), photoreceptor synaptic vesicles (VGluT1) and horizontal cells (calbindin) showed higher density of tips of the horizontal cell dendrites associated with photoreceptor axon terminals in CoQ10-treated animals compared to untreated animals, where this association was scarce. In addition, photoreceptor axon terminals displayed better preserved morphology in cone-pedicles and rod-spherules in treated compared to untreated animals.
Coenzyme Q10 is able to delay retinal function loss and synaptic contact disruption in rd10 mice. These results indicate that dietary supplementation with CoQ10 could be useful for the treatment of RP.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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