However, CoQ10 has significant potential for being a strong preventative and therapeutic nutrient for many common eye health concerns including glaucoma, diabetic retinopathy, retinal ischemia, and macular degeneration. CoQ10 promotes optimal blood flow and neutralizes free radicals to prevent oxidation of cells.

One study showed that CoQ10 reduces corneal damages after UVB exposure by preserving mitochondrial function. These actions help prevent some eye disorders including:.

Glaucoma is a disease marked by damage to the optic nerve caused by abnormally high pressure in the eye. CoQ10 supports mitochondrial function and is effective in reducing high intraocular pressure, thereby, reducing the risk of developing glaucoma and slowing the progression of existing glaucoma.

Diabetic retinopathy is a condition that causes damage to the blood vessels in the retina due to poorly controlled blood sugar. CoQ10 helps reduce free radicals in the eye and improves the thickness of the retina. These actions help reduce the risk of diabetic retinopathy.

Retinal ischemia is a condition that results from lack of oxygen in the retina. CoQ10 helps promote blood flow to the eyes to offer the much-needed oxygen to support retinal performance.

Dry macular degeneration is a condition where parts of the macula get thinner and tiny clumps of protein called drusen grow, obstructing vision.

CoQ10, when combined with acetyl-l-carnitine or omega-3 fatty acids, supports retinal functioning more than any of these nutrients on their own.

These nutrients assist with mitochondrial fat metabolism to improve and stabilize vision in people with early-stage age-related macular degeneration AMD. This powerhouse combination of antioxidants improves the retinal pigment cell tissue function and reduces the drusen-covered area of the retina, providing protection from macular degeneration.

CoQ10 is found in foods we eat including meat, fish, nuts, and colorful fruits and vegetables, but it is difficult to consume enough to significantly increase CoQ10 levels in your body — at least to levels that help support eye health and ward off ocular disease.

Support your eye health with powerful antioxidants that prevent oxidative damage while promoting blood flow to the eyes and circulation to the entire body with Viteyes® Optic Nerve Support.

Taken as part of your daily regimen, these powerful supplements offer the recommended dose of coenzyme Q10 to support eye health and reduce the risk of eye disorders including glaucoma, macular degeneration, and diabetic retinopathy.

By helping to prevent oxidative stress and optimize mitochondrial function within the retina, CoQ10 protects against the retinal damage caused by ischemia, as well as preventing ischemia associated with poor mitochondria function. In an animal study , a diet supplemented with CoQ10 ameliorated oxidative stress and mitochondrial alteration, as well as promoted retinal ganglion cell survival in ischemic retina induced by intraocular pressure elevation within two weeks following ischemic damage.

CoQ10 significantly prevented the upregulation of SOD2 and heme oxygenase-1 HO protein expression in the ischemic retina, blocked activation of astroglial and microglial cells in the retina, and blocked apoptosis by decreasing caspase-3 protein expression in ischemic retina.

Glaucoma is also caused by loss of retinal ganglion cells and optic neuropathy. Overactivation of N-methyl-D-aspartate NMDA and non-NMDA subtypes of glutamate receptors is a possible factor in cell loss. CoQ10 helps to restrain the accumulation of glutamate by reducing the effects of oxidative stress on mitochondrial function and energy production.

Many common eye conditions including glaucoma, dry eye, diabetic retinopathy, cataract, and age-related macular degeneration are directly caused by mitochondrial dysfunction and, specifically, a lack of adequate energy production.

Certainly oxidative stress plays a role in mitochondrial dysfunction; however, as a primary cofactor in mitochondria function, CoQ10 optimizes energy production directly and, therefore, helps to improve mitochondrial function in these eye conditions.

Levels of CoQ10 tend to naturally decrease with age, due to decreased synthesis and increased degradation. This trend has often been implicated in the rise of traditional age-related retinal conditions. For example, when CoQ10 levels were determined in plasma and platelets from 19 exudative age-related macular degeneration AMD patients and 19 age-matched controls, those with AMD were found to have lower CoQ10 levels and a lesser ability to oppose oxidative damage.

Supplementation may be an easy way to maintain healthy levels of this important antioxidant and retain retinal health. CoQ10 supplementation directly corresponds to plasma levels, indicating that supplementation is an effective way to raise levels for therapeutic applications.

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Coenzyme Q10 — A Natural Eye Preservative. April 30, - facebook twitter linkedin. CoQ10 significantly prevented the upregulation of SOD2 and heme oxygenase-1 HO-1 protein expression in the ischemic retina, blocked activation of astroglial and microglial cells in the retina, and blocked apoptosis by decreasing caspase-3 protein expression in ischemic retina.

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CoQ10 naturally declines with age so maintaining a healthy diet is increasingly important. Given the scientific evidence to date it seems unlikely that CoQ10 supplementation is helpful for vision in healthy people.

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Always seek the advice of your physician or other qualified health care provide. Louis, MO. Vehicle alone—treated cells were used as controls. The viability of RGC-5 cells or primary RGCs was evaluated microscopically and confirmed with a commercial reagent Guava ViaCount Assay with CytoSoft software, cat.

This assay distinguishes between viable and nonviable cells, based on their differential permeability to two fluorescent nucleic acid stains Annexin V and 7-AAD in the reagent. Briefly, cells or tissue were collected and solubilized in a lysis buffer containing 25 mM hydroxyethyl piperazineethanesulfonic acid HEPES , pH 7.

TMRE Staining of Mitochondrial Membrane Potential. The change in mΔΨ occurring during apoptosis was detected by a fluorescence-based assay. RGC-5 cells, cultured on coverslips, were subjected to apoptotic stimuli as indicated, followed by incubation with 50 nM tetramethylrhodamine ethyl ester perchlorate TMRE; Sigma-Aldrich in culture medium for 30 minutes at 37°C, allowing mitochondria to load with the dye in proportion to mitochondrial membrane potential.

After washing with PBS, coverslips were mounted on a glass slide with a drop of HEPES-Tris buffer pH 7. The glass slide was immediately mounted on a confocal microscope Nikon TE; Nikon Corp. html as described before in detail. All experiments in animal models were performed in compliance with the Italian law on animal care No.

Quantification of CoQ10 in the Rabbit Retina following Corneal Instillation. Three male New Zealand albino rabbits weighing 2. At 2, 7, and 15 minutes after CoQ10 instillations on corneas, venous blood samples 1 mL were withdrawn from the marginal vein of rabbits ear into heparinized tubes and centrifuged at g for 15 minutes at room temperature to obtain plasma.

After stirring for 2 minutes, to completely oxidize the CoQ10, the mixture was centrifuged at g for 10 minutes at room temperature to separate a supernatant, which was collected, dried under nitrogen stream, lyophilized, and suspended in ethanol.

The CoQ10 quantification in plasma and retinal extracts was carried out by high-performance liquid chromatography HPLC analysis according to Takada et al.

One drop of a CoQ10 solution 2. Immunohistofluorescence Analysis of Cleaved Caspase 3. Retinal sections of 4 μm were stained with cleaved caspase 3 Asp primary antibody Cell Signaling Technology, Danvers, MA , followed by fluorescent anti rabbit Cyconjugated secondary antibody Chemicon International, Inc.

Fluorescence was imaged Nikon TE Confocal Microscope and EZ-C1 Software; Nikon Corp. and digitally captured. Retinas were peeled off carefully and washed three times with PBS, and ganglion cells remaining in the retinas were identified as described in Nadal-Nicolas et al. Next day, the retinas were washed three times with PBS and incubated for 2 hours with Cy3-conjugated secondary antibody Chemicon International.

Subsequently, the retinas were washed three times with PBS and mounted on slides, vitreous side facing upward. Brn3a-positive RGCs in retinas were assessed microscopically using a confocal microscope Nikon TE using EZ-C1 Software; Nikon Corp.

For quantitative analysis, the positive cells were counted in four to six microscope fields of identical size located at approximately the same distance from the optic disc. Data are presented as means ± SEM of at least three to four independent experiments.

Statistical comparisons were made using unpaired Student's t -test or ANOVA followed by Newman—Keuls multiple comparison post test, as appropriate. CoQ10 Increases RGC Viability and Inhibits Apoptosis.

The neuroprotective property of CoQ10 was first evaluated in the cultured rat RGC-5 cell line on the basis of cell viability in response to Antimycin A μM or serum starvation 0.

As we demonstrated previously, 14 both Antimycin A and serum starvation do not induce apoptosis through the generation of free radicals in our experimental conditions.

Light microscopy examination of RGC-5 cells Fig. Scoring of viable cells by fluorescence-activated cell sorting FACS analysis with the ViaCount reagent on Guava PCA is shown in Figure 1 B.

Figure 1. View Original Download Slide. Untreated RGC-5 cells were used as controls. A Light microscopy examination of RGC-5 cells. B FACS analysis of viable and nonviable nucleated cells with commercial reagent ViaCount on Guava PCA. Data are means ± SEM of at least four to five experiments.

Data are means ± SEM of three experiments. Next, cell viability of primary rat RGCs, following a hour treatment with the excitotoxic aminoacid glutamate 50 μM preceded or not by a 2-hour pretreatment with CoQ10 10 μM was evaluated by FACS analysis Guava PC.

CoQ10 Inhibits Apoptosis by Preventing the Mitochondrial Depolarization. The ability of CoQ10 to prevent mitochondrial depolarization independently from its antioxidant properties was evaluated by the uptake of TMRE in RGC-5 cells treated with Antimycin A or serum starvation Fig.

Two hours before application of the apoptotic stimuli, cells were pretreated with 10 μM CoQ10 or with vehicle alone. Quantification of TMRE intensity Fig.

induced a marked loss of TMRE staining compared with the untreated controls 14, ± a. Pretreatment with CoQ10 successfully prevented the mitochondrial depolarization as indicated by the almost 5-fold ± a.

or 2-fold 12, ± a. increase of TMRE staining, respectively. Figure 2. TMRE staining of mitochondrial membrane potential. A The change in mΔΨ detected with 50 nM TMRE at the 24th hour following treatment with μM Antimycin A or at the 72nd hour following serum starvation, preceded or not by pretreatment with 10 μM CoQ Treated cells show reduced fluorescence as compared with nontreated uniformly stained controls, indicating loss of mitochondrial membrane potential.

The loss was significantly prevented by CoQ Each image is representative of at least three independent experiments with similar results. B Quantification of TMRE intensity in arbitrary units. AntA or 0. Instillation of 15 eye drops of CoQ10 solution Fig.

There were no significant changes in CoQ10 plasma content between CoQtreated and vehicle alone—treated rabbit eyes data not shown , which excluded transfer of CoQ10 to the retina through hematic circulation. Figure 3.

The oxidized CoQ10 exogenous in extracted eye tissues was quantified by HPLC. Topical Application of CoQ10 in a Mouse Model of KA-Induced Retinal Damage Protects Retinal Cells from Apoptosis.

As shown in Figure 4 A, at the 24th hour following KA intravitreal injection a substantial number of cells in the ganglion cell layer GCL and the inner nuclear layer INL stained positive for the cleaved caspase 3, showing green fluorescent cytoplasms of apoptotic cells.

Significantly, the KA-induced apoptotic cell death underwent a dramatic drop in the retina of mice treated with topical application of CoQ Figure 4. Application of CoQ10 to the mouse cornea prevents retinal cell apoptosis in response to intravitreal injection of KA.

A Evaluation of KA-induced apoptosis in retinal sections by immunohistofluorescence. GCL, INL, and ONL are indicated. Three animals in each group were used. C CoQ10 attenuated KA-induced loss of RGCs; 24 hours following KA intravitreal injection the loss of RGCs in flat-mounted retinas was determined by immunofluorescence staining with antibodies against Brn3a.

D Quantification of cells indicates that, whereas Brn3a-positive RGCs remained similar in untreated or CoQtreated control mice, Brn3a-positive RGCs were reduced significantly in mice treated with KA. In contrast, KA-induced cell loss was reversed when the mice were treated with CoQ Three mice in each group were used.

Next, we performed the quantification of RGCs in the GCL in flat-mounted retinas, to determine the extent of retinal cell loss and the level of protection exuded by topical application of CoQ10 in KA-treated mice.

Results presented in Figure 4 C indicate that at 24 hours after intravitreal injection of KA, the density of the Brn3a-positive RGCs was reduced in treated mice compared with nontreated controls. Instead, topical application of CoQ10 prevented the loss of RGCs and increased number of Brn3a-positive cells in the GCL layer.

Treatment with CoQ10 eye drops increased the number of the Brn3a-positive cells Neurodegenerative diseases, including glaucoma, 3 , 21 involve cell loss by apoptosis as the main pathogenetic event.

Notwithstanding a substantial amount of research that is focused on this area, effective treatments for most neurodegenerative diseases do not yet exist. Previously, we have shown that CoQ10 prevented apoptosis of corneal keratocytes both in vitro 12 and in vivo 13 in response to therapeutic excimer laser irradiation with markedly higher efficacy compared with that of other antioxidants vitamins A, C, and E.

We then demonstrated that keratocyte apoptosis prevention by CoQ10 also occurred in response to apoptotic stimuli that do not induce the formation of free radicals such as ceramide, hypoxia, and growth factor withdrawal and that this was consequent to the ability of CoQ10 to inhibit mitochondrial depolarization.

The effects of CoQ10 on the vision and, in particular, on the health of the retina have not been widely investigated. Only a few studies have indicated that oral or intravitreal administration of CoQ10 significantly improves eyesight 18 , 25 , 26 and protects RGCs against oxidative stress 27 or high IOP-induced ischemia.

Although the involvement of RGC excitotoxicity as a pathogenetic mechanism of glaucoma is debated, it has been proven that in most cases it could play a key role. In particular, Sucher et al.

Mali et al. In a parallel study, Kumada et al. A very recent study reports that KA induces a reactive gliosis that leads to RGC apoptosis by activating retinal matrix metalloproteinase-9, tPA, and uPA. Here, we demonstrate that CoQ10 protects RGCs from apoptosis independently from its antioxidant properties, in keeping with the previous results we obtained with corneal keratocytes.

Our results also indicate that CoQ10 increases RGC viability and inhibits apoptosis in response to different apoptotic stimuli such as glutamate, chemical hypoxia Antimycin A , and serum withdrawal FBS 0. On the basis of these observations, the effectiveness of corneal application of CoQ10 eye drops in protecting RGCs from KA-induced apoptosis in our study indicates that CoQ10 may act by mechanisms that are downstream of and overcome all the above pathways.

Finally, the ability of CoQ10 eye drops to deliver CoQ10 to the retina and to protect the retinal layers from apoptosis in the mouse model of KA-induced retinal damage reminiscent of glaucoma suggests that CoQ10 eye drops have a promising therapeutic applicability.

The ability of CoQ10 to reach the retina following corneal application is supported by an observation of Fato et al. Our results are in keeping with a report of Qu et al.

These authors speculate that enhancing CoQ10 levels in the retina of elderly patients could have therapeutic value. In conclusion, we propose that CoQ10 eye drops may be evaluated as a novel, simple, and noninvasive therapy for topical treatment of retinopathies with apoptosis as the main pathogenetic mechanism.

The authors thank Mary Forrest for accurate editing of this manuscript. Chen PP. Risk and risk factors for blindness from glaucoma. Curr Opin Ophthalmol. Henson DB Thampy R. Preventing blindness from glaucoma. Nucci C Schiavone N Carella E Capaccioli S Carella G.

Ganglionic cell apoptogenesis in glaucoma. Acta Ophthalmol Scand. Harada T Harada C Nakamura K The potential role of glutamate transporters in the pathogenesis of normal tension glaucoma.

Clin Invest. Lynch DR Guttmann RP. Excitotoxicity: perspectives based on N-methyl-D-aspartate receptor subtypes.

J Pharmacol Exp Ther. Nucci C Tartaglione R Rombolà L Morrone LA Fazzi E Bagetta G. Neurochemical evidence to implicate elevated glutamate in the mechanisms of high intraocular pressure IOP -induced retinal ganglion cell death in rat.

Sucher NJ Limpton SA Dreyer EB. Molecular basis of glutamate toxicity in retinal ganglion cells. Vision Res. Mali RS Cheng M Chintala SK. Plasminogen activators promote excitotoxicity-induced retinal damage. FASEB J. Johnson TV Tomarev SI.