Coenzyme Q10 Instilled as Eye Drops on the Cornea Reaches the Retina and Protects Retinal Layers from Apoptosis in a Mouse Model of Kainate-Induced Retinal Damage

Lulli, Matteo; Witort, Ewa; Papucci, Laura; Torre, Eugenio; Schipani, Christian; Bergamini, Christian; Monte, Massimo Dal; Capaccioli, S.

doi:10.1167/iovs.12-10374

Cited by 39 publications

(38 citation statements)

References 31 publications

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“…Since CoQ 10 is neuroprotective against retinal damage by high IOP-induced transient ischemic injury and other apoptotic insults [35, 36], we determined whether CoQ 10 promotes RGC survival in ischemic retina using whole-mount immunohistochemistry for Brn3a, a marker for RGCs. Mean RGC density per retina for each group is presented in Supplementary Table 1.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, CoQ 10 is neuroprotective in retinal cells in vivo and in vitro against oxidative stress and excitotoxicity [23, 35, 41]. It has been reported that that CoQ 10 supplements correlated with plasma CoQ 10 level and CoQ 10 in large doses was taken up all tissues including heart and brain mitochondria [43], suggesting that CoQ 10 could also be taken up by retina and lead to a beneficial effect in ischemic retina injury.…”

Section: Discussionmentioning

confidence: 99%

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Coenzyme Q10 ameliorates oxidative stress and prevents mitochondrial alteration in ischemic retinal injury

et al. 2013

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Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species for protecting neuronal cells against oxidative stress in neurodegenerative diseases. We tested whether a diet supplemented with CoQ10 ameliorates oxidative stress and mitochondrial alteration, as well as promotes retinal ganglion cell (RGC) survival in ischemic retina induced by intraocular pressure elevation. A CoQ10 significantly promoted RGC survival at 2 weeks after ischemia. Superoxide dismutase 2 (SOD2) and heme oxygenase-1 (HO-1) expression were significantly increased at 12 h after ischemic injury. In contrast, the CoQ10 significantly prevented the upregulation of SOD2 and HO-1 protein expression in ischemic retina. In addition, the CoQ10 significantly blocked activation of astroglial and microglial cells in ischemic retina. Interestingly, the CoQ10 blocked apoptosis by decreasing caspase-3 protein expression in ischemic retina. Bax and phosphorylated Bad (pBad) protein expression were significantly increased in ischemic retina at 12 h. Interestingly, while CoQ10 significantly decreased Bax protein expression in ischemic retina, CoQ10 showed greater increase of pBad protein expression. Of interest, ischemic injury significantly increased mitochondrial transcription factor A (Tfam) protein expression in the retina at 12 h, however, CoQ10 significantly preserved Tfam protein expression in ischemic retina. Interestingly, there were no differences in mitochondrial DNA content among control- or CoQ10-treated groups. Our findings demonstrate that CoQ10 protects RGCs against oxidative stress by modulating the Bax/Bad-mediated mitochondrial apoptotic pathway as well as prevents mitochondrial alteration by preserving Tfam protein expression in ischemic retina. Our results suggest that CoQ10 may provide neuroprotection against oxidative stress-mediated mitochondrial alterations in ischemic retinal injury.Electronic supplementary materialThe online version of this article (doi:10.1007/s10495-013-0956-x) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 ameliorates oxidative stress and prevents mitochondrial alteration in ischemic retinal injury

et al. 2013

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“…Because CoQ 10 protects RGCs against high IOP-induced transient ischemic injury 28 and other apoptotic insults, 26,41 we determined RGC survival following CoQ 10 supplementation in glaucomatous DBA/2J mice by whole-mount immunohisto-chemistry using antibody raised against Brn3a. There was no significant change in RGC survival between control and CoQ 10treated 10-month-old D2-Gpnmb þ mice ( Supplementary Fig.…”

Section: Coq 10 Promotes Rgc Survival In Glaucomatous Dba/2j Micementioning

confidence: 99%

“…8 Coenzyme Q10 (CoQ 10 ), an essential cofactor of the electron transport chain, acts by maintaining the mitochondrial membrane potential, supporting ATP synthesis and inhibiting reactive oxygen species generation for protecting neuronal cells against oxidative stress in neurodegenerative diseases. [21][22][23][24][25] Previous studies demonstrated that CoQ 10 protected retinal neurons against kainate-induced apoptotic injury 26 and against hydrogen peroxide-induced oxidative stress in vitro and N-methyl-D-aspartate-induced glutamate excitotoxicity in vivo. 27 Moreover, CoQ 10 prevented retinal damage caused by acute high IOP-induced transient ischemic injury.…”

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confidence: 99%

Coenzyme Q10 Inhibits Glutamate Excitotoxicity and Oxidative Stress–Mediated Mitochondrial Alteration in a Mouse Model of Glaucoma

Lee

Shim

Kim

et al. 2014

Invest. Ophthalmol. Vis. Sci.

155

123

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“…For example, in antiphospholipid syndrome, treatment with co-enzyme Q has been shown been shown to alter mitochondrial dynamics resulting in lower oxidative stress and slowing of the accelerated atherosclerosis (Perez-Sanchez et al2012). Co-enzyme Q has also been shown to prevent retinal cell apoptosis when given as eye drops in mouse models of kainate-induced retinal damage (Lulli et al2012). Quinones are also being investigated for the treatment of mitochondrial diseases (Enns et al2012) as well as age-related diseases (Skulachev et al2009).…”

Section: Quinones In Medicinementioning

confidence: 99%

A review on the role of quinones in renal disorders

2013

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Quinones are electron and proton carriers that play a primary role in the aerobic metabolism of virtually every cell in nature. Most physiological quinones are benzoquinones. They undergo highly regulated redox reactions in the mitochondria, Golgi apparatus, plasma membrane and endoplasmic reticulum. Important consequences of these electron transfer reactions are the production of and protection against reactive oxygen species (ROS). Quinones have been extensively studied for both their cytotoxic as well as cellular protective properties and they have been particularly useful in rational drug design. The role of quinones in medicine is explored in this literature review with a particular focus on renal diseases. Due to their high basal metabolism and detoxification role, the kidneys are particularly sensitive to oxidative stress. Regardless of the underlying etiology, ROS plays an important role in both acute kidney injury (AKI) and chronic kidney diseases (CKD). Depending on the oxidative state of the kidney, quinones can be nephrotoxoic or nephro-protective. Many factors play a role in the interaction between quinones and the kidney and the consequences of this are just beginning to be explored.Electronic supplementary materialThe online version of this article (doi:10.1186/2193-1801-2-139) contains supplementary material, which is available to authorized users.

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Coenzyme Q10 Instilled as Eye Drops on the Cornea Reaches the Retina and Protects Retinal Layers from Apoptosis in a Mouse Model of Kainate-Induced Retinal Damage

Cited by 39 publications

References 31 publications

Coenzyme Q10 ameliorates oxidative stress and prevents mitochondrial alteration in ischemic retinal injury

Coenzyme Q10 ameliorates oxidative stress and prevents mitochondrial alteration in ischemic retinal injury

Coenzyme Q10 Inhibits Glutamate Excitotoxicity and Oxidative Stress–Mediated Mitochondrial Alteration in a Mouse Model of Glaucoma

A review on the role of quinones in renal disorders

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