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Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 12732

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Special Issue Editors

Prof. Dr. Masaki Tanito

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Guest Editor

Department of Ophthalmology, Faculty of Medicine, Shimane University, Izumo 693-8501, Japan
Interests: glaucoma; cataract; oxidative stress; antioxidant; surgery

Prof. Dr. Akira Obana

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Guest Editor

1. Department of Ophthalmology, Seirei Hamamatsu General Hospital, 2-12-12 Sumiyoshi, Naka-ku, Hamamatsu City 430-8558, Shizuoka, Japan
2. Department of Medical Spectroscopy, Institute for Medical Photonics Research, Preeminent Medical Photonics Education & Research Center, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu City 431-3192, Shizuoka, Japan
Interests: retina; age-related macular degeneration; photooxidation; lasers; vitreous surgery
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Special Issue Information

Dear Colleagues,

Oxidative modifications on tissue and/or cellular proteins, nucleic acids, and lipids have been shown to be involved in various ocular pathologies. However, the underlying molecular mechanisms of these oxidative events are still not fully understood and require further research. In this Special Issue, basic research for exploring the mechanisms of oxidative stress on eye diseases can be included. Human clinical trials are mandatory to test the hypotheses generated by basic research into cures of ocular diseases. Therefore, any clinical trials testing therapeutic use of antioxidants/oxidative stress-modification methods on ocular diseases are very welcome in this issue. Human clinical studies that test the roles of biomarkers and imaging technologies for detection of oxidative stresses leading to accurate and early diagnosis of ocular diseases are also welcome.

The target diseases of interest in this Special Issue are cataract, glaucoma, vitreoretina, and macular diseases, but other age-related eye diseases will also be considered for inclusion. In vivo assessment of roles of oxidative stress-related systemic conditions on eye diseases are within the scope of this Special Issue. We look forward to your contributions.

Prof. Dr. Masaki Tanito
Prof. Dr. Akira Obana
Guest Editors

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Keywords

cataract
glaucoma
retina
macular degeneration
diabetic retinopathy
aging
systemic diseases
oxidative stress
phototoxicity
molecular mechanism
antioxidants
macular pigment
supplement
diagnostic technique
imaging
biomarker
ocular surgery
clinical trial

Published Papers (6 papers)

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Research

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23 pages, 8076 KiB

Open AccessArticle

Therapeutic Potential of Peucedanum japonicum Thunb. and Its Active Components in a Delayed Corneal Wound Healing Model Following Blue Light Irradiation-Induced Oxidative Stress

by Wan Seok Kang, Eun Kim, Hakjoon Choi, Ki Hoon Lee, Kyeong Jo Kim, Dosung Lim, Su-young Choi, Youngbae Kim, Seon ah Son, Jin Seok Kim and Sunoh Kim

Antioxidants 2023, 12(6), 1171; https://doi.org/10.3390/antiox12061171 - 29 May 2023

Cited by 2 | Viewed by 1301

Abstract

Blue light is reported to be harmful to eyes by inducing reactive oxygen species (ROS). Herein, the roles of Peucedanum japonicum Thunb. leaf extract (PJE) in corneal wound healing under blue light irradiation are investigated. Blue-light-irradiated human corneal epithelial cells (HCECs) show increased intracellular ROS levels and delayed wound healing without a change in survival, and these effects are reversed by PJE treatment. In acute toxicity tests, a single oral administration of PJE (5000 mg/kg) does not induce any signs of clinical toxicity or body weight changes for 15 days post-administration. Rats with OD (oculus dexter, right eye) corneal wounds are divided into seven treatment groups: NL (nonwounded OS (oculus sinister, left eye)), NR (wounded OD), BL (wounded OD + blue light (BL)), and PJE (BL + 25, 50, 100, 200 mg/kg). Blue-light-induced delayed wound healing is dose-dependently recovered by orally administering PJE once daily starting 5 days before wound generation. The reduced tear volume in both eyes in the BL group is also restored by PJE. Forty-eight hours after wound generation, the numbers of inflammatory and apoptotic cells and the expression levels of interleukin-6 (IL-6) largely increase in the BL group, but these values return to almost normal after PJE treatment. The key components of PJE, identified by high-performance liquid chromatography (HPLC) fractionation, are CA, neochlorogenic acid (NCA), and cryptochlorogenic acid (CCA). Each CA isomer effectively reverses the delayed wound healing and excessive ROS production, and their mixture synergistically enhances these effects. The expression of messenger RNAs (mRNAs) related to ROS, such as SOD1, CAT, GPX1, GSTM1, GSTP1, HO-1, and TRXR1, is significantly upregulated by PJE, its components, and the component mixture. Therefore, PJE protects against blue-light-induced delayed corneal wound healing via its antioxidative, anti-inflammatory, and antiapoptotic effects mechanistically related to ROS production. Full article

(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases)

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13 pages, 4142 KiB

Open AccessArticle

Dimethyl Fumarate Protects Retinal Pigment Epithelium from Blue Light-Induced Oxidative Damage via the Nrf2 Pathway

by Hideyuki Shimizu, Kei Takayama, Kazuhisa Yamada, Ayana Suzumura, Tomohito Sato, Yoshiaki Nishio, Masataka Ito, Hiroaki Ushida, Koji M Nishiguchi, Masaru Takeuchi and Hiroki Kaneko

Antioxidants 2023, 12(1), 45; https://doi.org/10.3390/antiox12010045 - 26 Dec 2022

Cited by 4 | Viewed by 1981

Abstract

The purpose of this study is to investigate the protective effect of dimethyl fumarate (DMF), the methyl-ester of fumaric acid, against blue-light (BL) exposure in retinal pigment epithelial (RPE) cells. ARPE-19 cells, a human RPE cell line, were cultured with DMF followed by exposure to BL. Reactive oxygen species (ROS) generation, cell viability, and cell death rate were determined. Real-time polymerase chain reaction and Western blotting were performed to determine the change in nuclear factor (erythroid-derived)-like 2 (NRF2) expression. Twenty-seven inflammatory cytokines in the supernatant of culture medium were measured. BL exposure induced ROS generation in ARPE-19 cells, which DMF alleviated in a concentration-dependent manner. BL exposure increased the ARPE-19 cell death rate, which DMF alleviated. BL exposure induced ARPE-19 cell apoptosis, again alleviated by DMF. Under BL exposure, DMF increased the NRF2 mRNA level and promoted NRF2 expression in the nucleus. BL also strongly increased interleukin (IL)-1β and fibroblast growth factor (FGF) expression. BL strongly induced RPE cell damage with apoptotic change while DMF mainly reduced inflammation in BL-induced RPE damage, resulting in blockade of cell death. DMF has a protective effect in RPE cells against BL exposure via activation of the NRF2 pathway. Full article

(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases)

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21 pages, 5387 KiB

Open AccessArticle

Mechanisms of Epithelial-Mesenchymal Transition and Prevention of Dispase-Induced PVR by Delivery of an Antioxidant αB Crystallin Peptide

by Iori Wada, Parameswaran G Sreekumar, Christine Spee, Andrew J MacKay, Michael Ip and Ram Kannan

Antioxidants 2022, 11(10), 2080; https://doi.org/10.3390/antiox11102080 - 21 Oct 2022

Cited by 3 | Viewed by 1888

Abstract

Proliferative Vitreoretinopathy (PVR) is a refractory retinal disease whose primary pathogenesis involves the epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells. At present, there is no effective treatment other than surgery for PVR. The purpose of this study was to investigate the effect of αB crystallin peptide (αBC-P) on EMT in PVR. We have previously shown that this peptide is antiapoptotic and regulates RPE redox status. Subconfluent primary human RPE (hRPE) cells were stimulated by TGFβ2 (10 ng/mL) with or without αBC-P (50 or 75 μg/mL) for 48 h and expression of EMT/mesenchymal to epithelial transition (MET) markers was determined. Mitochondrial ROS (mtROS) generation in hRPE cells treated with TGFβ2 was analyzed. The effect of TGFβ2 and αBC-P on oxidative phosphorylation (OXPHOS) and glycolysis in hRPE was studied. RPE cell migration was also assessed. A PVR-like phenotype was induced by intravitreal dispase injection in C57BL/6J mice. PVR progression and potential therapeutic efficiency of αBC-Elastin-like polypeptides (ELP) was studied using fundus photography, OCT imaging, ERG, and histologic analysis of the retina. αSMA, E-cadherin, Vimentin, Fibronectin and, RPE65, and CTGF were analyzed on Day 28. Additionally, the amount of VEGF-A in retinal cell lysates was measured. The EMT-associated αSMA, Vimentin, SNAIL and SLUG showed a significant upregulation with TGFβ2, and their expression was significantly suppressed by cotreatment with αBC-P. The MET-associated markers, E-cadherin and Sirt1, were significantly downregulated by TGFβ2 and were restored by αBC-P. Incubation of hRPE with TGFβ2 for 24 h showed a marked increase in mitochondrial ROS which was noticeably inhibited by αBC-ELP. We also showed that after TGFβ2 treatment, SMAD4 translocated to mitochondria which was blocked by αBC-ELP. Mitochondrial oxygen consumption rate increased with TGFβ2 treatment for 48 h, and αBC-P co-treatment caused a further increase in OCR. Glycolytic functions of RPE were significantly suppressed with αBC-P (75 μg/mL). In addition, αBC-P significantly inhibited the migration from TGFβ2 treatment in hRPE cells. The formation of proliferative membranes was suppressed in the αBC-ELP-treated group, as evidenced by fundus, OCT, and H&E staining in dispase-induced PVR in mice. Furthermore, ERG showed an improvement in c-wave amplitude. In addition, immunostaining showed significant suppression of αSMA and RPE65 expression. It was also observed that αBC-ELP significantly reduced the expression level of vimentin, fibronectin, and CTGF. Our findings suggest that the antioxidant αBC-P may have therapeutic potential in preventing PVR by reversing the phenotype of EMT/MET and improving the mitochondrial function in RPE cells. Full article

(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases)

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15 pages, 7133 KiB

Open AccessArticle

Intraocular Pressure-Induced Endothelial Dysfunction of Retinal Blood Vessels Is Persistent, but Does Not Trigger Retinal Ganglion Cell Loss

by Maoren Wang, Hanhan Liu, Ning Xia, Huige Li, Tim van Beers, Adrian Gericke and Verena Prokosch

Antioxidants 2022, 11(10), 1864; https://doi.org/10.3390/antiox11101864 - 21 Sep 2022

Cited by 9 | Viewed by 1517

Abstract

Research has been conducted into vascular abnormalities in the pathogenesis of glaucoma, but conclusions remain controversial. Our aim was to test the hypothesis that retinal endothelial dysfunction induced by elevated intraocular pressure (IOP) persists after IOP normalization, further triggering retinal ganglion cell (RGC) loss. High intraocular pressure (HP) was induced in mice by episcleral vein occlusion (EVO). Retinal vascular function was measured via video microscopy in vitro. The IOP, RGC and their axons survival, levels of oxidative stress and inflammation as well as vascular pericytes coverage, were determined. EVO caused HP for two weeks, which returned to baseline afterwards. Mice with HP exhibited endothelial dysfunction in retinal arterioles, reduced density of RGC and their axons, and loss of pericytes in retinal arterioles. Notably, these values were similar to those of mice with recovered IOP (RP). Levels of oxidative stress and inflammation were increased in HP mice but went back to normal in the RP mice. Our data demonstrate that HP induces persistent endothelial dysfunction in retinal arterioles, which persists one month after RP. Oxidative stress, inflammation, and loss of pericytes appear to be involved in triggering vascular functional deficits. Our data also suggest that retinal endothelial dysfunction does not affect RGC and their axon survival. Full article

(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases)

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Review

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14 pages, 1979 KiB

Open AccessReview

Mitochondrial Open Reading Frame of the 12S rRNA Type-c: Potential Therapeutic Candidate in Retinal Diseases

by Zahra Mohtashami, Mithalesh Kumar Singh, Farid Thomaz Neto, Nasim Salimiaghdam, Hossein Hasanpour and M. Cristina Kenney

Antioxidants 2023, 12(2), 518; https://doi.org/10.3390/antiox12020518 - 18 Feb 2023

Cited by 1 | Viewed by 1776

Abstract

Mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) is the most unearthed peptide encoded by mitochondrial DNA (mtDNA). It is an important regulator of the nuclear genome during times of stress because it promotes an adaptive stress response to maintain cellular homeostasis. Identifying MOTS-c specific binding partners may aid in deciphering the complex web of mitochondrial and nuclear-encoded signals. Mitochondrial damage and dysfunction have been linked to aging and the accelerated cell death associated with many types of retinal degenerations. Furthermore, research on MOTS-c ability to revive oxidatively stressed RPE cells has revealed a significant protective role for the molecule. Evidence suggests that senescent cells play a role in the development of age-related retinal disorders. This review examines the links between MOTS-c, mitochondria, and age-related diseases of the retina. Moreover, the untapped potential of MOTS-c as a treatment for glaucoma, diabetic retinopathy, and age-related macular degeneration is reviewed. Full article

(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases)

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16 pages, 1432 KiB

Open AccessReview

Oxidative Stress-Induced Cellular Senescence in Aging Retina and Age-Related Macular Degeneration

by Ryo Terao, Tazbir Ahmed, Ayana Suzumura and Hiroko Terasaki

Antioxidants 2022, 11(11), 2189; https://doi.org/10.3390/antiox11112189 - 05 Nov 2022

Cited by 14 | Viewed by 3326

Abstract

Aging leads to a gradual decline of function in multiple organs. Cataract, glaucoma, diabetic retinopathy, and age-related macular degeneration (AMD) are age-related ocular diseases. Because their pathogenesis is unclear, it is challenging to combat age-related diseases. Cellular senescence is a cellular response characterized by cell cycle arrest. Cellular senescence is an important contributor to aging and age-related diseases through the alteration of cellular function and the secretion of senescence-associated secretory phenotypes. As a driver of stress-induced premature senescence, oxidative stress triggers cellular senescence and age-related diseases by inducing senescence markers via reactive oxygen species and mitochondrial dysfunction. In this review, we focused on the mechanism of oxidative stress-induced senescence in retinal cells and its role in the pathogenesis of AMD. Full article

(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Eye Diseases)

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