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Antioxidants
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Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research
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Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research

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 (30 March 2024) | Viewed by 6787

Special Issue Editors

Prof. Dr. Wonkyu Ju

E-Mail Website
Guest Editor
Hamilton Glaucoma Center and Shiley Eye Institute, Viterbi Family Department of Ophthalmology, University of California, San Diego, La Jolla, CA 92039, USA
Interests: retinal ganglion cell; glial cells; oxidative stress; mitochondrial dysfunction; mitochondrial protection; neuroinflammation; glaucoma; Alzheimer’s disease
Dr. Niina Harju

E-Mail Website
Guest Editor
School of Pharmacy, Faculty of Health Sciences, University of Eastern Finland, 70210 Kuopio, Finland
Interests: retinal pigment epithelium; inflammation; oxidative stress; antioxidants; age-related macular degeneration; retinal detachment

Special Issue Information

Dear Colleagues,

Oxidative stress, mitochondrial dysfunction, and inflammation are critical to degenerative retinal diseases, a group of eye diseases (e.g., age-related macular degeneration, retinal detachment, retinitis pigmentosa, and glaucoma) that cause vision loss. Antioxidants are considered potential therapeutic strategies in retinal eye diseases. In age-related macular degeneration (AMD), retinal pigment epithelial (RPE) cell loss leads to retinal degeneration and visual defects. Dry AMD induces RPE cell degeneration, whereas the wet form causes neovascularization and exudate formation following RPE cell loss. Rhegmatogenous retinal detachment occurs because a tear or hole in the retina leads to vitreous fluid penetrating the sub-retinal space, which induces photoreceptors’ separation from the RPE cell layer. Glaucoma induces progressive retinal ganglion cell (RGC) axon degeneration, resulting in RGC death and visual deficits.

The retina is a thin layer in the posterior part of the eye that collects visual information and transfers it into the brain via the optic nerve. The retina consists of RPE cells, photoreceptor rods and cones, glial cells, and neuronal cells, including RGCs. All layers are essential for vision and are affected by retinal degeneration. RPE cells support the homeostasis of the retina and photoreceptors, complete the heterocycle of outer photoreceptor segments and enable nutrition transport from the choroid and removal of waste material into the choroid. RGCs are the most prominent cell type in the ganglion cell layer, which is the innermost neural layer of the retina. Both RPE and RGC degeneration leads to vision loss, and antioxidants could protect these cells against oxidative stress, mitochondrial dysfunction, and/or inflammation in degenerative retinal eye diseases.

We invite all scientists studying cellular responses of antioxidants related to pre-clinical degenerative retinal eye disease research to participate in this Special Issue. Original research articles, reviews, or shorter perspective articles on all aspects related to antioxidants in degenerative retinal eye diseases are welcome, including topics such as antioxidants, oxidative stress, mitochondrial dysfunction, inflammation, RPE cells, photoreceptors, glia cells, RGCs, and studies of potential new treatment options for retinal degeneration.

Prof. Dr. Wonkyu Ju
Dr. Niina Harju
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antioxidants
  • retinal degeneration
  • oxidative stress
  • mitochondrial dysfunction
  • mitochondrial protection
  • inflammation
  • retinal eye diseases
  • RPE cells
  • photoreceptors
  • retinal ganglion cells
  • glial cells

Published Papers (6 papers)

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Research

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18 pages, 3494 KiB  
Article
Glutathione and a Pool of Metabolites Partly Related to Oxidative Stress Are Associated with Low and High Myopia in an Altered Bioenergetic Environment
by Salvador Mérida, Amparo Návea, Carmen Desco, Bernardo Celda, Mercedes Pardo-Tendero, José Manuel Morales-Tatay and Francisco Bosch-Morell
Antioxidants 2024, 13(5), 539; https://doi.org/10.3390/antiox13050539 - 27 Apr 2024
Viewed by 547
Abstract
Oxidative stress forms part of the molecular basis contributing to the development and manifestation of myopia, a refractive error with associated pathology that is increasingly prevalent worldwide and that subsequently leads to an upsurge in degenerative visual impairment due to conditions that are [...] Read more.
Oxidative stress forms part of the molecular basis contributing to the development and manifestation of myopia, a refractive error with associated pathology that is increasingly prevalent worldwide and that subsequently leads to an upsurge in degenerative visual impairment due to conditions that are especially associated with high myopia. The purpose of our study was to examine the interrelation of potential oxidative-stress-related metabolites found in the aqueous humor of high-myopic, low-myopic, and non-myopic patients within a clinical study. We conducted a cross-sectional study, selecting two sets of patients undergoing cataract surgery. The first set, which was used to analyze metabolites through an NMR assay, comprised 116 patients. A total of 59 metabolites were assigned and quantified. The PLS-DA score plot clearly showed a separation with minimal overlap between the HM and control samples. The PLS-DA model allowed us to determine 31 major metabolite differences in the aqueous humor of the study groups. Complementary statistical analysis of the data allowed us to determine six metabolites that presented significant differences among the experimental groups (p < 005). A significant number of these metabolites were discovered to have a direct or indirect connection to oxidative stress linked with conditions of myopic eyes. Notably, we identified metabolites associated with bioenergetic pathways and metabolites that have undergone methylation, along with choline and its derivatives. The second set consisted of 73 patients who underwent a glutathione assay. Here, we showed significant variations in both reduced and oxidized glutathione in aqueous humor among all patient groups (p < 0.01) for the first time. Axial length, refractive status, and complete ophthalmologic examination were also recorded, and interrelations among metabolic and clinical parameters were evaluated. Full article
(This article belongs to the Special Issue Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research)
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19 pages, 11203 KiB  
Article
Lemon Peel Water Extract: A Novel Material for Retinal Health, Protecting Retinal Pigment Epithelial Cells against Dynamin-Related Protein 1-Mediated Mitochondrial Fission by Blocking ROS-Stimulated Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Pathway
by Shang-Chun Tsou, Chen-Ju Chuang, Inga Wang, Tzu-Chun Chen, Jui-Hsuan Yeh, Chin-Lin Hsu, Yu-Chien Hung, Ming-Chung Lee, Yuan-Yen Chang and Hui-Wen Lin
Antioxidants 2024, 13(5), 538; https://doi.org/10.3390/antiox13050538 - 27 Apr 2024
Viewed by 784
Abstract
Previous studies showed that NaIO3 can induce oxidative stress-mediated retinal pigment epithelium (RPE) damage to simulate age-related macular degeneration (AMD). Lemon peel is rich in antioxidants and components that can penetrate the blood–retinal barrier, but their role in retinal oxidative damage remains [...] Read more.
Previous studies showed that NaIO3 can induce oxidative stress-mediated retinal pigment epithelium (RPE) damage to simulate age-related macular degeneration (AMD). Lemon peel is rich in antioxidants and components that can penetrate the blood–retinal barrier, but their role in retinal oxidative damage remains unexplored. Here, we explore the protection of lemon peel ultrasonic-assisted water extract (LUWE), containing large amounts of flavonoids and polyphenols, against NaIO3-induced retinal degeneration. We initially demonstrated that LUWE, orally administered, prevented retinal distortion and thinning on the inner and outer nuclei layers, downregulating cleaved caspase-3 protein expression in RPE cells in NaIO3-induced mice. The effect of LUWE was achieved through the suppression of apoptosis and the associated proteins, such as cleaved PARP and cleaved caspase-3, as suggested by NaIO3-induced ARPE-19 cell models. This is because LUWE reduced reactive oxygen species-mediated mitochondrial fission via regulating p-Drp-1 and Fis1 expression. We further confirmed that LUWE suppresses the expression of p-MEK-1/2 and p-ERK-1/2 in NaIO3-induced ARPE-19 cells, thereby providing the protection described above, which was confirmed using PD98059 and U0126. These results indicated that LUWE prevents mitochondrial oxidative stress-mediated RPE damage via the MEK/ERK pathway. Elucidation of the molecular mechanism may provide a new protective strategy against retinal degeneration. Full article
(This article belongs to the Special Issue Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research)
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14 pages, 6180 KiB  
Article
Buspirone Enhances Cell Survival and Preserves Structural Integrity during Oxidative Injury to the Retinal Pigment Epithelium
by Manas R. Biswal, Ryan J. Paulson, Riddhi Vichare and Alfred S. Lewin
Antioxidants 2023, 12(12), 2129; https://doi.org/10.3390/antiox12122129 (registering DOI) - 17 Dec 2023
Viewed by 1231
Abstract
Chronic oxidative stress impairs the normal functioning of the retinal pigment epithelium (RPE), leading to atrophy of this cell layer in cases of advance age-related macular degeneration (AMD). The purpose of our study was to determine if buspirone, a partial serotonin 1A (5-HT1A) [...] Read more.
Chronic oxidative stress impairs the normal functioning of the retinal pigment epithelium (RPE), leading to atrophy of this cell layer in cases of advance age-related macular degeneration (AMD). The purpose of our study was to determine if buspirone, a partial serotonin 1A (5-HT1A) receptor agonist, protected against oxidative stress-induced changes in the RPE. We exposed differentiated human ARPE-19 cells to paraquat to induce oxidative damage in culture, and utilized a mouse model with sodium iodate (NaIO3)-induced oxidative injury to evaluate the effect of buspirone. To investigate buspirone’s effect on protective gene expression, we performed RT–PCR. Cellular toxicities and junctional abnormalities due to paraquat induction in ARPE-19 cells and buspirone’s impact were assessed via WST-1 assays and ZO-1 immunostaining. We used spectral-domain optical coherence tomography (SD-OCT) and ZO-1 immunostaining of RPE/choroid for structural analysis. WST-1 assays showed dose-dependent protection of viability in buspirone-treated ARPE-19 cells in culture and preservation of RPE junctional integrity under oxidative stress conditions. In the NaIO3 model, daily intraperitoneal injection (i.p.) of buspirone (30 mg/kg) for 12 days improved the survival of photoreceptors compared to those of vehicle-treated eyes. ZO-1-stained RPE flat-mounts revealed the structural preservation of RPE from oxidative damage in buspirone-treated mice, as well as in buspirone-induced Nqo1, Cat, Sqstm1, Gstm1, and Sod2 genes in the RPE/choroid compared to untreated eyes. Since oxidative stress is implicated in the pathogenesis AMD, repurposing buspirone, which is currently approved for the treatment of anxiety, might be useful in treating or preventing dry AMD. Full article
(This article belongs to the Special Issue Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research)
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24 pages, 16456 KiB  
Article
Intravitreal Injection of ZYAN1 Restored Autophagy and Alleviated Oxidative Stress in Degenerating Retina via the HIF-1α/BNIP3 Pathway
by Xiao-Na Hao, Na Zhao, Jie-Min Huang, Si-Yu Li, Dong Wei, Ning Pu, Guang-Hua Peng and Ye Tao
Antioxidants 2023, 12(11), 1914; https://doi.org/10.3390/antiox12111914 - 26 Oct 2023
Viewed by 1245
Abstract
Mitochondrial autophagy plays a contributary role in the pathogenesis of retina degeneration (RD). ZYAN1 is a novel proline hydroxylase domain (PHD) inhibitor that can enhance the expression of hypoxia-inducible factor 1-alpha (HIF-1α). This study investigated whether ZYAN1 could alleviate progressive photoreceptor loss and [...] Read more.
Mitochondrial autophagy plays a contributary role in the pathogenesis of retina degeneration (RD). ZYAN1 is a novel proline hydroxylase domain (PHD) inhibitor that can enhance the expression of hypoxia-inducible factor 1-alpha (HIF-1α). This study investigated whether ZYAN1 could alleviate progressive photoreceptor loss and oxidative damage in a pharmacologically induced RD model via the modulation of mitophagy. ZYAN1 was injected into the vitreous body of the RD model, and the retinal autophagy level was analyzed. The therapeutic effects of ZYAN1 were evaluated via a function examination, a morphological assay, in situ reactive oxygen species (ROS) detection, and an immunofluorescence assay. It was shown that the thickness of the outer nuclear layer (ONL) increased significantly, and visual function was efficiently preserved via ZYAN1 treatment. The mitochondria structure of photoreceptors was more complete in the ZYAN1-treated mice, and the number of autophagosomes also increased significantly. Membrane disc shedding and ROS overproduction were alleviated after ZYAN1 treatment, and the axonal cilia were more structurally intact. A Western blot analysis showed that the expression levels of the autophagy-related proteins LC3-B, Beclin-1, and ATG5 increased significantly after ZYAN1 treatment, while the expression of P62 was down-regulated. Moreover, the expression levels of HIF-1α and BNIP3 were up-regulated after ZYAN1 treatment. Therefore, an intravitreal injection of ZYAN1 can act as part of the pharmacologic strategy to modulate mitophagy and alleviate oxidative stress in RD. These findings enrich our knowledge of RD pathology and provide insights for the discovery of a therapeutic molecule. Full article
(This article belongs to the Special Issue Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research)
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14 pages, 1962 KiB  
Article
β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells
by Cheol Park, Hee-Jae Cha, Hyun Hwangbo, EunJin Bang, Su Hyun Hong, Kyoung Seob Song, Jeong Sook Noh, Do-Hyung Kim, Gi-Young Kim and Yung Hyun Choi
Antioxidants 2023, 12(7), 1410; https://doi.org/10.3390/antiox12071410 - 11 Jul 2023
Cited by 2 | Viewed by 1426
Abstract
Diabetic retinopathy (DR) is the leading cause of vision loss and a major complication of diabetes. Hyperglycemia-induced accumulation of reactive oxygen species (ROS) is an important risk factor for DR. β-asarone, a major component of volatile oil extracted from Acori graminei Rhizoma, exerts [...] Read more.
Diabetic retinopathy (DR) is the leading cause of vision loss and a major complication of diabetes. Hyperglycemia-induced accumulation of reactive oxygen species (ROS) is an important risk factor for DR. β-asarone, a major component of volatile oil extracted from Acori graminei Rhizoma, exerts antioxidant effects; however, its efficacy in DR remains unknown. In this study, we investigated whether β-asarone inhibits high-glucose (HG)-induced oxidative damage in human retinal pigment epithelial (RPE) ARPE-19 cells. We found that β-asarone significantly alleviated cytotoxicity, apoptosis, and DNA damage in HG-treated ARPE-19 cells via scavenging of ROS generation. β-Asarone also significantly attenuated the excessive accumulation of lactate dehydrogenase and mitochondrial ROS by increasing the manganese superoxide dismutase and glutathione activities. HG conditions markedly increased the release of interleukin (IL)-1β and IL-18 and upregulated their protein expression and activation of the nuclear factor-kappa B (NF-κB) signaling pathway, whereas β-asarone reversed these effects. Moreover, expression levels of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome multiprotein complex molecules, including thioredoxin-interacting protein, NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain, and cysteinyl aspartate-specific proteinase-1, were increased in ARPE-19 cells under HG conditions. However, their expression levels remained similar to those in the control group in the presence of β-asarone. Therefore, β-asarone protects RPE cells from HG-induced injury by blocking ROS generation and NF-κB/NLRP3 inflammasome activation, indicating its potential as a therapeutic agent for DR treatment. Full article
(This article belongs to the Special Issue Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research)
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Review

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43 pages, 1443 KiB  
Review
Antioxidants and Mechanistic Insights for Managing Dry Age-Related Macular Degeneration
by Deepak Basyal, Sooyeun Lee and Hye Jin Kim
Antioxidants 2024, 13(5), 568; https://doi.org/10.3390/antiox13050568 - 4 May 2024
Viewed by 842
Abstract
Age-related macular degeneration (AMD) severely affects central vision due to progressive macular degeneration and its staggering prevalence is rising globally, especially in the elderly population above 55 years. Increased oxidative stress with aging is considered an important contributor to AMD pathogenesis despite multifaceted [...] Read more.
Age-related macular degeneration (AMD) severely affects central vision due to progressive macular degeneration and its staggering prevalence is rising globally, especially in the elderly population above 55 years. Increased oxidative stress with aging is considered an important contributor to AMD pathogenesis despite multifaceted risk factors including genetic predisposition and environmental agents. Wet AMD can be managed with routine intra-vitreal injection of angiogenesis inhibitors, but no satisfactory medicine has been approved for the successful management of the dry form. The toxic carbonyls due to photo-oxidative degradation of accumulated bisretinoids within lysosomes initiate a series of events including protein adduct formation, impaired autophagy flux, complement activation, and chronic inflammation, which is implicated in dry AMD. Therapy based on antioxidants has been extensively studied for its promising effect in reducing the impact of oxidative stress. This paper reviews the dry AMD pathogenesis, delineates the effectiveness of dietary and nutrition supplements in clinical studies, and explores pre-clinical studies of antioxidant molecules, extracts, and formulations with their mechanistic insights. Full article
(This article belongs to the Special Issue Cellular Responses of Antioxidants Related to Degenerative Eye Disease Research)
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