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Antioxidants
Special Issues
Advances in Oxidative Stress and Eye Diseases
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Advances in Oxidative Stress and Eye Diseases

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 December 2021) | Viewed by 10242

Special Issue Editors

Dr. Adrian Gericke

E-Mail Website
Guest Editor
Augenklinik, Universitätsmedizin der, Johannes Gutenberg-Universität Mainz, Langenbeckstraße 1, 55131 Mainz, Germany
Interests: corneal regeneration; G protein-coupled receptors; inflammation; ocular perfusion; oxidative stress; retinal ischemia; vascular endothelial function
Special Issues, Collections and Topics in MDPI journals
Dr. Verena Prokosch

E-Mail Website
Co-Guest Editor
Department of Ophthalmology, University of Cologne, Kerpener Str. 62, 50937 Köln, Germany
Interests: eyes; western blot; genetic engineering; glaucoma; retinal ganglion cells; pharmacology; ophthalmology; retina; medicine

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are important signaling molecules that regulate numerous physiological actions, such as neuron function and vascular reactivity. However, excessive ROS levels can modify cellular molecules and impair their function. Moreover, ROS can stimulate the production of inflammatory cytokines, causing inflammation and cell death. Hence, it is not surprising that elevated ROS levels have been observed in various ocular diseases, such as glaucoma, diabetic retinopathy, and age-related macular degeneration (AMD), but also in ocular surface diseases. Different compounds with direct or indirect antioxidant activity have been used to reduce ROS accumulation in animal ocular disease models and humans. We invite submissions that cover the following topics to this Special Issue:

  • Studies that provide substantial mechanistic insight into the pathophysiology of ROS in eye diseases in animal models or patients.
  • Proof-of-concept studies for certain antioxidant agents demonstrating their influence on oxidative stress and ocular disease onset and/or progression. The studies should employ accepted state-of-the-art techniques to assess oxidative stress and/or inflammation.

Dr. Adrian Gericke
Dr. Verena Prokosch
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

  • oxidative stress
  • reactive oxygen species (ROS)
  • eye
  • pathophysiology
  • therapy

Published Papers (3 papers)

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Research

15 pages, 1763 KiB  
Article
An Assessment of Cataract Severity Based on Antioxidant Status and Ascorbic Acid Levels in Aqueous Humor
by Yu-Ting Tsao, Wei-Chi Wu, Kuan-Jen Chen, Chun-Fu Liu, Yi-Jen Hsueh, Chao-Min Cheng and Hung-Chi Chen
Antioxidants 2022, 11(2), 397; https://doi.org/10.3390/antiox11020397 - 16 Feb 2022
Cited by 7 | Viewed by 3055
Abstract
Cataract is the leading cause of blindness throughout the world. Currently, the cataract severity evaluation is based on the subjective LOCS III guideline. To ameliorate the evaluation system and develop an objective and quantitative analysis, we investigated the relationships among aqueous humor total [...] Read more.
Cataract is the leading cause of blindness throughout the world. Currently, the cataract severity evaluation is based on the subjective LOCS III guideline. To ameliorate the evaluation system and develop an objective and quantitative analysis, we investigated the relationships among aqueous humor total antioxidant capacity (AqTAC), ascorbic acid (AqAA) concentration, and cataract severity. In this study, we enrolled 130 cataract patients who underwent phacoemulsification between April 2019 and March 2020. The AqTAC and AqAA were measured by our own developed TAC assay and commercially available kit. Cataract severity was recorded by nuclear opalescence (NO) and cortical cataract (CC) degree according to LOCS III. Cumulative dissipated energy (CDE) during phacoemulsification was recorded to verify the severity of the cataract. As a result, we found a moderate correlation between AqTAC and CDE (p < 0.001). In addition, we found AqTAC independently associated with the CDE when analyzed by multivariate linear regression (p < 0.001). AqTAC also negatively correlated to cataract severity when measured by NO and CC (p = 0.012 in NO grade 3 vs. grade 1; p = 0.012 in CC grade 2 vs. grade 1; p < 0.001 in CC grade 3 vs. grade 1). We further found AqAA provided 71.9 ± 13.5% of AqTAC, and showed a high correlation (rho = 0.79, p < 0.001). In conclusion, we found a significant correlation between AqTAC/AqAA and cataract severity measured by CDE. The correlation was superior to the correlation between LOCS III and CDE. Aqueous humor TAC owns the potential to assess cataracts in an objective and quantitative way. Full article
(This article belongs to the Special Issue Advances in Oxidative Stress and Eye Diseases)
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18 pages, 5772 KiB  
Article
The Effects of Two Nrf2 Activators, Bardoxolone Methyl and Omaveloxolone, on Retinal Ganglion Cell Survival during Ischemic Optic Neuropathy
by Jia-Ying Chien, Yu-Yau Chou, Jhih-Wei Ciou, Fang-Yun Liu and Shun-Ping Huang
Antioxidants 2021, 10(9), 1466; https://doi.org/10.3390/antiox10091466 - 15 Sep 2021
Cited by 11 | Viewed by 3535
Abstract
Nonarteritic anterior ischemic optic neuropathy (NAION) is one of the most common acute optic neuropathies that affect the over 55-year-old population. NAION causes the loss of visual function, and it has no safe and effective therapy. Bardoxolone methyl (methyl 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oate; CDDO-Me; RTA 402) [...] Read more.
Nonarteritic anterior ischemic optic neuropathy (NAION) is one of the most common acute optic neuropathies that affect the over 55-year-old population. NAION causes the loss of visual function, and it has no safe and effective therapy. Bardoxolone methyl (methyl 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oate; CDDO-Me; RTA 402) is a semisynthetic triterpenoid with effects against antioxidative stress and inflammation in neurodegeneration and kidney disease that activates the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Moreover, RTA 402 is an FDA-approved compound for the treatment of solid tumors, lymphoid malignancies, melanoma, and chronic kidney disease. Omaveloxolone (RTA 408) is an activator of Nrf2 and an inhibitor of NFκB, possessing antioxidative and anti-inflammatory activities in mitochondrial bioenergetics. RTA 408 is also under clinical investigation for Friedreich ataxia (FA). In this study, a rodent anterior ischemic optic neuropathy (rAION) model induced by photothrombosis was used to examine the therapeutic effects of RTA 402 and RTA 408. Treatment with RTA402 results in antiapoptotic, antioxidative stress, anti-inflammatory, and myelin-preserving effects on retinal ganglion cell (RGC) survival and visual function via regulation of NQO1 and HO-1, reduced IL-6 and Iba1 expression in macrophages, and promoted microglial expression of TGF-β and Ym1 + 2 in the retina and optic nerve. However, these effects were not observed after RTA 408 treatment. Our results provide explicit evidence that RTA 402 modulates the Nrf2 and NFκB signaling pathways to protect RGCs from apoptosis and maintain the visual function in an rAION model. These findings indicate that RTA 402 may a potential therapeutic agent for ischemic optic neuropathy. Full article
(This article belongs to the Special Issue Advances in Oxidative Stress and Eye Diseases)
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17 pages, 5268 KiB  
Article
Protective Effects of Oroxylin A on Retinal Ganglion Cells in Experimental Model of Anterior Ischemic Optic Neuropathy
by Jia-Ying Chien, Shu-Fang Lin, Yu-Yau Chou, Chi-Ying F. Huang and Shun-Ping Huang
Antioxidants 2021, 10(6), 902; https://doi.org/10.3390/antiox10060902 - 3 Jun 2021
Cited by 9 | Viewed by 2970
Abstract
Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute vision loss in older people, and there is no effective therapy. The effect of the systemic or local application of steroids for NAION patients remains controversial. Oroxylin A (OA) (5,7-dihydroxy-6-methoxyflavone) [...] Read more.
Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute vision loss in older people, and there is no effective therapy. The effect of the systemic or local application of steroids for NAION patients remains controversial. Oroxylin A (OA) (5,7-dihydroxy-6-methoxyflavone) is a bioactive flavonoid extracted from Scutellariae baicalensis Georgi. with various beneficial effects, including anti-inflammatory and neuroprotective effects. A previous study showed that OA promotes retinal ganglion cell (RGC) survival after optic nerve (ON) crush injury. The purpose of this research was to further explore the potential actions of OA in ischemic injury in an experimental anterior ischemic optic neuropathy (rAION) rat model induced by photothrombosis. Our results show that OA efficiently attenuated ischemic injury in rats by reducing optic disc edema, the apoptotic death of retinal ganglion cells, and the infiltration of inflammatory cells. Moreover, OA significantly ameliorated the pathologic changes of demyelination, modulated microglial polarization, and preserved visual function after rAION induction. OA activated nuclear factor E2 related factor (Nrf2) signaling and its downstream antioxidant enzymes NAD(P)H:quinone oxidoreductase (NQO-1) and heme oxygenase 1 (HO-1) in the retina. We demonstrated that OA activates Nrf2 signaling, protecting retinal ganglion cells from ischemic injury, in the rAION model and could potentially be used as a therapeutic approach in ischemic optic neuropathy. Full article
(This article belongs to the Special Issue Advances in Oxidative Stress and Eye Diseases)
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