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Oxidative Stress and Retinal 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 (20 February 2023) | Viewed by 21962

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Dr. Marcella Nebbioso

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Department of Sense Organs, Faculty of Medicine and Odontology, Sapienza University of Rome, p. le A. Moro 5, 00185 Rome, Italy
Interests: neuro-ophthalmology; rare retinal diseases; diabetic retinopathy; inflammation; oxidative stress; ocular biomedical techniques; age-related macular degeneration; glaucoma

Special Issue Information

Dear Colleagues,

Numerous factors contribute to the breakdown of the balance between the production and elimination of free radicals, causing the onset of so-called oxidative stress. Among the most common factors are: inflammation, cigarette smoking, psycho-physical stress, alcohol consumption, diets rich in proteins and animal fats, exposure to polluted environments, and ionizing and ultraviolet radiation. The continuous oxidizing action of reactive oxygen species (ROS) is evident above all in the premature aging of cells, which is associated with the onset of various diseases such as diabetes mellitus, tumors, diseases of the cardiovascular system, Parkinson's disease, Alzheimer's, and many others. Thus, the neurodegeneration and dysfunction of vascular endothelial cells are caused by interactions between oxidative stress, inflammation, and free oxygen radicals.

A prolonged exposure to ROS determines the development of several retinal pathologies. Today, it is essential to investigate pathogenesis and develop novel strategies to reduce retinal complications. The body is able to defend itself against premature aging thanks to natural free radical scavengers, which have the task of providing free radicals with the electrons they lack. Other substances that play an important antioxidant role are taken with food, such as vegetable pigments (polyphenols, turmeric, bioflavonoids, anthocyanins), vitamins (ascorbic acid, α- or γ-tocopherol, beta-carotene), microelements (selenium, copper, zinc), enzymes (glutathione, coenzyme Q10, alpha-lipoic acid), etc.

Our Special Issue on oxidative stress and retinal diseases is intended to inspire researchers to experiment with animal models and human cells, and to provide interventional or observational studies. A better knowledge of these factors could be useful for spreading new therapies able to act directly or indirectly on their biochemical activity and therefore avoid the complications related to several retinopathies. In this Special Issue, review and meta-analysis studies will also be considered to take stock of the situation regarding the recently discovered etiopathogenesis of retinal disease and oxidative stress.

Prof. Dr. Marcella Nebbioso
Guest Editor

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Keywords

animal retinal models
adult human retinal pigment epithelial (ARPE-19) cells
cytokines
neurodegeneration
oxidative stress
reactive oxygen species (ROS)
retinal endothelial cell
retinal ganglion cells

Published Papers (10 papers)

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Research

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16 pages, 1953 KiB

Open AccessArticle

Sulodexide Prevents Hyperglycemia-Induced Endothelial Dysfunction and Oxidative Stress in Porcine Retinal Arterioles

by Alice Dauth, Andrzej Bręborowicz, Yue Ruan, Qi Tang, Jenia K. Zadeh, Elsa W. Böhm, Norbert Pfeiffer, Pratik H. Khedkar, Andreas Patzak, Ksenija Vujacic-Mirski, Andreas Daiber and Adrian Gericke

Antioxidants 2023, 12(2), 388; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12020388 - 6 Feb 2023

Cited by 8 | Viewed by 2190

Abstract

Diabetes mellitus may cause severe damage to retinal blood vessels. The central aim of this study was to test the hypothesis that sulodexide, a mixture of glycosaminoglycans, has a protective effect against hyperglycemia-induced endothelial dysfunction in the retina. Functional studies were performed in isolated porcine retinal arterioles. Vessels were cannulated and incubated with highly concentrated glucose solution (HG, 25 mM D-glucose) +/− sulodexide (50/5/0.5 μg/mL) or normally concentrated glucose solution (NG, 5.5 mM D-glucose) +/− sulodexide for two hours. Endothelium-dependent and endothelium-independent vasodilatation were measured by videomicroscopy. Reactive oxygen species (ROS) were quantified by dihydroethidium (DHE) fluorescence. Using high-pressure liquid chromatography (HPLC), the intrinsic antioxidant properties of sulodexide were investigated. Quantitative PCR was used to determine mRNA expression of regulatory, inflammatory, and redox genes in retinal arterioles, some of which were subsequently quantified at the protein level by immunofluorescence microscopy. Incubation of retinal arterioles with HG caused significant impairment of endothelium-dependent vasodilation, whereas endothelium-independent responses were not affected. In the HG group, ROS formation was markedly increased in the vascular wall. Strikingly, sulodexide had a protective effect against hyperglycemia-induced ROS formation in the vascular wall and had a concentration-dependent protective effect against endothelial dysfunction. Although sulodexide itself had only negligible antioxidant properties, it prevented hyperglycemia-induced overexpression of the pro-oxidant redox enzymes, NOX4 and NOX5. The data of the present study provide evidence that sulodexide has a protective effect against hyperglycemia-induced oxidative stress and endothelial dysfunction in porcine retinal arterioles, possibly by modulation of redox enzyme expression. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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13 pages, 1867 KiB

Open AccessArticle

Metabolic Imaging and Molecular Biology Reveal the Interplay between Lipid Metabolism and DHA-Induced Modulation of Redox Homeostasis in RPE Cells

by Giada Bianchetti, Maria Elisabetta Clementi, Beatrice Sampaolese, Cassandra Serantoni, Alessio Abeltino, Marco De Spirito, Shlomo Sasson and Giuseppe Maulucci

Antioxidants 2023, 12(2), 339; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12020339 - 31 Jan 2023

Cited by 2 | Viewed by 1709

Abstract

Diabetes-induced oxidative stress induces the development of vascular complications, which are significant causes of morbidity and mortality in diabetic patients. Among these, diabetic retinopathy (DR) is often caused by functional changes in the blood–retinal barrier (BRB) due to harmful oxidative stress events in lipids, proteins, and DNA. Docosahexaenoic acid (DHA) has a potential therapeutic effect against hyperglycemia-induced oxidative damage and apoptotic pathways in the main constituents of BRB, retinal pigment epithelium cells (ARPE-19). Effective antioxidant response elicited by DHA is driven by the activation of the Nrf2/Nqo1 signaling cascade, which leads to the formation of NADH, a reductive agent found in the cytoplasm. Nrf2 also induces the expression of genes encoding enzymes involved in lipid metabolism. This study, therefore, aims at investigating the modulation of lipid metabolism induced by high-glucose (HG) on ARPE-19 cells through the integration of metabolic imaging and molecular biology to provide a comprehensive functional and molecular characterization of the mechanisms activated in the disease, as well the therapeutic role of DHA. This study shows that HG augments RPE metabolic processes by enhancing lipid metabolism, from fatty acid uptake and turnover to lipid biosynthesis and β-oxidation. DHA exerts its beneficial effect by ameliorating lipid metabolism and reducing the increased ROS production under HG conditions. This investigation may provide novel insight for formulating novel treatments for DR by targeting lipid metabolism pathways. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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16 pages, 4647 KiB

Open AccessArticle

Phloroglucinol Attenuates DNA Damage and Apoptosis Induced by Oxidative Stress in Human Retinal Pigment Epithelium ARPE-19 Cells by Blocking the Production of Mitochondrial ROS

by Cheol Park, Hee-Jae Cha, Min Yeong Kim, EunJin Bang, Sung-Kwon Moon, Seok Joong Yun, Wun-Jae Kim, Jeong Sook Noh, Gi-Young Kim, Suengmok Cho, Hyesook Lee and Yung Hyun Choi

Antioxidants 2022, 11(12), 2353; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11122353 - 28 Nov 2022

Cited by 6 | Viewed by 1826

Abstract

Phloroglucinol, a phenolic compound, is known to possess a potent antioxidant ability. However, its role in retinal cells susceptible to oxidative stress has not been well elucidated yet. Thus, the objective of this study was to evaluate whether phloroglucinol could protect against oxidative damage in cultured human retinal pigment epithelium ARPE-19 cells. For this purpose, ARPE-19 cells were stimula ted with hydrogen peroxide (H₂O₂) to mimic oxidative stress. Cell viability, cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, mitochondrial function, DNA damage, and autophagy were then assessed. Our results revealed that phloroglucinol ameliorated cell viability, cytotoxicity, and DNA damage in H₂O₂-exposued ARPE-19 cells and blocked production of ROS. Phloroglucinol also counteracted H₂O₂-induced apoptosis by reducing Bax/Bcl-2 ratio, blocking activation of caspase-3, and inhibiting degradation of poly (ADP-ribose) polymerase. H₂O₂ caused mitochondrial impairment and increased expression levels of mitophagy markers such as PINK1and PARKIN known to be associated with mitochondrial ROS (mtROS) generation and cytosolic release of cytochrome c. However, these changes were significantly attenuated by phloroglucinol. Mito-TEMPO, a selective mitochondrial antioxidant, further enhanced the protective effect of phloroglucinol against dysfunctional mitochondria. Furthermore, H₂O₂ induced autophagy, but not when ARPE-19 cells were pretreated with phloroglucinol, meaning that autophagy by H₂O₂ contributed to the pro-survival mechanism and that phloroglucinol protected ARPE-19 cells from apoptosis by blocking autophagy. Taken together, these results suggest that phloroglucinol can inhibit oxidative stress-induced ARPE-19 cell damage and dysfunction by protecting DNA damage, autophagy, and subsequent apoptosis through mitigation of mtROS generation. Thus, phloroglucinol might have therapeutic potential to prevent oxidative stress-mediated damage in RPE cells. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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17 pages, 8138 KiB

Open AccessArticle

Antioxidant Effects of DPP-4 Inhibitors in Early Stages of Experimental Diabetic Retinopathy

by Hugo Ramos, Patricia Bogdanov, Jordi Huerta, Anna Deàs-Just, Cristina Hernández and Rafael Simó

Antioxidants 2022, 11(7), 1418; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11071418 - 21 Jul 2022

Cited by 5 | Viewed by 2419

Abstract

Hyperglycemia-induced oxidative stress plays a key role in the impairment of the retinal neurovascular unit, an early event in the pathogenesis of DR. The aim of this study was to assess the antioxidant properties of topical administration (eye drops) of sitagliptin in the diabetic retina. For this purpose, db/db mice received sitagliptin or vehicle eye drops twice per day for two weeks. Age-matched db/+ mice were used as the control group. We evaluated retinal mRNA (RT-PCR) and protein levels (Western blotting and immunohistochemistry) of different components from both the antioxidant system (NRF2, CAT, GPX, GR, CuZnSOD, and MnSOD) and the prooxidant machinery (PKC and TXNIP). We also studied superoxide levels (dihydroethidium staining) and oxidative damage to DNA/RNA (8-hydroxyguanosine immunostaining) and proteins (nitrotyrosine immunostaining). Finally, NF-кB translocation and IL-1β production were assessed through Western blotting and/or immunohistochemistry. We found that sitagliptin protected against diabetes-induced oxidative stress by reducing superoxide, TXNIP, PKC, and DNA/RNA/protein oxidative damage, and it prevented the downregulation of NRF2 and antioxidant enzymes, with the exception of catalase. Sitagliptin also exerted anti-inflammatory effects, avoiding both NF-кB translocation and IL-1β production. Sitagliptin prevents the diabetes-induced imbalance between ROS production and antioxidant defenses that occurs in diabetic retinas. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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10 pages, 577 KiB

Open AccessArticle

Relevance of Diabetic Retinopathy with AGEs and Carotenoid Levels Assessed by Skin Sensors

by Junichi Sasaki, Yuji Takayanagi, Yoichi Kadoh and Masaki Tanito

Antioxidants 2022, 11(7), 1370; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11071370 - 14 Jul 2022

Cited by 2 | Viewed by 1451

Abstract

Advanced glycation end products (AGEs) and carotenoids, the major prooxidants and antioxidants in vivo, respectively, are thought to be associated with diabetes mellitus (DM). To estimate AGEs and carotenoid levels simultaneously in patients with DM, we used noninvasive fingertip skin sensors. The study population included 249 eyes of 249 Japanese subjects (130 men, 119 women; mean age ± standard deviation, 69.9 ± 12.0 years). Ninety-three patients had DM, which included diabetic retinopathy (DR) (n = 44) and no DR (NDR) (n = 49), and 156 controls. Compared to the controls (0.44 ± 0.07 arbitrary unit (A.U.)), the AGEs scores were significantly higher in DM (0.47 ± 0.09, p = 0.029) and DR (0.49 ± 0.08, p = 0.0006) patients; no difference was seen between NDR (0.45 ± 0.09, p = 0.83) and controls. Multivariate analyses indicated that a higher AGEs level is a risk factor for DR (r = 0.030, p = 0.0025). However, the carotenoid scores did not differ in any comparisons between the controls (327.7 ± 137.0 O.D.) and patients with DM (324.7 ± 126.4, p = 0.86), NDR (320.4 ± 123.6, p = 0.93), or DR (329.4 ± 130.8, p = 0.93). The carotenoid scores correlated negatively with the AGEs scores (r = −0.21, p = 0.0007), and reflected the Veggie intake score (p < 0.0001). In patients with DM, estimations of AGEs and carotenoid levels using skin sensors can be useful for assessing their risk of DR and vegetable intake, respectively. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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14 pages, 3602 KiB

Open AccessArticle

PPARδ Inhibits Hyperglycemia-Triggered Senescence of Retinal Pigment Epithelial Cells by Upregulating SIRT1

by Eun Ji Lee, Jun Pil Won, Hyuk Gyoon Lee, Eunsu Kim, Jinwoo Hur, Won Jin Lee, Jung Seok Hwang and Han Geuk Seo

Antioxidants 2022, 11(6), 1207; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061207 - 20 Jun 2022

Cited by 2 | Viewed by 1976

Abstract

Emerging evidence shows that peroxisome proliferator-activated receptor delta (PPARδ) plays a pivotal role in cellular aging. However, its function in retinal disease processes such as hyperglycemia-associated diabetic retinopathy is unclear. Here, we demonstrate that PPARδ inhibits premature senescence of retinal pigment epithelial (RPE) cells induced by high glucose (HG) through SIRT1 upregulation. A specific ligand GW501516-activation of PPARδ suppressed premature senescence and production of reactive oxygen species induced by HG in ARPE-19 cells, a spontaneously arising human RPE cell line. These effects were accompanied by the regulation of the premature senescence-associated genes p53, p21, and SMP-30. Furthermore, GW501516-activated PPARδ almost completely abolished the effects of HG treatment on the formation of phosphorylated H2A histone family member X (γ-H2A.X) foci, a molecular marker of aging. These inhibitory effects of GW501516 were significantly reversed in ARPE-19 cells stably expressing small hairpin RNA targeting PPARδ. Notably, GW501516 significantly increased the mRNA and protein levels of SIRT1, indicating that GW501516-activated PPARδ exerted its beneficial effects through SIRT1. In addition, GW501516 restored HG-suppressed SIRT1 expression, corroborating the role of SIRT1 in the anti-senescence function of PPARδ. The effects of PPARδ on HG-induced premature senescence and the expression of the senescence-associated genes p53, p21, and SMP-30 were mimicked by the SIRT1 activator resveratrol, but blocked by the SIRT1 inhibitor sirtinol. Collectively, these results indicate that GW501516-activated PPARδ inhibits HG-triggered premature senescence of RPE cells by modulating SIRT1 signaling. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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14 pages, 1672 KiB

Open AccessArticle

Investigation of DHA-Induced Regulation of Redox Homeostasis in Retinal Pigment Epithelium Cells through the Combination of Metabolic Imaging and Molecular Biology

by Giada Bianchetti, Maria Elisabetta Clementi, Beatrice Sampaolese, Cassandra Serantoni, Alessio Abeltino, Marco De Spirito, Shlomo Sasson and Giuseppe Maulucci

Antioxidants 2022, 11(6), 1072; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061072 - 28 May 2022

Cited by 10 | Viewed by 2188

Abstract

Diabetes-induced oxidative stress leads to the onset of vascular complications, which are major causes of disability and death in diabetic patients. Among these, diabetic retinopathy (DR) often arises from functional alterations of the blood-retinal barrier (BRB) due to damaging oxidative stress reactions in lipids, proteins, and DNA. This study aimed to investigate the impact of the ω3-polyunsaturated docosahexaenoic acid (DHA) on the regulation of redox homeostasis in the human retinal pigment epithelial (RPE) cell line (ARPE-19) under hyperglycemic-like conditions. The present results show that the treatment with DHA under high-glucose conditions activated erythroid 2-related factor Nrf2, which orchestrates the activation of cellular antioxidant pathways and ultimately inhibits apoptosis. This process was accompanied by a marked increase in the expression of NADH (Nicotinamide Adenine Dinucleotide plus Hydrogen) Quinone Oxidoreductase 1 (Nqo1), which is correlated with a contextual modulation and intracellular re-organization of the NAD+/NADH redox balance. This investigation of the mechanisms underlying the impairment induced by high levels of glucose on redox homeostasis of the BRB and the subsequent recovery provided by DHA provides both a powerful indicator for the detection of RPE cell impairment as well as a potential metabolic therapeutic target for the early intervention in its treatment. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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13 pages, 4472 KiB

Open AccessArticle

Oxidative-Induced Angiogenesis Is Modulated by Small Extracellular Vesicle miR-302a-3p Cargo in Retinal Pigment Epithelium Cells

by Maria Oltra, Miriam Martínez-Santos, María Ybarra, Hugo Rowland, María Muriach, Javier Romero, Javier Sancho-Pelluz and Jorge M. Barcia

Antioxidants 2022, 11(5), 818; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050818 - 22 Apr 2022

Cited by 7 | Viewed by 1931

Abstract

Extracellular vesicles are released from cells under diverse conditions. Widely studied in cancer, they are associated with different diseases playing major roles. Recent reports indicate that oxidative damage promotes the release of small extracellular vesicle (sEVs) from the retinal pigment epithelium (RPE), with an angiogenic outcome and changes in micro-RNA (miRNA) levels. The aim of this study was to determine the role of the miRNA miR-302a-3p, included within RPE-released sEVs, as an angiogenic regulator in cultures of endothelial cells (HUVEC). ARPE-19 cell cultures, treated with H₂O₂ to cause an oxidative insult, were transfected with a miR-302a-3p mimic. Later, sEVs from the medium were isolated and added into HUVEC or ARPE-19 cultures. sEVs from ARPE-19 cells under oxidative damage presented a decrease of miR-302a-3p levels and exhibited proangiogenic properties. In contrast, sEVs from miR-302a-3p-mimic transfected cells resulted in control angiogenic levels. The results herein indicate that miR-302a-3p contained in sEVs can modify VEGFA mRNA expression levels as part of its antiangiogenic features. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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Review

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26 pages, 694 KiB

Open AccessReview

Diabetic Retinopathy: Are lncRNAs New Molecular Players and Targets?

by Simona Cataldi, Mariagiovanna Tramontano, Valerio Costa, Marianna Aprile and Alfredo Ciccodicola

Antioxidants 2022, 11(10), 2021; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11102021 - 12 Oct 2022

Cited by 8 | Viewed by 2688

Abstract

The growing incidence of diabetes mellitus worldwide implies the increasing prevalence of several related macro- (e.g., hypertension and atherosclerosis) and micro-vascular (e.g., nephropathy and retinopathy) complications. Notably, diabetic retinopathy (DR) is the leading cause of blindness in older diabetic patients and can occur with different degrees of severity. Chronic hyperglycemia is the main determinant of the functional damage of retinal cells. The oxidative stress, inflammatory factors and vascular endothelial growth factor signaling have been widely reported as contributors of DR onset and progression, and an emerging role has been described for different classes of non-coding RNA, including several long non-coding RNAs (lncRNAs). Here, we report the main results of all research articles (i.e., 150) listed on PubMed database from 2014 to 2022 regarding the putative role of lncRNAs in DR, including small nucleolar RNA host genes (SNHGs). Particularly, in this review we describe all lncRNAs and SNHGs with altered expression in DR and related contexts, discussing their association with DR outcomes, their mechanism of action related to DR, the molecular/functional effects, as well as the biological and experimental contexts. Thus, herein we provide an overview of the current state of knowledge regarding the putative involvement of 50 lncRNAs and SNHGs in the pathogenesis of DR, highlighting their potential as therapeutic targets or biomarkers for improving the clinical management of DR. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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18 pages, 2561 KiB

Open AccessReview

Oxidative Stress Implication in Retinal Diseases—A Review

by Marcella Nebbioso, Federica Franzone, Alessandro Lambiase, Vincenza Bonfiglio, Paolo Giuseppe Limoli, Marco Artico, Samanta Taurone, Enzo Maria Vingolo, Antonio Greco and Antonella Polimeni

Antioxidants 2022, 11(9), 1790; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11091790 - 10 Sep 2022

Cited by 19 | Viewed by 2540

Abstract

Oxidative stress (OS) refers to an imbalance between free radicals (FRs), namely highly reactive molecules normally generated in our body by several pathways, and intrinsic antioxidant capacity. When FR levels overwhelm intrinsic antioxidant defenses, OS occurs, inducing a series of downstream chemical reactions. Both reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced by numerous chemical reactions that take place in tissues and organs and are then eliminated by antioxidant molecules. In particular, the scientific literature focuses more on ROS participation in the pathogenesis of diseases than on the role played by RNS. By its very nature, the eye is highly exposed to ultraviolet radiation (UVR), which is directly responsible for increased OS. In this review, we aimed to focus on the retinal damage caused by ROS/RNS and the related retinal pathologies. A deeper understanding of the role of oxidative and nitrosative stress in retinal damage is needed in order to develop targeted therapeutic interventions to slow these pathologies. Full article

(This article belongs to the Special Issue Oxidative Stress and Retinal Diseases)

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