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Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation

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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 (30 June 2022) | Viewed by 39966

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Special Issue Editor

Dr. Fabrizio Gentile

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Guest Editor

Department of Medicine & Health Sciences, Universita' del Molise, Campobasso, Italy

Special Issue Information

Dear Colleagues,

A growing body of evidence highlights the role played by reactive aldehydes produced by free-radical attack to cell membrane phospholipids, polyunsaturated fatty acids, carbohydrates and their derivatives during oxidative stress in the pathogenesis of inflammation, autoimmunity and immunity-driven inflammation. Lipid peroxidation (LPO) and glycoxidation products accumulate in tissues and act both as second messengers of redox imbalance and as covalent modifiers of molecular effectors of signal transduction, cytoskeletal organization, cell adhesion and other critical processes. Ischemia/reperfusion damage, endothelial dysfunction, lung perivascular edema and injury, atherosclerosis, adipose tissue inflammation, diabetic vascular disease and neuropathy are but a few examples evidencing the pivotal role of LPO and glycoxidation products in acute and chronic inflammatory disorders. Furthermore, the adducts of reactive aldehydes with cell proteins and DNA, referred to as mixed advanced lipoxidation end-products (ALEs) and glycoxidation end-products (AGEs), represent oxidation-specific epitopes, which act both as: 1) damage-associated molecular patterns, inciting flogosis and activating antigen-presenting cells, by binding to pattern-recognition receptors; and 2) neoepitopes derived from the modification of self epitopes, which can be instrumental in breaking the tolerance of autoreactive T and B cells to self antigens, as repeatedly observed in systemic lupus erythematosus, Sjogren’s syndrome and other autoimmune disease conditions, both in experimental animals and in humans. Direct immunological responses incited by self epitopes modified with LPO and glycoxidation products can be spread intramolecularly to unmodified epitopes of parent, formerly tolerated self antigens. Moreover, the ability of these reactive species to form adducts with a broad range of biomolecules may favour the intermolecular spreading of autoimmune responses to different proteins and nucleic acids. This Special Issue of Antioxidants aims to provide an update of this intriguing subject.

Dr. Fabrizio Gentile
Guest Editor

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Keywords

lipid peroxidation
reactive aldehydes
autoimmunity
immunity-driven inflammation
epitope spreading
tolerance breaking

Published Papers (10 papers)

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Research

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19 pages, 2390 KiB

Open AccessArticle

Oxidant/Antioxidant Status Is Impaired in Sepsis and Is Related to Anti-Apoptotic, Inflammatory, and Innate Immunity Alterations

by Marianna Miliaraki, Panagiotis Briassoulis, Stavroula Ilia, Kalliopi Michalakakou, Theodoros Karakonstantakis, Aikaterini Polonifi, Kalliopi Bastaki, Efrossini Briassouli, Konstantinos Vardas, Aikaterini Pistiki, Maria Theodorakopoulou, Theonymfi Tavladaki, Anna-Maria Spanaki, Eumorfia Kondili, Helen Dimitriou, Maria Venihaki, Sotirios Tsiodras, Dimitrios Georgopoulos, Marina Mantzourani, Serafeim Nanas, Apostolos Armaganidis, George L. Daikos, Ioannis Papassotiriou and George Briassoulis Show full author list Hide full author list

Antioxidants 2022, 11(2), 231; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020231 - 25 Jan 2022

Cited by 11 | Viewed by 3712

Abstract

Oxidative stress is considered pivotal in the pathophysiology of sepsis. Oxidants modulate heat shock proteins (Hsp), interleukins (IL), and cell death pathways, including apoptosis. This multicenter prospective observational study was designed to ascertain whether an oxidant/antioxidant imbalance is an independent sepsis discriminator and mortality predictor in intensive care unit (ICU) patients with sepsis (n = 145), compared to non-infectious critically ill patients (n = 112) and healthy individuals (n = 89). Serum total oxidative status (TOS) and total antioxidant capacity (TAC) were measured by photometric testing. IL-6, -8, -10, -27, Hsp72/90 (ELISA), and selected antioxidant biomolecules (Ζn, glutathione) were correlated with apoptotic mediators (caspase-3, capsase-9) and the central anti-apoptotic survivin protein (ELISA, real-time PCR). A wide scattering of TOS, TAC, and TOS/TAC in all three groups was demonstrated. Septic patients had an elevated TOS/TAC, compared to non-infectious critically ill patients and healthy individuals (p = 0.001). TOS/TAC was associated with severity scores, procalcitonin, IL-6, -10, -27, IFN-γ, Hsp72, Hsp90, survivin protein, and survivin isoforms -2B, -ΔΕx3, -WT (p < 0.001). In a propensity probability (age-sex-adjusted) logistic regression model, only sepsis was independently associated with TOS/TAC (Exp(B) 25.4, p < 0.001). The AUC_TOS/TAC (0.96 (95% CI = 0.93–0.99)) was higher than AUC_TAC (z = 20, p < 0.001) or AUC_TOS (z = 3.1, p = 0.002) in distinguishing sepsis. TOS/TAC, TOS, survivin isoforms -WT and -2B, Hsp90, IL-6, survivin protein, and repressed TAC were strong predictors of mortality (p < 0.01). Oxidant/antioxidant status is impaired in septic compared to critically ill patients with trauma or surgery and is related to anti-apoptotic, inflammatory, and innate immunity alterations. The unpredicted TOS/TAC imbalance might be related to undefined phenotypes in patients and healthy individuals. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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17 pages, 3152 KiB

Open AccessArticle

2-Oxo-Imidazole-Containing Dipeptides Play a Key Role in the Antioxidant Capacity of Imidazole-Containing Dipeptides

by Shingo Kasamatsu, Somei Komae, Kana Matsukura, Yuki Kakihana, Koji Uchida and Hideshi Ihara

Antioxidants 2021, 10(9), 1434; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10091434 - 08 Sep 2021

Cited by 7 | Viewed by 2915

Abstract

There is substantial evidence for the antioxidant functions of imidazole-containing dipeptides (IDPs), including carnosine and anserine, under physiological and pathological conditions in vivo. However, the detailed mechanism underlying the antioxidant functions is still poorly understood. Recently, we discovered the endogenous production of 2-oxo-imidazole-containing dipeptides (2-oxo-IDPs), such as 2-oxo-carnosine and 2-oxo-anserine, as novel derivatives of IDPs in mouse tissues and revealed that the antioxidant capacity of 2-oxo-carnosine was much greater than that of carnosine. However, the antioxidant capacity of 2-oxo-IDPs still remains unclear. In this study, we evaluated 2-oxo-carnosine and 2-oxo-anserine by multiple in vitro assays, such as 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging, ferric reducing/antioxidant power, and oxygen radical absorbance capacity assays in comparison with the corresponding IDPs, carnosine and anserine. All the assays employed herein demonstrated that 2-oxo-carnosine and 2-oxo-anserine exhibited a greater antioxidant capacity than that of the corresponding IDPs. Quantitative high-performance liquid chromatography tandem mass spectrometry revealed that commercial IDPs standards were contaminated with a certain amount of 2-oxo-IDPs, which was correlated with the antioxidant capacity. DPPH radical scavenging assay revealed that the elimination of contaminated 2-oxo-IDPs from the IDPs standards caused a significant decrease in the antioxidant capacity compared to the original IDPs standards. These results suggest that the main driver of the antioxidant capacity of IDPs is 2-oxo-IDPs; accordingly, the conversion of IDPs to 2-oxo-IDPs may be a critical step in the antioxidant functions. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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21 pages, 4272 KiB

Open AccessArticle

A Novel ALDH2 Activator AD-9308 Improves Diastolic and Systolic Myocardial Functions in Streptozotocin-Induced Diabetic Mice

by Hsiao-Lin Lee, Siow-Wey Hee, Chin-Feng Hsuan, Wenjin Yang, Jing-Yong Huang, Ya-Ling Lin, Chih-Neng Hsu, Juey-Jen Hwang, Shiau-Mei Chen, Zhi-Zhong Ding, Tung-Yuan Lee, Yu-Chiao Lin, Feng-Chiao Tsai, Wei-Lun Su, Li-Yun Chueh, Meng-Lun Hsieh, Che-Hong Chen, Daria Mochly-Rosen, Yi-Cheng Chang and Lee-Ming Chuang

Antioxidants 2021, 10(3), 450; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030450 - 13 Mar 2021

Cited by 6 | Viewed by 3888

Abstract

Diabetes mellitus has reached epidemic proportion worldwide. One of the diabetic complications is cardiomyopathy, characterized by early left ventricular (LV) diastolic dysfunction, followed by development of systolic dysfunction and ventricular dilation at a late stage. The pathogenesis is multifactorial, and there is no effective treatment yet. In recent years, 4-hydroxy-2-nonenal (4-HNE), a toxic aldehyde generated from lipid peroxidation, is implicated in the pathogenesis of cardiovascular diseases. Its high bioreactivity toward proteins results in cellular damage. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is the major enzyme that detoxifies 4-HNE. The development of small-molecule ALDH2 activator provides an opportunity for treating diabetic cardiomyopathy. This study found that AD-9308, a water-soluble andhighly selective ALDH2 activator, can improve LV diastolic and systolic functions, and wall remodeling in streptozotocin-induced diabetic mice. AD-9308 treatment dose-dependently lowered serum 4-HNE levels and 4-HNE protein adducts in cardiac tissue from diabetic mice, accompanied with ameliorated myocardial fibrosis, inflammation, and apoptosis. Improvements of mitochondrial functions, sarco/endoplasmic reticulumcalcium handling and autophagy regulation were also observed in diabetic mice with AD-9308 treatment. In conclusion, ADLH2 activation effectively ameliorated diabetic cardiomyopathy, which may be mediated through detoxification of 4-HNE. Our findings highlighted the therapeutic potential of ALDH2 activation for treating diabetic cardiomyopathy. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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15 pages, 2729 KiB

Open AccessArticle

CUPRAC-Reactive Advanced Glycation End Products as Prognostic Markers of Human Acute Myocardial Infarction

by Govigerel Bayarsaikhan, Delger Bayarsaikhan, Pyung Chun Oh, Woong Chol Kang and Bonghee Lee

Antioxidants 2021, 10(3), 434; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030434 - 11 Mar 2021

Cited by 4 | Viewed by 2608

Abstract

Cardiovascular disorders, especially acute coronary syndromes, are among the leading causes of mortality worldwide, and advanced glycation end products (AGEs) are associated with cardiovascular disease and serve as biomarkers for diagnosis and prediction. In this study, we investigated the utility of AGEs as prognostic biomarkers for acute myocardial infarction (AMI). We measured AGEs in serum samples of AMI patients (N = 27) using the cupric ion reducing antioxidant capacity (CUPRAC) method on days 0, 2, 14, 30, and 90 after AMI, and the correlation of serum AGE concentration and post-AMI duration was determined using Spearman’s correlation analysis. Compared to total serum protein, the level of CUPRAC reactive AGEs was increased from 0.9 to 2.1 times between 0–90 days after AMI incident. Furthermore, the glycation pattern and Spearman’s correlation analysis revealed four dominant patterns of AGE concentration changes in AMI patients: stable AGE levels (straight line with no peak), continuous increase, single peak pattern, and multimodal pattern (two or more peaks). In conclusion, CUPRAC-reactive AGEs can be developed as a potential prognostic biomarker for AMI through long-term clinical studies. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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13 pages, 12691 KiB

Open AccessArticle

Prevention of Autoimmune Diabetes in NOD Mice by Dimethyl Fumarate

by Shiri Li, Nosratola D. Vaziri, Lourdes Swentek, Chie Takasu, Kelly Vo, Michael J. Stamos, Camillo Ricordi and Hirohito Ichii

Antioxidants 2021, 10(2), 193; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10020193 - 29 Jan 2021

Cited by 8 | Viewed by 2515

Abstract

Oxidative stress plays critical roles in the pathogenesis of diabetes. This study tested the hypothesis that by protecting β-cells against oxidative stress and inflammation, an Nrf2 activator, dimethyl fumarate (DMF), may prevent or delay the onset of type 1 diabetes in non-obese diabetic (NOD) mice. Firstly, islet isolation was conducted to confirm the antioxidative effects of DMF oral administration on islet cells. Secondly, in a spontaneous diabetes model, DMF (25 mg/kg) was fed to mice once daily starting at the age of 8 weeks up to the age of 22 weeks. In a cyclophosphamide-induced accelerated diabetes model, DMF (25 mg/kg) was fed to mice twice daily for 2 weeks. In the islet isolation study, DMF administration improved the isolation yield, attenuated oxidative stress and enhanced GCLC and NQO1 expression in the islets. In the spontaneous model, DMF significantly reduced the onset of diabetes compared to the control group (25% vs. 54.2%). In the accelerated model, DMF reduced the onset of diabetes from 58.3% to 16.7%. The insulitis score in the islets of the DMF treatment group (1.6 ± 0.32) was significantly lower than in the control group (3.47 ± 0.21). The serum IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-9, IL-12p70, IFN-γ, TNF-α, MCP-1 and CXCL16 levels in the DMF-treated group were lower than in the control group. In conclusion, DMF may protect islet cells and reduce the incidence of autoimmune diabetes in NOD mice by attenuating insulitis and proinflammatory cytokine production. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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14 pages, 1934 KiB

Open AccessArticle

Serum Selenium Status and Its Interrelationship with Serum Biomarkers of Thyroid Function and Antioxidant Defense in Hashimoto’s Thyroiditis

by Rahim Rostami, Sarmad Nourooz-Zadeh, Afshin Mohammadi, Hamid Reza Khalkhali, Gordon Ferns and Jaffar Nourooz-Zadeh

Antioxidants 2020, 9(11), 1070; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9111070 - 31 Oct 2020

Cited by 19 | Viewed by 4089

Abstract

Selenium (Se) deficiency has been implicated in the pathogenesis of Hashimoto’s thyroiditis (HT), although the available evidence is limited. The present study aimed to explore the interrelationships between serum Se status with measures of thyroid function and antioxidant defense in new cases of HT patients with hypoechogenic thyroid. HT patients (n = 49) and matched controls (n = 50) were recruited. Selenium, thyroid hormone panel, thyroid volume (TVol), glutathione (GSH), glutathione peroxidase3 (GPx3) activity, urinary iodine concentration (UIC), and urinary creatinine (Cr) were assessed. HT patients exhibited lower Se levels compared to controls (p < 0.001) with the rates of Se-deficient (<0.85 µmol/L) participants being 58.8% and 34%, respectively. Se-deficient patients exhibited higher thyroid stimulating hormone (TSH), Thyroid volume (TVol), thyroglobulin, antibody-titers, GPx3 activity and UIC/Cr compared to Se-sufficient patients (all p < 0.001). In the Se-deficient patients, inverse correlations were seen between Se-levels with TSH, TVol, and Thyroid peroxidase antibody (TPO-Ab) (all p < 0.001). This study is the first to uncover that coexisting Se-deficiency and elevated iodine in HT may enhance autoimmune reactions and accelerate the deterioration of thyroid function through oxidative stress. Our study also highlights the importance of optimal Se status in this disease, thus providing a rationale for the execution of intervention trials for the evaluation of the clinical benefits of antioxidant-status improvement in HT. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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Review

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21 pages, 950 KiB

Open AccessReview

Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress

by Govigerel Bayarsaikhan, Delger Bayarsaikhan, Jaewon Lee and Bonghee Lee

Antioxidants 2022, 11(5), 936; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050936 - 09 May 2022

Cited by 7 | Viewed by 3075

Abstract

Oxidative stress and inflammation cannot be considered as diseases themselves; however, they are major risk factors for the development and progression of the pathogenesis underlying many illnesses, such as cancer, neurological disorders (including Alzheimer’s disease and Parkinson’s disease), autoimmune and metabolic disorders, etc. According to the results obtained from extensive studies, oxidative stress–induced biomolecules, such as advanced oxidation protein products, advanced glycation end products, and advanced lipoxidation end products, are critical for an accelerated level of inflammation and oxidative stress–induced cellular damage, as reflected in their strong affinity to a wide range of scavenger receptors. Based on the limitations of antioxidative and anti-inflammatory molecules in practical applications, targeting such interactions between harmful molecules and their cellular receptors/signaling with advances in gene engineering technology, such as CRISPR or TALEN, may prove to be a safe and effective alternative. In this review, we summarize the findings of recent studies focused on the deletion of scavenger receptors under oxidative stress as a development in the therapeutic approaches against the diseases linked to inflammation and the contribution of advanced glycation end products (AGEs), advanced lipid peroxidation products (ALEs), and advanced oxidation protein products (AOPPs). Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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27 pages, 1997 KiB

Open AccessReview

Sickle Cell Disease: Role of Oxidative Stress and Antioxidant Therapy

by Rosa Vona, Nadia Maria Sposi, Lorenza Mattia, Lucrezia Gambardella, Elisabetta Straface and Donatella Pietraforte

Antioxidants 2021, 10(2), 296; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10020296 - 16 Feb 2021

Cited by 40 | Viewed by 7452

Abstract

Sickle cell disease (SCD) is the most common hereditary disorder of hemoglobin (Hb), which affects approximately a million people worldwide. It is characterized by a single nucleotide substitution in the β-globin gene, leading to the production of abnormal sickle hemoglobin (HbS) with multi-system consequences. HbS polymerization is the primary event in SCD. Repeated polymerization and depolymerization of Hb causes oxidative stress that plays a key role in the pathophysiology of hemolysis, vessel occlusion and the following organ damage in sickle cell patients. For this reason, reactive oxidizing species and the (end)-products of their oxidative reactions have been proposed as markers of both tissue pro-oxidant status and disease severity. Although more studies are needed to clarify their role, antioxidant agents have been shown to be effective in reducing pathological consequences of the disease by preventing oxidative damage in SCD, i.e., by decreasing the oxidant formation or repairing the induced damage. An improved understanding of oxidative stress will lead to targeted antioxidant therapies that should prevent or delay the development of organ complications in this patient population. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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Graphical abstract

21 pages, 1040 KiB

Open AccessReview

Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations

by Helena Beatriz Ferreira, Tânia Melo, Artur Paiva and Maria do Rosário Domingues

Antioxidants 2021, 10(1), 45; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10010045 - 02 Jan 2021

Cited by 38 | Viewed by 5065

Abstract

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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13 pages, 19743 KiB

Open AccessReview

Systematic Review and Meta-Analysis of the Blood Glutathione Redox State in Chronic Obstructive Pulmonary Disease

by Salvatore Sotgia, Panagiotis Paliogiannis, Elisabetta Sotgiu, Sabrina Mellino, Elisabetta Zinellu, Alessandro G. Fois, Pietro Pirina, Ciriaco Carru, Arduino A. Mangoni and Angelo Zinellu

Antioxidants 2020, 9(11), 1146; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9111146 - 18 Nov 2020

Cited by 17 | Viewed by 3119

Abstract

The aim of this systematic review and meta-analysis was to assess the blood concentrations of the total and reduced forms of the low-molecular-weight antioxidant thiol glutathione (GSH) in chronic obstructive pulmonary disease (COPD) patients in comparison to healthy individuals. A literature search was conducted in the PubMed and Web of Science databases from inception until June 2020. In the 18 studies identified (involving a total of 974 COPD patients and 631 healthy controls), the pooled reduced GSH concentrations were significantly lower in patients with COPD than controls (SMD = −3.04, 95% CI = −4.42 to −1.67; p < 0.001). By contrast, the pooled total GSH concentrations were significantly higher in patients with COPD than controls (SMD = 0.42, 95% CI = 0.11 to 0.73; p = 0.009). Our meta-analysis showed that the blood concentrations of reduced GSH, even in the presence of higher total GSH concentrations, were significantly lower in patients with COPD when compared to healthy controls. This suggests that an impaired antioxidant defense system plays an important role in the pathogenesis of COPD. Full article

(This article belongs to the Special Issue Oxidative Stress, Lipid Peroxidation and Glycoxidation Products in Inflammation, Autoimmunity and Immunity-Driven Inflammation)

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