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Oxidative Stress, Metabolic and Inflammatory 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 (10 August 2022) | Viewed by 30326

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Special Issue Editors

Dr. Pilar Zafrilla

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Department of Pharmacy, Faculty of Health Sciences, Universidad Católica San Antonio de Murcia (UCAM), Campus de los Jerónimos, Guadalupe, 30107 Murcia, Spain
Interests: clinical trials; oxidative stress; bioavailability; bioactive compounds; inflammation; Endothelial damage markers
Special Issues, Collections and Topics in MDPI journals

Dr. Javier Marhuenda

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Department of Pharmacy, Faculty of Health Sciences, Universidad Católica San Antonio de Murcia (UCAM), Campus de los Jerónimos, 30107 Guadalupe, Murcia, Spain
Interests: oxidative stress; polyphenols; bioactive compounds; bioavailability; metabolomics
Special Issues, Collections and Topics in MDPI journals

Dr. Begoña Cerdá

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Department of Pharmacy, Faculty of Pharmacy and Nutrition, Universidad Católica San Antonio de Murcia (UCAM), Campus de los Jerónimos, Guadalupe, 30107 Murcia, Spain
Interests: oxidative stress; bioavailability; ellagitanins; bioactive compounds; microbiota; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Metabolic pathologies syndrome, also known as metabolic syndrome, and inflammatory diseases represent a public health problem worldwide. The latest studies propose that these pathologies may result from different pathophysiological mechanisms, which could be participating simultaneously. Among them, oxidative stress stands out, produced by the alteration of the balance between antioxidant mechanisms and the production of pro-oxidant molecules. Oxidative stress stimulates the production of cytokines (interleukin (IL) 6, Tumor Necrosis Factor alpha (TNF-α), IL-8 and IL-18, among others) that initiate an inflammatory response and thus an alteration in the metabolism of carbohydrates, lipids and proteins. In addition, the increase in pro-oxidant secretion is suggested to be responsible for the generation of insulin resistance in skeletal muscle, adipose tissue and the alteration in insulin secretion by the α cells of the pancreas. The accumulation of pro-oxidant molecules in the body causes damage and induces the activation of specific pathways—both of these events lead to cell proliferation, dysfunction, adaptation or death.

Therefore, with regard to the latest advances in the detection of oxidative damage and the new bioactive compounds described in recent years, we consider it important to collect information on new advances in the treatment of this type of disease.

Dr. Pilar Zafrilla
Dr. Javier Marhuenda
Dr. Begoña Cerdá
Guest Editors

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Keywords

oxidative stress
metabolic syndrome
inflammation
metabolic diseases

Published Papers (10 papers)

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Research

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14 pages, 1756 KiB

Open AccessArticle

Ability of a Polyphenol-Rich Nutraceutical to Reduce Central Nervous System Lipid Peroxidation by Analysis of Oxylipins in Urine: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial

by Raúl Arcusa, Juan Ángel Carillo, Begoña Cerdá, Thierry Durand, Ángel Gil-Izquierdo, Sonia Medina, Jean-Marie Galano, María Pilar Zafrilla and Javier Marhuenda

Antioxidants 2023, 12(3), 721; https://doi.org/10.3390/antiox12030721 - 14 Mar 2023

Cited by 2 | Viewed by 1418

Abstract

Isoprostanes (IsoPs) are lipid peroxidation biomarkers that reveal the oxidative status of the organism without specifying which organs or tissues it occurs in. Similar compounds have recently been identified that can assess central nervous system (CNS) lipid peroxidation status, usually oxidated by reactive oxygen species. These compounds are the neuroprostanes (NeuroPs) derived from eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and the F_2t-dihomo-isoprotanes derived from adrenic acid (AdA). The aim of the present investigation was to evaluate whether the long-term nutraceutical consumption of high polyphenolic contents (600 mg) from fruits (such as berries) and vegetables shows efficacy against CNS lipid peroxidation in urine biomarkers. A total of 92 subjects (47 females, 45 males, age 34 ± 11 years old, weight 73.10 ± 14.29 kg, height 1.72 ± 9 cm, body mass index (BMI) 24.40 ± 3.43 kg/m²) completed a randomized, cross-over, double-blind study after an intervention of two periods of 16 weeks consuming either extract (EXT) or placebo (PLA) separated by a 4-week washout period. The results showed significant reductions in three AdA-derived metabolites, namely, 17-epi-17-F_2t-dihomo-IsoPs (Δ −1.65 ng/mL; p < 0.001), 17-F_2t-dihomo-IsoPs (Δ −0.17 ng/mL; p < 0.015), and ent-7(RS)-7-F_2t-dihomo-IsoPs (Δ −1.97 ng/mL; p < 0.001), and one DHA-derived metabolite, namely, 4-F_4t-NeuroP (Δ −7.94 ng/mL; p < 0.001), after EXT consumption, which was not observed after PLA consumption. These data seem to show the effectiveness of the extract for preventing CNS lipid peroxidation, as determined by measurements of oxylipins in urine through Ultra-High-Performance Liquid Chromatography triple quadrupole tandem mass spectrometry (UHPLC-QqQ-ESI-MS/MS). Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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23 pages, 5208 KiB

Open AccessArticle

Carob Extract Supplementation Together with Caloric Restriction and Aerobic Training Accelerates the Recovery of Cardiometabolic Health in Mice with Metabolic Syndrome

by Maria de la Fuente-Fernández, Mario de la Fuente-Muñoz, Marta Román-Carmena, Sara Amor, Ana Belén García-Redondo, Javier Blanco-Rivero, Daniel González-Hedström, Alberto E. Espinel, Ángel Luís García-Villalón and Miriam Granado

Antioxidants 2022, 11(9), 1803; https://doi.org/10.3390/antiox11091803 - 13 Sep 2022

Cited by 2 | Viewed by 2261

Abstract

Carob, the fruit of Ceratonia siliqua L. exerts antidiabetic, anti-inflammatory, and antioxidant effects and could be a useful strategy for the treatment and/or prevention of metabolic syndrome (MetS). The aim of this study was to analyze whether supplementation with a carob fruit extract (CSAT+^®), alone or in combination with aerobic training, accelerates the recovery of cardiometabolic health in mice with MetS subjected to a caloric restriction. For this purpose, mice were fed with a high fat (58% kcal from fat)/high sugar diet for 23 weeks to induce MetS. During the next two weeks, mice with MetS were switched to a diet with a lower caloric content (25% kcal from fat) supplemented or not with CSAT+^® (4.8%) and/or subjected to aerobic training. Both caloric reduction and aerobic training improved the lipid profile and attenuated MetS-induced insulin resistance measured as HOMA-IR. However, only supplementation with CSAT+^® enhanced body weight loss, increased the circulating levels of adiponectin, and lowered the plasma levels of IL-6. Moreover, CSAT+^® supplementation was the only effective strategy to reduce the weight of epidydimal adipose tissue and to improve insulin sensitivity in the liver and in skeletal muscle. Although all interventions improved endothelial function in aorta segments, only supplementation with CSAT+^® reduced obesity-induced hypertension, prevented endothelial dysfunction in mesenteric arteries, and decreased the vascular response of aorta segments to the vasoconstrictor AngII. The beneficial cardiometabolic effects of CSAT+^® supplementation, alone or in combination with aerobic training, were associated with decreased mRNA levels of pro-inflammatory markers such as MCP-1, TNFα, IL-1β, and IL-6 and with increased gene expression of antioxidant enzymes, such as GSR, GPX-3, and SOD-1 in the liver, gastrocnemius, retroperitoneal adipose tissue, and aorta. In conclusion, supplementation with CSAT+^®, alone or in combination with aerobic training, to mice with MetS subjected to caloric restriction for two weeks enhances body weight loss, improves the lipid profile and insulin sensitivity, and exerts antihypertensive effects through its anti-inflammatory and antioxidant properties. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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16 pages, 1618 KiB

Open AccessArticle

Anti-Inflammatory and Antioxidant Capacity of a Fruit and Vegetable-Based Nutraceutical Measured by Urinary Oxylipin Concentration in a Healthy Population: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial

by Raúl Arcusa, Juan Ángel Carrillo, Begoña Cerdá, Thierry Durand, Ángel Gil-Izquierdo, Sonia Medina, Jean-Marie Galano, Débora Villaño Valencia, Javier Marhuenda and Pilar Zafrilla

Antioxidants 2022, 11(7), 1342; https://doi.org/10.3390/antiox11071342 - 8 Jul 2022

Cited by 4 | Viewed by 2178

Abstract

Oxylipins, lipid biomarkers of inflammation are considered the gold standard method to evaluate the inflammatory and antioxidant status. The aim of the present study was to investigate whether the administration of a polyphenolic extract shot in the form of a nutraceutical was able to reduce inflammation, measured in urine markers. Ninety-two participants (45 males, 47 females, age 34 ± 11 years, weight 73.10 ± 14.29 kg, height 1.72 ± 9 cm, BMI 24.40 ± 3.43 kg/m²) completed the study after an intervention of two 16-week periods consuming extract or placebo separated by a 4-week washout period. The results showed significant differences in terms of reduction of different pro-inflammatory oxylipins (15-keto-PGF_2α (from 0.90 ± 0.25 ng/mL to 0.74 ± 0.19 ng/mL p < 0.05), ent-PGF_2α (from 1.59 ± 0.37 ng/mL to 1.44 ± 0.32 ng/mL p < 0.05), 2,3-dinor-15-F_2t-Isop) (from 1.17 ± 0.35 ng/mL to 1.02 ± 0.27 ng/mL p < 0.05), in total oxylipins count (from 8.03 ± 1.86 ng/mL to 7.25 ± 1.23 ng/mL p < 0.05), and increase in PGE₂ (from 1.02 ± 0.38 ng/mL to 1.26 ± 0.38 ng/mL p < 0.05) which has an anti-inflammatory character, after extract consumption compared to placebo. The available data seem to indicate that long-term consumption of a nutraceutical with high polyphenol content improves inflammation and oxidation parameters measured in urine, through UHPLC-QqQ-ESI-MS/MS. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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11 pages, 2001 KiB

Open AccessArticle

Substance P Hinders Bile Acid-Induced Hepatocellular Injury by Modulating Oxidative Stress and Inflammation

by Dahyeon Lee, Jeong Seop Park, Doyoung Kim and Hyun Sook Hong

Antioxidants 2022, 11(5), 920; https://doi.org/10.3390/antiox11050920 - 7 May 2022

Cited by 8 | Viewed by 1824

Abstract

Liver failure is an outcome of chronic liver disease caused by steatohepatitis and cholestatic injury. This study examined substance P (SP) effect on liver injury due to cholestatic stress caused by excessive bile acid (BA) accumulation. Chenodeoxycholic acid (CDCA) was added to HepG2 cells to induce hepatic injury, and cellular alterations were observed within 8 h. After confirming BA-mediated cellular injury, SP was added, and its restorative effect was evaluated through cell viability, reactive oxygen species (ROS)/inflammatory cytokines/endothelial cell media expression, and adjacent liver sinusoidal endothelial cell (LSEC) function. CDCA treatment provoked ROS production, followed by IL-8 and ICAM-1 expression in hepatocytes within 8 h, which accelerated 24 h post-treatment. Caspase-3 signaling was activated, reducing cell viability and promoting alanine aminotransferase release. Interestingly, hepatocyte alteration by CDCA stress could affect LSEC activity by decreasing cell viability and disturbing tube-forming ability. In contrast, SP treatment reduced ROS production and blocked IL-8/ICAM-1 in CDCA-injured hepatocytes. SP treatment ameliorated the effect of CDCA on LSECs, preserving cell viability and function. Collectively, SP could protect hepatocytes and LSECs from BA-induced cellular stress, possibly by modulating oxidative stress and inflammation. These results suggest that SP can be used to treat BA-induced liver injury. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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15 pages, 1850 KiB

Open AccessArticle

The Influence of Coronary Artery Disease in the Development of Aortic Stenosis and the Importance of the Albumin Redox State

by Tamara Sastre-Oliva, Nerea Corbacho-Alonso, Diego Albo-Escalona, Juan A. Lopez, Luis F. Lopez-Almodovar, Jesús Vázquez, Luis R. Padial, Laura Mourino-Alvarez and Maria G. Barderas

Antioxidants 2022, 11(2), 317; https://doi.org/10.3390/antiox11020317 - 5 Feb 2022

Cited by 6 | Viewed by 1955

Abstract

Calcific aortic valve and coronary artery diseases are related cardiovascular pathologies in which common processes lead to the calcification of the corresponding affected tissue. Among the mechanisms involved in calcification, the oxidative stress that drives the oxidation of sulfur-containing amino acids such ascysteines is of particular interest. However, there are important differences between calcific aortic valve disease and coronary artery disease, particularly in terms of the reactive oxygen substances and enzymes involved. To evaluate what effect coronary artery disease has on aortic valves, we analyzed valve tissue from patients with severe calcific aortic stenosis with and without coronary artery disease. Proteins and peptides with oxidized cysteines sites were quantified, leading to the identification of 16 proteins with different levels of expression between the two conditions studied, as well as differences in the redox state of the tissue. We also identified two specific sites of cysteine oxidation in albumin that have not been described previously. These results provide evidence that coronary artery disease affects valve calcification, modifying the molecular profile of aortic valve tissue. In addition, the redox proteome is also altered when these conditions coincide, notably affecting human serum albumin. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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16 pages, 7054 KiB

Open AccessArticle

Hepatic Homeostasis of Metal Ions Following Acute Repeated Stress Exposure in Rats

by Jereme G. Spiers, Li Si Tan, Stephen T. Anderson, Andrew F. Hill, Nickolas A. Lavidis and Hsiao-Jou Cortina Chen

Antioxidants 2022, 11(1), 85; https://doi.org/10.3390/antiox11010085 - 29 Dec 2021

Cited by 2 | Viewed by 2059

Abstract

Essential metals such as copper, iron, and zinc are cofactors in various biological processes including oxygen utilisation, cell growth, and biomolecular synthesis. The homeostasis of these essential metals is carefully controlled through a system of protein transporters involved in the uptake, storage, and secretion. Some metal ions can be transformed by processes including reduction/oxidation (redox) reactions, and correspondingly, the breakdown of metal ion homeostasis can lead to formation of reactive oxygen and nitrogen species. We have previously demonstrated rapid biochemical responses to stress involving alterations in the redox state to generate free radicals and the resultant oxidative stress. However, the effects of stress on redox-active metals including iron and copper and redox-inert zinc have not been well characterised. Therefore, this study aims to examine the changes in these essential metals following exposure to short-term repeated stress, and to further elucidate the alterations in metal homeostasis through expression analysis of different metal transporters. Outbred male Wistar rats were exposed to unrestrained (control), 1 day, or 3 days of 6 h restraint stress (n = 8 per group). After the respective stress treatment, blood and liver samples were collected for the analysis of biometal concentrations and relative gene expression of metal transporter and binding proteins. Exposure to repeated restraint stress was highly effective in causing hepatic redox imbalance. Stress was also shown to induce hepatic metal redistribution, while modulating the mRNA levels of key metal transporters. Overall, this study is the first to characterise the gene expression profile of metal homeostasis following stress and provide insight into the changes occurring prior to the onset of chronic stress conditions. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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20 pages, 4273 KiB

Open AccessArticle

Oxidative Stress Does Not Influence Subjective Pain Sensation in Inflammatory Bowel Disease Patients

by Anna Krystyna Zielińska, Maciej Sałaga, Paweł Siwiński, Marcin Włodarczyk, Adam Dziki and Jakub Fichna

Antioxidants 2021, 10(8), 1237; https://doi.org/10.3390/antiox10081237 - 1 Aug 2021

Cited by 11 | Viewed by 2321

Abstract

Oxidative stress (OS) has been proposed as a significant causative and propagating factor in inflammatory bowel diseases (IBDs). Modulation of OS is possible through antioxidants and inhibition of oxidizing enzymes. Thirty-one IBD patients and thirty-two controls were included in the study. The aim was to examine the levels of OS in colonic tissue of IBD requiring surgical intervention and control group, and their association with pain intensity. Total antioxidant capacity (TAC), superoxide dismutase (SOD) and catalase (CAT) activity, glutathione (GSH) and oxidized glutathione (GSSG) levels, and glutathione peroxidase (GPX) activity as markers of antioxidant defense were determined. Cyclooxygenases activities (Total COX, COX-1 and COX-2) were measured as prooxidant enzymes. Thiobarbituric acid reactive substances (TBARS) concentrations were measured to evaluate lipid peroxidation. Disease activity was assessed, and each subject filled out VAS and Laitinen’s pain assessment scales. Correlation between the OS, pain intensity, disease activity parameters, C-reactive protein (CRP), number of stools passed daily, disease duration, and dietary habits was investigated. No TAC differences were found between the groups. A significant decrease of SOD activity and GSH and GSSG levels was seen in IBD patients vs. controls, while GPX activity was diminished significantly only in CD patients. CAT and COX-1 activity was increased, and COX-2 significantly decreased in IBD. TBARS were significantly higher in CD patients compared to control group. No correlation was found between pain scores, inflammatory status, disease activity, disease duration, or dietary habits and OS markers. In our study, OS did not influence pain sensation reported by IBD patients. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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18 pages, 4431 KiB

Open AccessArticle

Hydroquinone Exposure Worsens Rheumatoid Arthritis through the Activation of the Aryl Hydrocarbon Receptor and Interleukin-17 Pathways

by Cintia Scucuglia Heluany, Paula Barbim Donate, Ayda Henriques Schneider, André Luis Fabris, Renan Augusto Gomes, Isadora Maria Villas-Boas, Denise Vilarinho Tambourgi, Tarcilia Aparecida da Silva, Gustavo Henrique Goulart Trossini, Giovanna Nalesso, Eduardo Lani Volpe Silveira, Fernando Queiroz Cunha and Sandra Helena Poliselli Farsky

Antioxidants 2021, 10(6), 929; https://doi.org/10.3390/antiox10060929 - 7 Jun 2021

Cited by 5 | Viewed by 2699

Abstract

Rheumatoid arthritis (RA) development is strongly associated with cigarette smoke exposure, which activates the aryl hydrocarbon receptor (AhR) as a trigger for Th17 inflammatory pathways. We previously demonstrated that the exposure to hydroquinone (HQ), one of the major compounds of cigarette tar, aggravates the arthritis symptomatology in rats. However, the mechanisms related to the HQ-related RA still remain elusive. Cell viability, cytokine secretion, and gene expression were measured in RA human fibroblast-like synoviocytes (RAHFLS) treated with HQ and stimulated or not with TNF-α. Antigen-induced arthritis (AIA) was also elicited in wild type (WT), AhR ^−/− or IL-17R ^−/− C57BL/6 mice upon daily exposure to nebulized HQ (25ppm) between days 15 to 21. At day 21, mice were challenged with mBSA and inflammatory parameters were assessed. The in vitro HQ treatment up-regulated TNFR1, TNFR2 expression, and increased ROS production. The co-treatment of HQ and TNF-α enhanced the IL-6 and IL-8 secretion. However, the pre-incubation of RAHFLS with an AhR antagonist inhibited the HQ-mediated cell proliferation and gene expression profile. About the in vivo approach, the HQ exposure worsened the AIA symptoms (edema, pain, cytokines secretion and NETs formation) in WT mice. These AIA effects were abolished in HQ-exposed AhR ^−/− and IL-17R ^−/− animals though. Our data demonstrated the harmful HQ influence over the onset of arthritis through the activation and proliferation of synoviocytes. The HQ-related RA severity was also associated with the activation of AhR and IL-17 pathways, highlighting how cigarette smoke compounds can contribute to the RA progression. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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Review

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23 pages, 1184 KiB

Open AccessReview

Macrophage Polarization and Reprogramming in Acute Inflammation: A Redox Perspective

by Salvador Pérez and Sergio Rius-Pérez

Antioxidants 2022, 11(7), 1394; https://doi.org/10.3390/antiox11071394 - 19 Jul 2022

Cited by 58 | Viewed by 8703

Abstract

Macrophage polarization refers to the process by which macrophages can produce two distinct functional phenotypes: M1 or M2. The balance between both strongly affects the progression of inflammatory disorders. Here, we review how redox signals regulate macrophage polarization and reprogramming during acute inflammation. In M1, macrophages augment NADPH oxidase isoform 2 (NOX2), inducible nitric oxide synthase (iNOS), synaptotagmin-binding cytoplasmic RNA interacting protein (SYNCRIP), and tumor necrosis factor receptor-associated factor 6 increase oxygen and nitrogen reactive species, which triggers inflammatory response, phagocytosis, and cytotoxicity. In M2, macrophages down-regulate NOX2, iNOS, SYNCRIP, and/or up-regulate arginase and superoxide dismutase type 1, counteract oxidative and nitrosative stress, and favor anti-inflammatory and tissue repair responses. M1 and M2 macrophages exhibit different metabolic profiles, which are tightly regulated by redox mechanisms. Oxidative and nitrosative stress sustain the M1 phenotype by activating glycolysis and lipid biosynthesis, but by inhibiting tricarboxylic acid cycle and oxidative phosphorylation. This metabolic profile is reversed in M2 macrophages because of changes in the redox state. Therefore, new therapies based on redox mechanisms have emerged to treat acute inflammation with positive results, which highlights the relevance of redox signaling as a master regulator of macrophage reprogramming. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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18 pages, 886 KiB

Open AccessReview

A Comprehensive Analysis of the Role of Oxidative Stress in the Pathogenesis and Chemoprevention of Oral Submucous Fibrosis

by Luciano Saso, Ahmad Reza, Emily Ng, Kimtrang Nguyen, Sheng Lin, Pangzhen Zhang, Paolo Junior Fantozzi, Guliz Armagan, Umberto Romeo and Nicola Cirillo

Antioxidants 2022, 11(5), 868; https://doi.org/10.3390/antiox11050868 - 28 Apr 2022

Cited by 13 | Viewed by 3372

Abstract

Oral submucous fibrosis (OSMF) is a chronic oral potentially malignant disorder (OPMD). It is described as a scarring disease of the oral mucosa associated with excess oxidants and insufficient antioxidants. While it is becoming increasingly accepted that oxidative stress results in excessive accumulation of collagen and progressive fibrosis of the submucosal tissues, there is limited data regarding the moderation of oxidative stress to initiate or prevent OSMF. To assess the scope for mechanism-based approaches to prevent or reverse OSMF, we systematically evaluated the existing literature and investigated the role of oxidative stress in the pathogenesis and chemoprevention of OSMF. A search for relevant articles on PubMed and Scopus was undertaken using pre-defined inclusion and exclusion criteria. A total of 78 articles were selected in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines. The articles eligible for assessment investigated both OSMF and/or oxidative stress biomarkers or specific antioxidants. Both in vitro and human studies consistently demonstrated variations in oxidative stress biomarker levels in OSMF and revealed an increase in oxidative stress, paralleling the development of the disease. Furthermore, the use of antioxidant supplements was overall associated with an improvement in clinical outcomes. Having identified the significance of oxidative stress in OSMF and the therapeutic potential of antioxidant supplements, this scoping review highlights the need for further well-designed studies in the development of mechanism-based interventions for managing OSMF. Full article

(This article belongs to the Special Issue Oxidative Stress, Metabolic and Inflammatory Diseases)

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