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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 (31 May 2023) | Viewed by 8544

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Dr. Vicente C. Zanon-Moreno

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Guest Editor

Faculty of Health Sciences, International University of Valencia, 46002 Valencia, Spain
Interests: ophthalmology; epidemiology; public health; omic sciences; molecular biology
Special Issues, Collections and Topics in MDPI journals

Dr. Vicente Andreu-Fernández

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Faculty of Health Sciences, International University of Valencia, 46002 Valencia, Spain
Interests: rare diseases; fetal alcohol spectrum disorders; perinatal environment; addictions; alcohol; epidemiology
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Dear Colleagues,

As you well know, oxidation is a process inherent to life. Oxygen allows us to breathe and helps the human body to perform many functions. However, it is also the cause of certain harmful effects, such as oxidative stress.

Oxidative stress, an imbalance between the production of reactive oxygen species and antioxidant compounds and molecules, has been associated with chronic diseases (diabetes, eye diseases, heart disease, cancer, kidney diseases, respiratory diseases, etc.). Free radicals cause alterations in lipids, proteins, fatty acids, and nucleic acids, leading to cell death by apoptosis.

A proper diet can help to combat oxidative stress by incorporating foods high in antioxidants. Nevertheless, it is necessary to properly design the diet since some foods that contain antioxidants also contain pro-oxidant compounds, so their consumption could be counterproductive to combat oxidative stress.

This Special Issue on "Oxidative Stress, Diet and Chronic Disease" aims to collect original articles and systematic reviews on oxidative stress and risk of chronic disease, as well as dietetic interventions to reduce the harmful effect of oxidative stress.

Dr. Vicente Zanon-Moreno
Dr. Vicente Andreu-Fernández
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
nutrition
natural therapy
prevention
chronic disease

Published Papers (4 papers)

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Research

29 pages, 3585 KiB

Open AccessArticle

Associations between the New DNA-Methylation-Based Telomere Length Estimator, the Mediterranean Diet and Genetics in a Spanish Population at High Cardiovascular Risk

by Oscar Coltell, Eva M. Asensio, José V. Sorlí, Carolina Ortega-Azorín, Rebeca Fernández-Carrión, Eva C. Pascual, Rocío Barragán, José I. González, Ramon Estruch, Juan F. Alzate, Alejandro Pérez-Fidalgo, Olga Portolés, Jose M. Ordovas and Dolores Corella

Antioxidants 2023, 12(11), 2004; https://doi.org/10.3390/antiox12112004 - 15 Nov 2023

Viewed by 1325

Abstract

Biological aging is a relevant risk factor for chronic diseases, and several indicators for measuring this factor have been proposed, with telomere length (TL) among the most studied. Oxidative stress may regulate telomere shortening, which is implicated in the increased risk. Using a novel estimator for TL, we examined whether adherence to the Mediterranean diet (MedDiet), a highly antioxidant-rich dietary pattern, is associated with longer TL. We determined TL using DNA methylation algorithms (DNAmTL) in 414 subjects at high cardiovascular risk from Spain. Adherence to the MedDiet was assessed by a validated score, and genetic variants in candidate genes and at the genome-wide level were analyzed. We observed several significant associations (p < 0.05) between DNAmTL and candidate genes (TERT, TERF2, RTEL1, and DCAF4), contributing to the validity of DNAmTL as a biomarker in this population. Higher adherence to the MedDiet was associated with lower odds of having a shorter TL in the whole sample (OR = 0.93; 95% CI: 0.85–0.99; p = 0.049 after fully multivariate adjustment). Nevertheless, this association was stronger in women than in men. Likewise, in women, we observed a direct association between adherence to the MedDiet score and DNAmTL as a continuous variable (beta = 0.015; SE: 0.005; p = 0.003), indicating that a one-point increase in adherence was related to an average increase of 0.015 ± 0.005 kb in TL. Upon examination of specific dietary items within the global score, we found that fruits, fish, “sofrito”, and whole grains exhibited the strongest associations in women. The novel score combining these items was significantly associated in the whole population. In the genome-wide association study (GWAS), we identified ten polymorphisms at the suggestive level of significance (p < 1 × 10⁻⁵) for DNAmTL (intergenics, in the IQSEC1, NCAPG2, and ABI3BP genes) and detected some gene–MedDiet modulations on DNAmTL. As this is the first study analyzing the DNAmTL estimator, genetics, and modulation by the MedDiet, more studies are needed to confirm these findings. Full article

(This article belongs to the Special Issue Oxidative Stress, Diet and Chronic Disease)

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19 pages, 3518 KiB

Open AccessArticle

Effect of Postnatal Epigallocatechin-Gallate Treatment on Cardiac Function in Mice Prenatally Exposed to Alcohol

by Vicente Andreu-Fernández, Mariona Serra-Delgado, Laura Almeida-Toledano, Àgueda García-Meseguer, Melina Vieiros, Anna Ramos-Triguero, Concha Muñoz-Lozano, Elisabet Navarro-Tapia, Leopoldo Martínez, Óscar García-Algar and María D. Gómez-Roig

Antioxidants 2023, 12(5), 1067; https://doi.org/10.3390/antiox12051067 - 09 May 2023

Cited by 1 | Viewed by 2048

Abstract

Prenatal alcohol exposure affects the cardiovascular health of the offspring. Epigallocatechin-3-gallate (EGCG) may be a protective agent against it, but no data are available regarding its impact on cardiac dysfunction. We investigated the presence of cardiac alterations in mice prenatally exposed to alcohol and the effect of postnatal EGCG treatment on cardiac function and related biochemical pathways. C57BL/6J pregnant mice received 1.5 g/kg/day (Mediterranean pattern), 4.5 g/kg/day (binge pattern) of ethanol, or maltodextrin until Day 19 of pregnancy. Post-delivery, treatment groups received EGCG-supplemented water. At post-natal Day 60, functional echocardiographies were performed. Heart biomarkers of apoptosis, oxidative stress, and cardiac damage were analyzed by Western blot. BNP and Hif1α increased and Nrf2 decreased in mice prenatally exposed to the Mediterranean alcohol pattern. Bcl-2 was downregulated in the binge PAE drinking pattern. Troponin I, glutathione peroxidase, and Bax increased in both ethanol exposure patterns. Prenatal alcohol exposure led to cardiac dysfunction in exposed mice, evidenced by a reduced ejection fraction, left ventricle posterior wall thickness at diastole, and Tei index. EGCG postnatal therapy restored the physiological levels of these biomarkers and improved cardiac dysfunction. These findings suggest that postnatal EGCG treatment attenuates the cardiac damage caused by prenatal alcohol exposure in the offspring. Full article

(This article belongs to the Special Issue Oxidative Stress, Diet and Chronic Disease)

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15 pages, 18992 KiB

Open AccessArticle

Smooth Muscle Cells from a Rat Model of Obesity and Hyperleptinemia Are Partially Resistant to Leptin-Induced Reactive Oxygen Species Generation

by Ocarol López-Acosta, Magdalena Cristóbal-García, Guillermo Cardoso-Saldaña, Karla Carvajal-Aguilera and Mohammed El-Hafidi

Antioxidants 2023, 12(3), 728; https://doi.org/10.3390/antiox12030728 - 16 Mar 2023

Cited by 2 | Viewed by 1366

Abstract

The aim of this study was to evaluate the effect of leptin on reactive oxygen species’ (ROS) generation of smooth muscle cells (SMCs) from a rat model of obesity and hyperleptinemia. Obesity and hyperleptinemia were induced in rats by a sucrose-based diet for 24 weeks. ROS generation was detected by using dichloro-dihydrofluorescein (DCF), a fluorescent ROS probe in primary SMCs culture. An increase in plasma leptin and oxidative stress markers was observed in sucrose-fed (SF) rats. At baseline SMCs from SF rats showed a more than twofold increase in fluorescence intensity (FI) compared to that obtained in control (C) cells. When the C cells were treated with 20 ng leptin, the FI increased by about 250%, whereas the leptin-induced FI in the SF cells increased only by 28%. In addition, sucrose feeding increased the levels of p22phox and gp91phox, subunits of Nox as an O₂^•− source in SMCs. Treatment of cells with leptin significantly increased p22phox and gp91phox levels in C cells and did not affect SF cells. Regarding STAT3 phosphorylation and the content of PTP1B and SOCS3 as protein markers of leptin resistance, they were found to be significantly increased in SF cells. These results suggest that SF aortic SMCs are partially resistant to leptin-induced ROS generation. Full article

(This article belongs to the Special Issue Oxidative Stress, Diet and Chronic Disease)

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15 pages, 6387 KiB

Open AccessArticle

Dissecting Causal Associations of Diet-Derived Circulating Antioxidants with Six Major Mental Disorders: A Mendelian Randomization Study

by Hao Zhao, Xue Han, Xuening Zhang, Lingjiang Li, Yanzhi Li, Wanxin Wang, Roger S. McIntyre, Kayla M. Teopiz, Lan Guo and Ciyong Lu

Antioxidants 2023, 12(1), 162; https://doi.org/10.3390/antiox12010162 - 10 Jan 2023

Cited by 1 | Viewed by 3290

Abstract

Although observational studies have suggested associations between circulating antioxidants and many mental disorders, causal inferences have not been confirmed. Mendelian randomization (MR) analyses were conducted using summary-level statistics from genome-wide association studies (GWASs) to explore whether genetically determined absolute circulating antioxidants (i.e., ascorbate, retinol, β-carotene, and lycopene) and metabolites (i.e., α- and γ-tocopherol, ascorbate, and retinol) were causally associated with the risk of six major mental disorders, including anxiety disorders (AD), major depressive disorder (MDD), bipolar disorder (BIP), schizophrenia (SCZ), post-traumatic stress disorder (PTSD), and obsessive–compulsive disorder (OCD). MR analyses were performed per specific-outcome databases, including the largest GWAS published to date (from 9725 for OCD to 413,466 for BIP participants), UK Biobank (over 370,000 participants), and FinnGen (over 270,000 participants), followed by meta-analyses. We found no significant evidence that genetically determined diet-derived circulating antioxidants were significantly causally associated with the risk of the six above-mentioned major mental disorders. For absolute antioxidant levels, the odds ratios (ORs) ranged from 0.91 (95% CI, 0.67–1.23) for the effect of β-carotene on OCD to 1.18 (95% CI, 0.90–1.54) for the effect of ascorbate on OCD. Similarly, for antioxidant metabolites, ORs ranged from 0.87 (95% CI, 0.55–1.38) for the effect of ascorbate on MDD to 1.08 (95% CI, 0.88–1.33) for the effect of ascorbate on OCD. Our study does not support significant causal associations of genetically determined diet-derived circulating antioxidants with the risk of major mental disorders. Full article

(This article belongs to the Special Issue Oxidative Stress, Diet and Chronic Disease)

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