Submit to Antioxidants Review for Antioxidants Propose a Special Issue

Journal Menu

Journal Browser

Oxidative-Stress in Human Diseases—2nd Edition

Special Issue Editors
Special Issue Information
Keywords
Published Papers

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 November 2023) | Viewed by 14085

Share This Special Issue

Special Issue Editor

Dr. Soliman Khatib

E-Mail Website
Guest Editor

1. Department of Natural Products and Nutrition, MIGAL—Galilee Research Institute, Kiryat Shmona 11016, Israel
2. Faculty of Sciences, Tel Hai Academic College, Qiryat Shemona 12208, Israel
Interests: natural compounds; analytical chemistry; metabolomics; oxidative stress; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) plays an essential role in the pathogenesis of human chronic diseases such as cardiovascular and kidney diseases, diabetes, neurodegenerative disorders, cancer, inflammation-related diseases, and aging. OS is a condition characterized by an imbalance between production and accumulation of oxygen and nitrogen reactive species (ROS/RNS) in cells and tissues, and it occurs when the generation of these compounds exceeds the ability of the biological system to neutralize them.

ROS/RNS, such as superoxide (O₂^•−), hydrogen peroxide (H₂O₂), hydroxyl radical (HO^•), nitrogen oxide (NO^•), peroxynitrite (ONOO⁻), and hypochlorous acid (HOCl), are all products of normal metabolic pathways in humans, and their production may be increased as a result of the influence of external factors, such as pollution, cigarette smoke, or internally, as a result of impaired intracellular metabolism. Long-term exposure to increased levels of ROS/RNS can cause structural defects of lipids, proteins, DNA, and RNA, as well as functional alteration of several enzymes and cellular structures, leading to an increase in OS and pathogenesis.

We invite you to share with our community your latest original and innovative research findings or review articles in the upcoming Special Issue “Oxidative-Stress in Human Diseases II”. We welcome clinical and pre-clinical studies of the relationship between OS and human diseases, novel diagnosis methods and mechanisms, as well as approaches for the prevention and treatment of diseases related to OS.

Dr. Soliman Khatib
Guest Editor

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
ROS/RNS
human diseases
antioxidants
OS biomarkers

Published Papers (9 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

14 pages, 1006 KiB

Open AccessArticle

Changes in Cortisol and in Oxidative/Nitrosative Stress Indicators after ADHD Treatment

by Laura Garre-Morata, Tomás de Haro, Raquel González Villén, María Luisa Fernández-López, Germaine Escames, Antonio Molina-Carballo and Darío Acuña-Castroviejo

Antioxidants 2024, 13(1), 92; https://doi.org/10.3390/antiox13010092 - 12 Jan 2024

Viewed by 1079

Abstract

Although ADHD is one of the most prevalent diseases during childhood, we still do not know its precise origin; oxidative/nitrosative stress and the hypothalamic–pituitary–adrenal axis are suggested contributors. Methylphenidate, among others, is the main drug used in ADHD patients, but its effects on relevant markers and structures remain unclear. This study, involving 59 patients diagnosed with ADHD according to DSM-5 criteria, aimed to assess changes in cortisol levels (using cortisol awakening response, CAR) and oxidative/nitrosative status with the treatment. Blood samples before and 3 months after treatment with methylphenidate were used to measure oxidative and inflammatory markers, as well as the endogenous antioxidant activity, while saliva samples tracked cortisol awakening response (CAR). The results showed a treatment-related improvement in the redox profile, with the reduction in advanced oxidation protein products (AOPP), lipid peroxidation (LPO), and nitrite plus nitrate (NOx) levels, and the increase in the enzymatic activities of glutathione reductase (GRd) and catalase (CAT). Moreover, the area under the curve (AUC) of CAR increased significantly, indicating increased reactivity of the HPA axis. These results support, for the first time, the involvement of the endogenous antioxidant system in the pathophysiology of ADHD. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

12 pages, 316 KiB

Open AccessArticle

Association Study between Antioxidant Nutrient Intake and Low Bone Mineral Density with Oxidative Stress-Single Nucleotide Variants: GPX1 (rs1050450 and rs17650792), SOD2 (rs4880) and CAT (rs769217) in Mexican Women

by Rogelio F. Jiménez-Ortega, Diana I. Aparicio-Bautista, Adriana Becerra-Cervera, Priscilla López-Montoya, Guadalupe León-Reyes, Jeny Flores-Morales, Manuel Castillejos-López, Alberto Hidalgo-Bravo, Jorge Salmerón, Berenice Rivera-Paredez and Rafael Velázquez-Cruz

Antioxidants 2023, 12(12), 2089; https://doi.org/10.3390/antiox12122089 - 08 Dec 2023

Viewed by 917

Abstract

Oxidative stress is essential in developing multiple bone metabolism diseases, including osteoporosis. Single-nucleotide variants (SNVs) have been associated with oxidative stress, promoting an imbalance between the production of reactive oxygen species and the ability to neutralize them, and it has been reported that antioxidant nutrient intake can influence bone mineral density (BMD). This work reports the association between oxidative stress-related SNVs (GPX1-rs1050450, rs17650792, SOD2-rs4880, and CAT-rs769217), BMD, and antioxidant nutrient intake. The study included 1269 Mexican women from the Health Workers Cohort Study. Genotyping was performed using predesigned TaqMan assays. Dietary data were collected using a 116-item semi-quantitative food frequency questionnaire. A dietary antioxidant quality score (DAQS) was used to estimate antioxidant–nutrient intake. Association analysis was estimated via linear, logistic, or quantile regression models. The results showed an association of the rs1050450-A and rs17650792-A alleles with femoral neck BMD (p = 0.038 and p = 0.017, respectively) and the SNV rs4880-A allele with total hip BMD (p = 0.026) in respondents aged 45 years or older. In addition, antioxidant–nutrient intake was associated with the rs4880-GG genotype, being significant for fiber (p = 0.007), riboflavin (p = 0.005), vitamin B6 (p = 0.034), and vitamin D (p = 0.002). The study showed an association between oxidative stress-related SNVs, BMD, and antioxidant–nutrient intake in Mexican women. Therefore, treatments for low BMD could be developed based on antioxidant supplementation. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

13 pages, 1341 KiB

Open AccessArticle

Association of Mitochondrial Variants with the Joint Occurrence of Polycystic Ovary Syndrome and Hashimoto’s Thyroiditis

by Natalia Zeber-Lubecka, Maria Kulecka, Katarzyna Suchta, Michalina Dąbrowska, Michał Ciebiera and Ewa E. Hennig

Antioxidants 2023, 12(11), 1983; https://doi.org/10.3390/antiox12111983 - 08 Nov 2023

Cited by 1 | Viewed by 1033

Abstract

Background. The prevalence of Hashimoto’s thyroiditis (HT) among women with polycystic ovary syndrome (PCOS) is higher than in the general female population, but the factors predisposing to the coexistence of these disorders remain unclear. This study employed whole genome sequencing of mitochondrial DNA to identify genetic variants potentially associated with the development of PCOS and HT and predisposing to their joint occurrence. Results. A total of 84 women participated, including patients with PCOS, HT, coexisting PCOS and HT (PCOS + HT) and healthy women. Both Fisher’s exact and Mann–Whitney U statistical analyses were performed to compare the frequency of variants between groups. Ten differentiating variants were common to both analyses in PCOS + HT vs. PCOS, one in PCOS + HT vs. HT, and six in PCOS + HT vs. control. Several variants differentiating the PCOS + HT group from PCOS and controls were identified, located both in the mitochondrial genes (including the MT-CYB, MT-ND1, MT-ND2, MT-ND4, MT-ND6, MT-CO1, MT-CO3) and the D-loop region. Only two variants differentiated PCOS + HT and HT groups. One variant (13237a in MT-ND5) was common for all three comparisons and underrepresented in the PCOS + HT group. Functional enrichment analysis showed 10 pathways that were unique for the comparison of PCOS + HT and PCOS groups, especially related to ATP production and oxidative phosphorylation, and one pathway, the NADH-quinone oxidoreductase, chain M/4, that was unique for the comparison of PCOS + HT and control groups. Notably, nine pathways shared commonality between PCOS + HT vs. PCOS and PCOS + HT vs. control, related to the biogenesis and assembly of Complex I. Conclusion. This study provides novel insights into the genetic variants associated with oxidative stress in women with coexisting PCOS and HT. Mitochondrial dysfunction and oxidative stress appear to play a role in the pathogenesis of both conditions. However, more mitochondrial variants were found to differentiate women with both PCOS and HT from those with PCOS alone than from those with HT alone. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

21 pages, 963 KiB

Open AccessArticle

Differential Modulation of Markers of Oxidative Stress and DNA Damage in Arterial Hypertension

by Moritz Kreutzmann, Bettina J. Kraus, Martin Christa, Stefan Störk, Eugène H. J. M. Jansen, Helga Stopper and Nicole Schupp

Antioxidants 2023, 12(11), 1965; https://doi.org/10.3390/antiox12111965 - 04 Nov 2023

Cited by 1 | Viewed by 1230

Abstract

Patients with arterial hypertension have an increased risk of developing tumors, particularly renal cell carcinoma. Arterial hypertension is linked to DNA damage via the generation of oxidative stress, in which an upregulated renin–angiotensin–aldosterone system plays a crucial role. The current study investigated surrogates of oxidative stress and DNA damage in a group of hypertensive patients (HypAll, n = 64) and subgroups of well (HypWell, n = 36) and poorly (HypPoor, n = 28) controlled hypertensive patients compared to healthy controls (n = 8). In addition, a longitudinal analysis was performed with some of the hypertensive patients. Markers for oxidative stress in plasma (SHp, D-ROM, and 3-nitrotyrosine) and urine (8-oxodG, 15-F_2t-isoprostane, and malondialdehyde) and markers for DNA damage in lymphocytes (γ-H2AX and micronuclei) were measured. In HypAll, all markers of oxidative stress except malondialdehyde were increased compared to the controls. After adjustment for age, this association was maintained for the protein stress markers SHp and 3-nitrotyrosine. With regard to the markers for DNA damage, there was no difference between HypAll and the controls. Further, no significant differences became apparent in the levels of both oxidative stress and DNA damage between HypWell and HypPoor. Finally, a positive correlation between the development of blood pressure and oxidative stress was observed in the longitudinal study based on the changes in D-ROM and systolic blood pressure. In conclusion, we found increased oxidative stress in extensively treated hypertensive patients correlating with the level of blood-pressure control but no association with DNA damage. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

12 pages, 3065 KiB

Open AccessArticle

Mitochondrial Oxidative Stress Mediates Bradyarrhythmia in Leigh Syndrome Mitochondrial Disease Mice

by Biyi Chen, Nastaran Daneshgar, Hsiang-Chun Lee, Long-Sheng Song and Dao-Fu Dai

Antioxidants 2023, 12(5), 1001; https://doi.org/10.3390/antiox12051001 - 26 Apr 2023

Cited by 2 | Viewed by 1812

Abstract

Mitochondrial oxidative stress has been implicated in aging and several cardiovascular diseases, including heart failure and cardiomyopathy, ventricular tachycardia, and atrial fibrillation. The role of mitochondrial oxidative stress in bradyarrhythmia is less clear. Mice with a germline deletion of Ndufs4 subunit respiratory complex I develop severe mitochondrial encephalomyopathy resembling Leigh Syndrome (LS). Several types of cardiac bradyarrhythmia are present in LS mice, including a frequent sinus node dysfunction and episodic atrioventricular (AV) block. Treatment with the mitochondrial antioxidant Mitotempo or mitochondrial protective peptide SS31 significantly ameliorated the bradyarrhythmia and extended the lifespan of LS mice. Using an ex vivo Langendorff perfused heart with live confocal imaging of mitochondrial and total cellular reactive oxygen species (ROS), we showed increased ROS in the LS heart, which was potentiated by ischemia-reperfusion. A simultaneous ECG recording showed a sinus node dysfunction and AV block concurrent with the severity of the oxidative stress. Treatment with Mitotempo abolished ROS and restored the sinus rhythm. Our study reveals robust evidence of the direct mechanistic roles of mitochondrial and total ROS in bradyarrhythmia in the setting of LS mitochondrial cardiomyopathy. Our study also supports the potential clinical application of mitochondrial-targeted antioxidants or SS31 for the treatment of LS patients. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

17 pages, 2501 KiB

Open AccessArticle

Copper Exposure Induces Epithelial-Mesenchymal Transition-Related Fibrotic Change via Autophagy and Increase Risk of Lung Fibrosis in Human

by Hsin-Ying Clair Chiou, Chih-Wen Wang, Szu-Chia Chen, Mei-Lan Tsai, Ming-Hong Lin, Chih-Hsing Hung and Chao-Hung Kuo

Antioxidants 2023, 12(2), 532; https://doi.org/10.3390/antiox12020532 - 20 Feb 2023

Cited by 4 | Viewed by 2192

Abstract

Copper is an essential trace element involved in several vital biological processes of the human body. However, excess exposure to copper caused by occupational hazards and environmental contamination, such as food, water, and air, damages human health. In this study, in vitro cell culture model and epidemiologic studies were conducted to evaluate the effect of copper on lung fibrosis. In vitro, treatment of CuSO₄ in lung epithelial cells at 100 μM consistently decreases cell viability in alveolar type (A549) and human bronchial epithelial (HBE) cells. CuSO₄ promotes epithelial-mesenchymal transition (EMT) as shown by increased cell migration and increased EMT marker and fibrotic gene expressions. Besides, CuSO₄ induced cell autophagy, with an increased LC3, PINK, and decreased p62 expression. Inhibition of ROS by N-acetylcysteine reversed the CuSO₄-induced PINK1, LC3, and Snail expressions. Inhibition of autophagy by chloroquine reverses the CuSO₄-induced EMT changes. Nature flavonoids, especially kaempferol, and fustin, were shown to inhibit Copper-induced EMT. In humans, a unit increase in urinary copper concentration was significantly associated with an increased risk of lung fibrotic changes (odds ratio [OR] = 1.17, 95% confidence interval [CI] = 1.01–1.36, p = 0.038). These results indicated that Copper is a risk factor for lung fibrosis through activation of the ROS-autophagy-EMT pathway, which can be reversed by flavonoids. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

11 pages, 1936 KiB

Open AccessArticle

Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress

by Drew Theobald and Srinivas Sriramula

Antioxidants 2023, 12(1), 150; https://doi.org/10.3390/antiox12010150 - 08 Jan 2023

Cited by 1 | Viewed by 1755

Abstract

Hypertension is associated with increased expression of kinin B1 receptors (B1R) and increased levels of pro-inflammatory cytokines within the neurons. We previously reported that angiotensin II (Ang II) upregulates B1R expression and can induce neuroinflammation and oxidative stress in primary hypothalamic neurons. However, the order in which B1R activation, neuroinflammation, and oxidative stress occur has not yet been studied. Using primary hypothalamic neurons from neonatal mice, we show that tumor necrosis factor (TNF), lipopolysaccharides (LPS), and hydrogen peroxide (H₂O₂) can upregulate B1R expression and increase oxidative stress. Furthermore, our study shows that B1R blockade with R715, a specific B1R antagonist, can attenuate these effects. To further confirm our findings, we used a deoxycorticosterone acetate (DOCA)-salt model of hypertension to show that oxidative stress is upregulated in the hypothalamic paraventricular nucleus (PVN) of the brain. Together, these data provide novel evidence that relationship between oxidative stress, neuroinflammation, and B1R upregulation in the brain is bidirectional, and that B1R antagonism may have beneficial effects on neuroinflammation and oxidative stress in various disease pathologies. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

Review

Jump to: Research

15 pages, 1576 KiB

Open AccessReview

Niemann-Pick Disease Type C (NPDC) by Mutation of NPC1 and NPC2: Aberrant Lysosomal Cholesterol Trafficking and Oxidative Stress

by Dongun Lee and Jeong Hee Hong

Antioxidants 2023, 12(12), 2021; https://doi.org/10.3390/antiox12122021 - 21 Nov 2023

Viewed by 1018

Abstract

Cholesterol trafficking is initiated by the endocytic pathway and transported from endo/lysosomes to other intracellular organelles. Deficiencies in cholesterol-sensing and binding proteins NPC1 and NPC2 induce accumulation in lysosomes and the malfunction of trafficking to other organelles. Each organelle possesses regulatory factors to induce cholesterol trafficking. The mutation of NPC1 and NPC2 genes induces Niemann-Pick disease type C (NPDC), which is a hereditary disease and causes progressive neurodegeneration, developmental disability, hypotonia, and ataxia. Oxidative stress induces damage in NPDC-related intracellular organelles. Although studies on the relationship between NPDC and oxidation are relatively rare, several studies have reported the therapeutic potential of antioxidants in treating NPDC. Investigating antioxidant drugs to relieve oxidative stress and cholesterol accumulation is suggested to be a powerful tool for developing treatments for NPDC. Understanding NPDC provides challenging issues in understanding the oxidative stress–lysosome metabolism of the lipid axis. Thus, we elucidated the relationship between complexes of intracellular organelles and NPDC to develop our knowledge and suggested potential antioxidant reagents for NPDC therapy. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Figure 1

54 pages, 5917 KiB

Open AccessReview

Oxidative Stress: A Suitable Therapeutic Target for Optic Nerve Diseases?

by Francesco Buonfiglio, Elsa Wilma Böhm, Norbert Pfeiffer and Adrian Gericke

Antioxidants 2023, 12(7), 1465; https://doi.org/10.3390/antiox12071465 - 20 Jul 2023

Cited by 5 | Viewed by 2242

Abstract

Optic nerve disorders encompass a wide spectrum of conditions characterized by the loss of retinal ganglion cells (RGCs) and subsequent degeneration of the optic nerve. The etiology of these disorders can vary significantly, but emerging research highlights the crucial role of oxidative stress, an imbalance in the redox status characterized by an excess of reactive oxygen species (ROS), in driving cell death through apoptosis, autophagy, and inflammation. This review provides an overview of ROS-related processes underlying four extensively studied optic nerve diseases: glaucoma, Leber’s hereditary optic neuropathy (LHON), anterior ischemic optic neuropathy (AION), and optic neuritis (ON). Furthermore, we present preclinical findings on antioxidants, with the objective of evaluating the potential therapeutic benefits of targeting oxidative stress in the treatment of optic neuropathies. Full article

(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—2nd Edition)

► Show Figures

Journal Menu

Journal Browser

Oxidative-Stress in Human Diseases—2nd Edition

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Published Papers (9 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI