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Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0
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Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 5746

Special Issue Editors

Dr. Rossana Morabito

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: physiology; ion trasport; band 3 protein; erythrocytes; oxidative stress; aging
Special Issues, Collections and Topics in MDPI journals
Dr. Alessia Remigante

E-Mail Website
Guest Editor
1. Biophysics Institute, National Research Council, 16149 Genoa, Italy
2. Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: oxidative stress events; glycation; aging; membrane transport systems
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) is frequently described as the balance between the production of reactive species (RS), including oxygen and nitrogen, in biological systems and the ability of the latter to defend through the sophisticated antioxidant machinery. At physiological levels, some oxidants, in controlled amounts, possess important signaling functions within the cell. Specifically, cells can generate RS with the function of second messengers, using them for intracellular signaling and for stimulating redox-sensitive signaling pathways to modify the cellular content of the cytoprotective regulatory proteins. In fact, the redox state in the cell is normally regulated by a complex endogenous antioxidant system composed of proteins with enzymatic activity and non-enzymatic proteins able to quickly neutralize or ensure a low production of RS. Nevertheless, when oxidants are produced in excess, or when the antioxidant defenses that regulate them are ineffective, this balance can be perturbed, thus resulting in an oxidative condition. Oxidative products are highly reactive and can directly or indirectly modulate the functions of many enzymes and transcription factors through complex signaling cascades. In particular, some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death, and constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or, alternatively, attenuating its consequences. Furthermore, the magnitude and exposure of the insult, as well as the cell type involved, are key elements in defining which pathways are activated, as well as the final cell outcome.

The aim of this Special Issue is to collect and contribute to the dissemination of high-quality research articles, as well as review articles, focusing on the relationship between oxidative stress-related diseases and cellular responses in different pathologies, including ischemic stroke, diabetes, kidney disease, cardiovascular, and neurodegenerative diseases. In addition, molecular targets of cellular membranes, as well as their potential modulation under oxidative stress, will be also considered, in an attempt to provide more information about cell responses to oxidative stress and its possible modulation by novel pharmacological strategies.

Dr. Rossana Morabito
Dr. Alessia Remigante
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • molecular targets of oxidative stress in oxidative stress related-diseases
  • oxidative stress and oxidative stress-related pathologies
  • cellular response to oxidative stress
  • oxidative stress and apoptosis in oxidative stress-related diseases
  • oxidative stress and related cell signaling
  • cell adaptation to oxidative stress
  • biomarkers of oxidative stress in disease
  • beneficial effects of natural or synthetic antioxidants in oxidative stress-related diseases

Related Special Issues

Published Papers (5 papers)

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Research

12 pages, 8545 KiB  
Article
Buffering Mitigates Chondrocyte Oxidative Stress, Metabolic Dysfunction, and Death Induced by Normal Saline: Formulation of a Novel Arthroscopic Irrigant
by Arman Hlas, Venkateswaran Ganesh, Jaison Marks, Rui He, Aliasger K. Salem, Joseph A. Buckwalter, Kyle R. Duchman, Kyungsup Shin, James A. Martin and Dongrim Seol
Int. J. Mol. Sci. 2024, 25(2), 1286; https://doi.org/10.3390/ijms25021286 - 20 Jan 2024
Viewed by 605
Abstract
For decades, surgeons have utilized 0.9% normal saline (NS) for joint irrigation to improve visualization during arthroscopic procedures. This continues despite mounting evidence that NS exposure impairs chondrocyte metabolism and compromises articular cartilage function. We hypothesized that chondrocyte oxidative stress induced by low [...] Read more.
For decades, surgeons have utilized 0.9% normal saline (NS) for joint irrigation to improve visualization during arthroscopic procedures. This continues despite mounting evidence that NS exposure impairs chondrocyte metabolism and compromises articular cartilage function. We hypothesized that chondrocyte oxidative stress induced by low pH is the dominant factor driving NS toxicity, and that buffering NS to increase its pH would mitigate these effects. Effects on chondrocyte viability, reactive oxygen species (ROS) production, and overall metabolic function were assessed. Even brief exposure to NS caused cell death, ROS overproduction, and disruption of glycolysis, pentose phosphate, and tricarboxylic acid (TCA) cycle pathways. NS also stimulated ROS overproduction in synovial cells that could adversely alter the synovial function and subsequently the entire joint health. Buffering NS with 25 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES) significantly increased chondrocyte viability, reduced ROS production, and returned metabolite levels to near control levels while also reducing ROS production in synovial cells. These results confirm that chondrocytes and synoviocytes are vulnerable to insult from the acidic pH of NS and demonstrate that adding a buffering agent to NS averts many of its most harmful effects. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0)
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16 pages, 2007 KiB  
Article
Propolis Protects GC-1spg Spermatogonial Cells against Tert-Butyl Hydroperoxide-Induced Oxidative Damage
by Filipa Duarte, Mariana Feijó, Ângelo Luís, Sílvia Socorro, Cláudio J. Maia and Sara Correia
Int. J. Mol. Sci. 2024, 25(1), 614; https://doi.org/10.3390/ijms25010614 - 03 Jan 2024
Viewed by 792
Abstract
Propolis is a natural resin produced by honeybees with plenty of pharmacologic properties, including antioxidant activity. Oxidative stress disrupts germ cell development and sperm function, with demonstrated harmful effects on male reproduction. Several natural antioxidants have been shown to reduce oxidative damage and [...] Read more.
Propolis is a natural resin produced by honeybees with plenty of pharmacologic properties, including antioxidant activity. Oxidative stress disrupts germ cell development and sperm function, with demonstrated harmful effects on male reproduction. Several natural antioxidants have been shown to reduce oxidative damage and increase sperm fertility potential; however, little is known about the effects of propolis. This work evaluated the role of propolis in protecting spermatogonial cells from oxidative damage. Propolis’ phytochemical composition and antioxidant potential were determined, and mouse GC-1spg spermatogonial cells were treated with 0.1–500 µg/mL propolis (12–48 h) in the presence or absence of an oxidant stimulus (tert-butyl hydroperoxide, TBHP, 0.005–3.6 µg/mL, 12 h). Cytotoxicity was assessed by MTT assays and proliferation by Ki-67 immunocytochemistry. Apoptosis, reactive oxygen species (ROS), and antioxidant defenses were evaluated colorimetrically. Propolis presented high phenolic and flavonoid content and moderate antioxidant activity, increasing the viability of GC-1spg cells and counteracting TBHP’s effects on viability and proliferation. Additionally, propolis reduced ROS levels in GC-1spg, regardless of the presence of TBHP. Propolis decreased caspase-3 and increased glutathione peroxidase activity in TBHP-treated GC-1spg cells. The present study shows the protective action of propolis against oxidative damage in spermatogonia, opening the possibility of exploiting its benefits to male fertility. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0)
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26 pages, 5421 KiB  
Article
Endoplasmic Reticulum Stress Promotes the Expression of TNF-α in THP-1 Cells by Mechanisms Involving ROS/CHOP/HIF-1α and MAPK/NF-κB Pathways
by Nadeem Akhter, Ajit Wilson, Hossein Arefanian, Reeby Thomas, Shihab Kochumon, Fatema Al-Rashed, Mohamed Abu-Farha, Ashraf Al-Madhoun, Fahd Al-Mulla, Rasheed Ahmad and Sardar Sindhu
Int. J. Mol. Sci. 2023, 24(20), 15186; https://doi.org/10.3390/ijms242015186 - 14 Oct 2023
Cited by 4 | Viewed by 1752
Abstract
Obesity and metabolic syndrome involve chronic low-grade inflammation called metabolic inflammation as well as metabolic derangements from increased endotoxin and free fatty acids. It is debated whether the endoplasmic reticulum (ER) stress in monocytic cells can contribute to amplify metabolic inflammation; if so, [...] Read more.
Obesity and metabolic syndrome involve chronic low-grade inflammation called metabolic inflammation as well as metabolic derangements from increased endotoxin and free fatty acids. It is debated whether the endoplasmic reticulum (ER) stress in monocytic cells can contribute to amplify metabolic inflammation; if so, by which mechanism(s). To test this, metabolic stress was induced in THP-1 cells and primary human monocytes by treatments with lipopolysaccharide (LPS), palmitic acid (PA), or oleic acid (OA), in the presence or absence of the ER stressor thapsigargin (TG). Gene expression of tumor necrosis factor (TNF)-α and markers of ER/oxidative stress were determined by qRT-PCR, TNF-α protein by ELISA, reactive oxygen species (ROS) by DCFH-DA assay, hypoxia-inducible factor 1-alpha (HIF-1α), p38, extracellular signal-regulated kinase (ERK)-1,2, and nuclear factor kappa B (NF-κB) phosphorylation by immunoblotting, and insulin sensitivity by glucose-uptake assay. Regarding clinical analyses, adipose TNF-α was assessed using qRT-PCR/IHC and plasma TNF-α, high-sensitivity C-reactive protein (hs-CRP), malondialdehyde (MDA), and oxidized low-density lipoprotein (OX-LDL) via ELISA. We found that the cooperative interaction between metabolic and ER stresses promoted TNF-α, ROS, CCAAT-enhancer-binding protein homologous protein (CHOP), activating transcription factor 6 (ATF6), superoxide dismutase 2 (SOD2), and nuclear factor erythroid 2-related factor 2 (NRF2) expression (p ≤ 0.0183),. However, glucose uptake was not impaired. TNF-α amplification was dependent on HIF-1α stabilization and p38 MAPK/p65 NF-κB phosphorylation, while the MAPK/NF-κB pathway inhibitors and antioxidants/ROS scavengers such as curcumin, allopurinol, and apocynin attenuated the TNF-α production (p ≤ 0.05). Individuals with obesity displayed increased adipose TNF-α gene/protein expression as well as elevated plasma levels of TNF-α, CRP, MDA, and OX-LDL (p ≤ 0.05). Our findings support a metabolic–ER stress cooperativity model, favoring inflammation by triggering TNF-α production via the ROS/CHOP/HIF-1α and MAPK/NF-κB dependent mechanisms. This study also highlights the therapeutic potential of antioxidants in inflammatory conditions involving metabolic/ER stresses. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0)
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18 pages, 2127 KiB  
Article
Electrophoretic Determination of L-Carnosine in Health Supplements Using an Integrated Lab-on-a-Chip Platform with Contactless Conductivity Detection
by Iva Pukleš, Csilla Páger, Nikola Sakač, Bojan Šarkanj, Brunislav Matasović, Mirela Samardžić, Mateja Budetić, Dean Marković and Marija Jozanović
Int. J. Mol. Sci. 2023, 24(19), 14705; https://doi.org/10.3390/ijms241914705 - 28 Sep 2023
Cited by 1 | Viewed by 777
Abstract
The health supplement industry is one of the fastest growing industries in the world, but there is a lack of suitable analytical methods for the determination of active compounds in health supplements such as peptides. The present work describes an implementation of contactless [...] Read more.
The health supplement industry is one of the fastest growing industries in the world, but there is a lack of suitable analytical methods for the determination of active compounds in health supplements such as peptides. The present work describes an implementation of contactless conductivity detection on microchip technology as a new strategy for the electrophoretic determination of L-carnosine in complex health supplement formulations without pre-concentration and derivatization steps. The best results were obtained in the case of +1.00 kV applied for 20 s for injection and +2.75 kV applied for 260 s for the separation step. Under the selected conditions, a linear detector response of 5 × 10−6 to 5 × 10−5 M was achieved. L-carnosine retention time was 61 s. The excellent reproducibility of both migration time and detector response confirmed the high precision of the method. The applicability of the method was demonstrated by the determination of L-carnosine in three different samples of health supplements. The recoveries ranged from 91 to 105%. Subsequent analysis of the samples by CE-UV-VIS and HPLC-DAD confirmed the accuracy of the obtained results. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0)
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19 pages, 3750 KiB  
Article
Impact of Truncated Oxidized Phosphatidylcholines on Phospholipase A2 Activity in Mono- and Polyunsaturated Biomimetic Vesicles
by Vesela Yordanova, Rusina Hazarosova, Victoria Vitkova, Albena Momchilova, Bozhil Robev, Biliana Nikolova, Plamen Krastev, Philippe Nuss, Miglena I. Angelova and Galya Staneva
Int. J. Mol. Sci. 2023, 24(13), 11166; https://doi.org/10.3390/ijms241311166 - 06 Jul 2023
Cited by 1 | Viewed by 1247
Abstract
The interplay between inflammatory and redox processes is a ubiquitous and critical phenomenon in cell biology that involves numerous biological factors. Among them, secretory phospholipases A2 (sPLA2) that catalyze the hydrolysis of the sn-2 ester bond of phospholipids are key [...] Read more.
The interplay between inflammatory and redox processes is a ubiquitous and critical phenomenon in cell biology that involves numerous biological factors. Among them, secretory phospholipases A2 (sPLA2) that catalyze the hydrolysis of the sn-2 ester bond of phospholipids are key players. They can interact or be modulated by the presence of truncated oxidized phosphatidylcholines (OxPCs) produced under oxidative stress from phosphatidylcholine (PC) species. The present study examined this important, but rarely considered, sPLA2 modulation induced by the changes in biophysical properties of PC vesicles comprising various OxPC ratios in mono- or poly-unsaturated PCs. Being the most physiologically active OxPCs, 1-palmitoyl-2-(5′-oxo-valeroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine (PGPC) have been selected for our study. Using fluorescence spectroscopy methods, we compared the effect of OxPCs on the lipid order as well as sPLA2 activity in large unilamellar vesicles (LUVs) made of the heteroacid PC, either monounsaturated [1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC)], or polyunsaturated [1-palmitoyl-2-docosahexaenoyl-sn-glycero-3-phosphocholine (PDPC)] at a physiological temperature. The effect of OxPCs on vesicle size was also assessed in both the mono- and polyunsaturated PC matrices. Results: OxPCs decrease the membrane lipid order of POPC and PDPC mixtures with PGPC inducing a much larger decrease in comparison with POVPC, indicative that the difference takes place at the glycerol level. Compared with POPC, PDPC was able to inhibit sPLA2 activity showing a protective effect of PDPC against enzyme hydrolysis. Furthermore, sPLA2 activity on its PC substrates was modulated by the OxPC membrane content. POVPC down-regulated sPLA2 activity, suggesting anti-inflammatory properties of this truncated oxidized lipid. Interestingly, PGPC had a dual and opposite effect, either inhibitory or enhancing on sPLA2 activity, depending on the protocol of lipid mixing. This difference may result from the chemical properties of the shortened sn-2-acyl chain residues (aldehyde group for POVPC, and carboxyl for PGPC), being, respectively, zwitterionic or anionic under hydration at physiological conditions. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 3.0)
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