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Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 25415

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Dr. Alessia Remigante

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Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: human physiology; cell physiology; membrane transport systems; bioactive compound; oxidative stress; human health
Special Issues, Collections and Topics in MDPI journals

Dr. Rossana Morabito

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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

Special Issue Information

Dear Colleagues,

Among the key factors influencing human health are chronic diseases and aging, which have been increasing in recent decades. These pathological states are produced by several causes, and a common factor involved in most of them is oxidative stress. Oxidative stress is defined as an imbalance between oxidative status, mainly by the formation of reactive species (RS), and antioxidant defense mechanisms. 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 oxidative conditions. Oxidative products are highly reactive, and can directly or indirectly modulate the functions of many enzymes and transcription factors through a complex signaling cascade. This phenomenon increases with age and affects the normal functioning of several cells and tissues. Due to the broad and profound biological effects of RS, numerous experimental and clinical studies have focused their attention on the participation of oxidative stress as a key regulator in chronic pathological status and aging. This Special Issue will focus on the investigation of the molecular mechanisms underlying oxidative stress, and pathophysiological consequences in cell and tissue function, in order to open new avenues in therapy, and drug design (natural or synthetic). It welcomes manuscripts collecting and contributing to the dissemination of high quality research articles, as well as review articles, focusing on the relationship between oxidative stress and cellular responses in chronic diseases and aging. 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 response to oxidative stress and its possible modulation by novel pharmacological strategies. Studies using animal or cell models, as well as clinical studies are welcomed.

Dr. Alessia Remigante
Prof. Dr. Rossana Morabito
Guest Editors

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Keywords

oxidative stress
antioxidants
aging
human health and diseases

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Published Papers (10 papers)

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Editorial

Jump to: Research, Review

5 pages, 189 KiB

Open AccessEditorial

Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health

by Alessia Remigante and Rossana Morabito

Cells 2024, 13(22), 1871; https://doi.org/10.3390/cells13221871 - 11 Nov 2024

Viewed by 417

Abstract

Chronic diseases and aging have increased significantly in recent decades [...] Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

Research

Jump to: Editorial, Review

19 pages, 4317 KiB

Open AccessArticle

Chlorine-Induced Toxicity on Murine Cornea: Exploring the Potential Therapeutic Role of Antioxidants

by Seungwon An, Khandaker Anwar, Mohammadjavad Ashraf, Kyu-Yeon Han and Ali R. Djalilian

Cells 2024, 13(5), 458; https://doi.org/10.3390/cells13050458 - 5 Mar 2024

Cited by 1 | Viewed by 1534

Abstract

Chlorine (Cl₂) exposure poses a significant risk to ocular health, with the cornea being particularly susceptible to its corrosive effects. Antioxidants, known for their ability to neutralize reactive oxygen species (ROS) and alleviate oxidative stress, were explored as potential therapeutic agents to counteract chlorine-induced damage. In vitro experiments using human corneal epithelial cells showed decreased cell viability by chlorine-induced ROS production, which was reversed by antioxidant incubation. The mitochondrial membrane potential decreased due to both low and high doses of Cl₂ exposure; however, it was recovered through antioxidants. The wound scratch assay showed that antioxidants mitigated impaired wound healing after Cl₂ exposure. In vivo and ex vivo, after Cl₂ exposure, increased corneal fluorescein staining indicates damaged corneal epithelial and stromal layers of mice cornea. Likewise, Cl₂ exposure in human ex vivo corneas led to corneal injury characterized by epithelial fluorescein staining and epithelial erosion. However, antioxidants protected Cl₂-induced damage. These results highlight the effects of Cl₂ on corneal cells using in vitro, ex vivo, and in vivo models while also underscoring the potential of antioxidants, such as vitamin A, vitamin C, resveratrol, and melatonin, as protective agents against acute chlorine toxicity-induced corneal injury. Further investigation is needed to confirm the antioxidants’ capacity to alleviate oxidative stress and enhance the corneal healing process. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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18 pages, 2693 KiB

Open AccessArticle

Allyl Isothiocianate Induces Ca²⁺ Signals and Nitric Oxide Release by Inducing Reactive Oxygen Species Production in the Human Cerebrovascular Endothelial Cell Line hCMEC/D3

by Roberto Berra-Romani, Valentina Brunetti, Giorgia Pellavio, Teresa Soda, Umberto Laforenza, Giorgia Scarpellino and Francesco Moccia

Cells 2023, 12(13), 1732; https://doi.org/10.3390/cells12131732 - 27 Jun 2023

Cited by 8 | Viewed by 1807

Abstract

Nitric oxide (NO) represents a crucial mediator to regulate cerebral blood flow (CBF) in the human brain both under basal conditions and in response to somatosensory stimulation. An increase in intracellular Ca²⁺ concentrations ([Ca²⁺]_i) stimulates the endothelial NO synthase to produce NO in human cerebrovascular endothelial cells. Therefore, targeting the endothelial ion channel machinery could represent a promising strategy to rescue endothelial NO signalling in traumatic brain injury and neurodegenerative disorders. Allyl isothiocyanate (AITC), a major active constituent of cruciferous vegetables, was found to increase CBF in non-human preclinical models, but it is still unknown whether it stimulates NO release in human brain capillary endothelial cells. In the present investigation, we showed that AITC evoked a Ca²⁺-dependent NO release in the human cerebrovascular endothelial cell line, hCMEC/D3. The Ca²⁺ response to AITC was shaped by both intra- and extracellular Ca²⁺ sources, although it was insensitive to the pharmacological blockade of transient receptor potential ankyrin 1, which is regarded to be among the main molecular targets of AITC. In accord, AITC failed to induce transmembrane currents or to elicit membrane hyperpolarization, although NS309, a selective opener of the small- and intermediate-conductance Ca²⁺-activated K⁺ channels, induced a significant membrane hyperpolarization. The AITC-evoked Ca²⁺ signal was triggered by the production of cytosolic, but not mitochondrial, reactive oxygen species (ROS), and was supported by store-operated Ca²⁺ entry (SOCE). Conversely, the Ca²⁺ response to AITC did not require Ca²⁺ mobilization from the endoplasmic reticulum, lysosomes or mitochondria. However, pharmacological manipulation revealed that AITC-dependent ROS generation inhibited plasma membrane Ca²⁺-ATPase (PMCA) activity, thereby attenuating Ca²⁺ removal across the plasma membrane and resulting in a sustained increase in [Ca²⁺]_i. In accord, the AITC-evoked NO release was driven by ROS generation and required ROS-dependent inhibition of PMCA activity. These data suggest that AITC could be exploited to restore NO signalling and restore CBF in brain disorders that feature neurovascular dysfunction. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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25 pages, 3628 KiB

Open AccessArticle

Palmitate-Induced Cardiac Lipotoxicity Is Relieved by the Redox-Active Motif of SELENOT through Improving Mitochondrial Function and Regulating Metabolic State

by Carmine Rocca, Anna De Bartolo, Rita Guzzi, Maria Caterina Crocco, Vittoria Rago, Naomi Romeo, Ida Perrotta, Ernestina Marianna De Francesco, Maria Grazia Muoio, Maria Concetta Granieri, Teresa Pasqua, Rosa Mazza, Loubna Boukhzar, Benjamin Lefranc, Jérôme Leprince, Maria Eugenia Gallo Cantafio, Teresa Soda, Nicola Amodio, Youssef Anouar and Tommaso Angelone

Cells 2023, 12(7), 1042; https://doi.org/10.3390/cells12071042 - 29 Mar 2023

Cited by 6 | Viewed by 3411

Abstract

Cardiac lipotoxicity is an important contributor to cardiovascular complications during obesity. Given the fundamental role of the endoplasmic reticulum (ER)-resident Selenoprotein T (SELENOT) for cardiomyocyte differentiation and protection and for the regulation of glucose metabolism, we took advantage of a small peptide (PSELT), derived from the SELENOT redox-active motif, to uncover the mechanisms through which PSELT could protect cardiomyocytes against lipotoxicity. To this aim, we modeled cardiac lipotoxicity by exposing H9c2 cardiomyocytes to palmitate (PA). The results showed that PSELT counteracted PA-induced cell death, lactate dehydrogenase release, and the accumulation of intracellular lipid droplets, while an inert form of the peptide (I-PSELT) lacking selenocysteine was not active against PA-induced cardiomyocyte death. Mechanistically, PSELT counteracted PA-induced cytosolic and mitochondrial oxidative stress and rescued SELENOT expression that was downregulated by PA through FAT/CD36 (cluster of differentiation 36/fatty acid translocase), the main transporter of fatty acids in the heart. Immunofluorescence analysis indicated that PSELT also relieved the PA-dependent increase in CD36 expression, while in SELENOT-deficient cardiomyocytes, PA exacerbated cell death, which was not mitigated by exogenous PSELT. On the other hand, PSELT improved mitochondrial respiration during PA treatment and regulated mitochondrial biogenesis and dynamics, preventing the PA-provoked decrease in PGC1-α and increase in DRP-1 and OPA-1. These findings were corroborated by transmission electron microscopy (TEM), revealing that PSELT improved the cardiomyocyte and mitochondrial ultrastructures and restored the ER network. Spectroscopic characterization indicated that PSELT significantly attenuated infrared spectral-related macromolecular changes (i.e., content of lipids, proteins, nucleic acids, and carbohydrates) and also prevented the decrease in membrane fluidity induced by PA. Our findings further delineate the biological significance of SELENOT in cardiomyocytes and indicate the potential of its mimetic PSELT as a protective agent for counteracting cardiac lipotoxicity. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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19 pages, 2013 KiB

Open AccessArticle

Mercury Chloride Affects Band 3 Protein-Mediated Anionic Transport in Red Blood Cells: Role of Oxidative Stress and Protective Effect of Olive Oil Polyphenols

by Pasquale Perrone, Sara Spinelli, Gianluca Mantegna, Rosaria Notariale, Elisabetta Straface, Daniele Caruso, Giuseppe Falliti, Angela Marino, Caterina Manna, Alessia Remigante and Rossana Morabito

Cells 2023, 12(3), 424; https://doi.org/10.3390/cells12030424 - 27 Jan 2023

Cited by 17 | Viewed by 2284

Abstract

Mercury is a toxic heavy metal widely dispersed in the natural environment. Mercury exposure induces an increase in oxidative stress in red blood cells (RBCs) through the production of reactive species and alteration of the endogenous antioxidant defense system. Recently, among various natural antioxidants, the polyphenols from extra-virgin olive oil (EVOO), an important element of the Mediterranean diet, have generated growing interest. Here, we examined the potential protective effects of hydroxytyrosol (HT) and/or homovanillyl alcohol (HVA) on an oxidative stress model represented by human RBCs treated with HgCl₂ (10 µM, 4 h of incubation). Morphological changes as well as markers of oxidative stress, including thiobarbituric acid reactive substance (TBARS) levels, the oxidation of protein sulfhydryl (-SH) groups, methemoglobin formation (% MetHb), apoptotic cells, a reduced glutathione/oxidized glutathione ratio, Band 3 protein (B3p) content, and anion exchange capability through B3p were analyzed in RBCs treated with HgCl₂ with or without 10 μM HT and/or HVA pre-treatment for 15 min. Our data show that 10 µM HT and/or HVA pre-incubation impaired both acanthocytes formation, due to 10 µM HgCl₂, and mercury-induced oxidative stress injury and, moreover, restored the endogenous antioxidant system. Interestingly, HgCl₂ treatment was associated with a decrease in the rate constant for SO₄²⁻ uptake through B3p as well as MetHb formation. Both alterations were attenuated by pre-treatment with HT and/or HVA. These findings provide mechanistic insights into benefits deriving from the use of naturally occurring polyphenols against oxidative stress induced by HgCl₂ on RBCs. Thus, dietary supplementation with polyphenols might be useful in populations exposed to HgCl₂ poisoning. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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17 pages, 4063 KiB

Open AccessArticle

Fresh Medium or L-Cystine as an Effective Nrf2 Inducer for Cytoprotection in Cell Culture

by Wujing Dai and Qin M. Chen

Cells 2023, 12(2), 291; https://doi.org/10.3390/cells12020291 - 12 Jan 2023

Cited by 3 | Viewed by 2615

Abstract

The Nrf2 gene encodes a transcription factor best known for regulating the expression of antioxidant and detoxification genes. A long list of small molecules has been reported to induce Nrf2 protein via Keap1 oxidation or alkylation. Many of these Nrf2 inducers exhibit off-target or toxic effects due to their nature as electrophiles. In searching for non-toxic Nrf2 inducers, we found that a culture medium change to fresh DMEM is capable of inducing Nrf2 protein in HeLa, HEK293, AC16 and MCF7 cells. Testing the components of DMEM led to the discovery of L-Cystine as an effective Nrf2 inducer. L-Cystine induces a dose-dependent increase of Nrf2 protein, from 0.1 to 1.6 mM. RNA-seq analyses and RT-PCR revealed an induction of multiple Nrf2 downstream genes, including NQO1, HMOX1, GCLC, GCLM, SRXN1, TXNRD1, AKR1C and OSGIN1 by 0.8 mM L-Cystine. The induction of Nrf2 protein was dependent on L-Cystine entering cells via the cystine/glutamate antiporter and the presence of Keap1. The half-life of Nrf2 protein increased from 19.4 min to 30.9 min with 0.8 mM L-Cystine treatment. L-Cystine was capable of eliciting cytoprotection by reducing ROS generation and protecting against oxidant- or doxorubicin-induced apoptosis. As an amino acid derivative, L-Cystine is considered a non-toxic Nrf2 inducer that exhibits the potential for protection against oxidative stress and tissue injury. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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10 pages, 948 KiB

Open AccessArticle

Evaluation of Malondialdehyde Levels, Oxidative Stress and Host–Bacteria Interactions: Escherichia coli and Salmonella Derby

by Vardan Tsaturyan, Armen Poghosyan, Michał Toczyłowski and Astghik Pepoyan

Cells 2022, 11(19), 2989; https://doi.org/10.3390/cells11192989 - 26 Sep 2022

Cited by 19 | Viewed by 2782

Abstract

Either extracts, cell-free suspensions or bacterial suspensions are used to study bacterial lipid peroxidation processes. Along with gas chromatography-mass spectrometry, liquid chromatography-mass spectrometry, and several other strategies, the thiobarbituric acid test is used for the determination of malondialdehyde (MDA) as the basis for the commercial test kits and the colorimetric detection of lipid peroxidation. The aim of the current study was to evaluate lipid peroxidation processes levels in the suspensions, extracts and culture supernatants of Escherichia coli and Salmonella Derby strains. The dependence of the formation of thiobarbituric acid-reactive substances levels in the cell extracts, the suspensions and cell-free supernatants on bacterial species, and their concentration and growth phase were revealed. The effect of bacterial concentrations on MDA formation was also found to be more pronounced in bacterial suspensions than in extracts, probably due to the dynamics of MDA release into the intercellular space. This study highlights the possible importance of MDA determination in both cell-free suspensions and extracts, as well as in bacterial suspensions to elucidate the role of lipid peroxidation processes in bacterial physiology, bacteria–host interactions, as well as in host physiology. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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20 pages, 8466 KiB

Open AccessArticle

Açai Berry Mitigates Vascular Dementia-Induced Neuropathological Alterations Modulating Nrf-2/Beclin1 Pathways

by Daniela Impellizzeri, Ramona D’Amico, Roberta Fusco, Tiziana Genovese, Alessio Filippo Peritore, Enrico Gugliandolo, Rosalia Crupi, Livia Interdonato, Davide Di Paola, Rosanna Di Paola, Salvatore Cuzzocrea, Rosalba Siracusa and Marika Cordaro

Cells 2022, 11(16), 2616; https://doi.org/10.3390/cells11162616 - 22 Aug 2022

Cited by 22 | Viewed by 3439

Abstract

The second-most common cause of dementia is vascular dementia (VaD). The majority of VaD patients experience cognitive impairment, which is brought on by oxidative stress and changes in autophagic function, which ultimately result in neuronal impairment and death. In this study, we examine a novel method for reversing VaD-induced changes brought on by açai berry supplementation in a VaD mouse model. The purpose of this study was to examine the impact of açai berries on the molecular mechanisms underlying VaD in a mouse model of the disease that was created by repeated ischemia–reperfusion (IR) of the whole bilateral carotid artery. Here, we found that açai berry was able to reduce VaD-induced behavioral alteration, as well as hippocampal death, in CA1 and CA3 regions. These effects are probably due to the modulation of nuclear factor erythroid 2-related factor 2 (Nrf-2) and Beclin-1, suggesting a possible crosstalk between these molecular pathways. In conclusion, the protective effects of açai berry could be a good supplementation in the future for the management of vascular dementia. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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23 pages, 3566 KiB

Open AccessArticle

Açaì (Euterpe oleracea) Extract Protects Human Erythrocytes from Age-Related Oxidative Stress

by Alessia Remigante, Sara Spinelli, Elisabetta Straface, Lucrezia Gambardella, Daniele Caruso, Giuseppe Falliti, Silvia Dossena, Angela Marino and Rossana Morabito

Cells 2022, 11(15), 2391; https://doi.org/10.3390/cells11152391 - 3 Aug 2022

Cited by 23 | Viewed by 2628

Abstract

Aging is a process characterised by a general decline in physiological functions. The high bioavailability of reactive oxygen species (ROS) plays an important role in the aging rate. Due to the close relationship between aging and oxidative stress (OS), functional foods rich in flavonoids are excellent candidates to counteract age-related changes. This study aimed to verify the protective role of Açaì extract in a d-Galactose (d-Gal)-induced model of aging in human erythrocytes. Markers of OS, including ROS production, thiobarbituric acid reactive substances (TBARS) levels, oxidation of protein sulfhydryl groups, as well as the anion exchange capability through Band 3 protein (B3p) and glycated haemoglobin (A1c) have been analysed in erythrocytes treated with d-Gal for 24 h, with or without pre-incubation for 1 h with 0.5–10 µg/mL Açaì extract. Our results show that the extract avoided the formation of acanthocytes and leptocytes observed after exposure to 50 and 100 mM d-Gal, respectively, prevented d-Gal-induced OS damage, and restored alterations in the distribution of B3p and CD47 proteins. Interestingly, d-Gal exposure was associated with an acceleration of the rate constant of SO₄²⁻ uptake through B3p, as well as A1c formation. Both alterations have been attenuated by pre-treatment with the Açaì extract. These findings contribute to clarify the aging mechanisms in human erythrocytes and propose functional foods rich in flavonoids as natural antioxidants for the treatment and prevention of OS-related disease conditions. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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Review

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21 pages, 2025 KiB

Open AccessReview

Transient Receptor Potential Ankyrin 1 (TRPA1) Channel as a Sensor of Oxidative Stress in Cancer Cells

by Francesco Moccia and Daniela Montagna

Cells 2023, 12(9), 1261; https://doi.org/10.3390/cells12091261 - 26 Apr 2023

Cited by 8 | Viewed by 3019

Abstract

Moderate levels of reactive oxygen species (ROS), such as hydrogen peroxide (H₂O₂), fuel tumor metastasis and invasion in a variety of cancer types. Conversely, excessive ROS levels can impair tumor growth and metastasis by triggering cancer cell death. In order to cope with the oxidative stress imposed by the tumor microenvironment, malignant cells exploit a sophisticated network of antioxidant defense mechanisms. Targeting the antioxidant capacity of cancer cells or enhancing their sensitivity to ROS-dependent cell death represent a promising strategy for alternative anticancer treatments. Transient Receptor Potential Ankyrin 1 (TRPA1) is a redox-sensitive non-selective cation channel that mediates extracellular Ca²⁺ entry upon an increase in intracellular ROS levels. The ensuing increase in intracellular Ca²⁺ concentration can in turn engage a non-canonical antioxidant defense program or induce mitochondrial Ca²⁺ dysfunction and apoptotic cell death depending on the cancer type. Herein, we sought to describe the opposing effects of ROS-dependent TRPA1 activation on cancer cell fate and propose the pharmacological manipulation of TRPA1 as an alternative therapeutic strategy to enhance cancer cell sensitivity to oxidative stress. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidant Strategies: Relationships and Cellular Pathways for Human Health)

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