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Antioxidants
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Oxidative Stress and NRF2 in Health and Disease
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Oxidative Stress and NRF2 in Health and Disease

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: 20 May 2024 | Viewed by 22532

Special Issue Editor

Dr. Lidija Milković

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Guest Editor
Laboratory for Oxidative Stress, Division of Molecular Medicine, Rudjer Boskovic Institute, 10000 Zagreb, Croatia
Interests: oxidative stress; reactive oxygen species (ROS); lipid peroxidation; cancer; cancer stem cells; cellular and extracellular antioxidants; Nrf2; metabolic reprogramming
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) has long been considered a cause of various noncommunicable diseases. The term refers to the increased formation of reactive oxygen species (ROS) and other byproducts that can react with cellular macromolecules such as proteins, DNA, and lipids to impair cellular function. Earlier research opinions assumed that OS only leads to various pathologies and referred to it as a harmful process that should be abolished. However, further research has revealed that OS byproducts, such as hydrogen peroxide, are also important for redox signaling. Depending on the cue, cells use their signaling abilities, which include turning certain protein targets on and off, to provide signal transduction that regulates their own functions or the functions of neighboring cells. The extent of OS is closely intertwined with metabolic switches and antioxidant machinery. While some ROS, such as hydrogen peroxide, are essential for normal physiology, their increase leads to pathology. The NRF2 pathway is the main pathway activated as a response to OS. The NRF2 pathway is the major signaling pathway activated in response to OS. The transcription factor NRF2 (nuclear factor, erythroid 2) is mainly regulated by Kelch-like ECH-associated protein 1 (KEAP1), although its regulation/activation is more complex. NRF2 regulates the expression of more than 250 genes, not only antioxidant enzymes but also others involved in autophagy, metabolism, detoxification, protein turnover, etc. Its mode of action is not always beneficial to humans and is not fully understood.

We invite researchers in this field and participants of the COST Action CA20121, Bench to Bedside Transition for Pharmacological regulation of NRF2 in non-communicable diseases (BenBedPhar) to submit their latest research to this Special Issue. Potential topics include but are not limited to deciphering the role of oxidative stress and NRF2 in physiology and pathology, linkage to other signaling pathways, the “omics” approach to identify specific targets and key molecules, potential therapeutic strategies, etc.

text

Dr. Lidija Milković
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
  • redox signaling
  • nrf2 and its regulation
  • redox-modifying therapeutic approach
  • omics approach
  • physiology
  • non-communicable diseases
  • metabolism
  • aging

Published Papers (10 papers)

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Research

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22 pages, 3371 KiB  
Article
Cellular Pre-Adaptation to the High O2 Concentration Used in Standard Cell Culture Confers Resistance to Subsequent H2O2-Induced Cell Death
by Jack B. Jordan, Miranda J. Smallwood, Gary R. Smerdon and Paul G. Winyard
Antioxidants 2024, 13(3), 269; https://doi.org/10.3390/antiox13030269 - 22 Feb 2024
Viewed by 783
Abstract
The addition of hydrogen peroxide (H2O2) to cultured cells is widely used as a method to modulate redox-regulated cellular pathways, including the induction of programmed cell death in cell culture experiments and the testing of pro- and antioxidant compounds. [...] Read more.
The addition of hydrogen peroxide (H2O2) to cultured cells is widely used as a method to modulate redox-regulated cellular pathways, including the induction of programmed cell death in cell culture experiments and the testing of pro- and antioxidant compounds. Here, we assessed the effect on the cellular response to H2O2 of pre-adapting squamous cell carcinoma cells (A431) to the standard cell culture oxygenation of 18.6% O2, compared to cells pre-adapted to a physiological skin O2 concentration (3.0% O2). We showed that cells pre-adapted to 18.6% O2 resisted H2O2-induced cell death compared to cells pre-adapted to 3.0% O2 for 96 h prior to treatment with H2O2. Moreover, the enzymatic activities of catalase and glutathione reductase, as well as the protein expression levels of catalase, were higher in cells pre-adapted to 18.6% O2 compared to cells pre-adapted to 3.0% O2. H2O2-resistant cells, pre-adapted to 18.6% O2, exhibited increased nuclear Nrf-2 levels. It is concluded that A431 cells pre-adapted to standard cell culture oxygenation conditions resist H2O2-induced cell death. This effect may be related to their heightened activation of Nrf-2. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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14 pages, 1980 KiB  
Article
Oxidative Stress Induces Skin Pigmentation in Melasma by Inhibiting Hedgehog Signaling
by Nan-Hyung Kim and Ai-Young Lee
Antioxidants 2023, 12(11), 1969; https://doi.org/10.3390/antiox12111969 - 06 Nov 2023
Viewed by 1315
Abstract
There is growing evidence that oxidative stress plays a role in melasma and disrupts primary cilia formation. Additionally, primary cilia have been suggested to have an inhibitory role in melanogenesis. This study examined the potential link between oxidative stress, skin hyperpigmentation, and primary [...] Read more.
There is growing evidence that oxidative stress plays a role in melasma and disrupts primary cilia formation. Additionally, primary cilia have been suggested to have an inhibitory role in melanogenesis. This study examined the potential link between oxidative stress, skin hyperpigmentation, and primary cilia. We compared the expression levels of the nuclear factor E2-related factor 2 (NRF2), intraflagellar transport 88 (IFT88), and glioma-associated oncogene homologs (GLIs) in skin samples from patients with melasma, both in affected and unaffected areas. We also explored the roles of NRF2, IFT88, and GLIs in ciliogenesis and pigmentation using cultured adult human keratinocytes, with or without melanocytes. Our findings revealed decreased levels of NRF2, heme oxygenase-1, IFT88, and GLIs in lesional skin from melasma patients. The knockdown of NRF2 resulted in reduced expressions of IFT88 and GLI1, along with fewer ciliated cells. Furthermore, NRF2, IFT88, or GLI1 knockdown led to increased expressions in protease-activated receptor-2 (PAR2), K10, involucrin, tyrosinase, and/or melanin. These effects were reversed by the smoothened agonist 1.1. Calcium also upregulated these proteins, but not NRF2. The upregulation of involucrin and PAR2 after NRF2 knockdown was mitigated with a calcium chelator. In summary, our study suggests that oxidative stress in NRF2-downregulated melasma keratinocytes impedes ciliogenesis and related molecular processes. This inhibition stimulates keratinocyte differentiation, resulting in melanin synthesis and melanosome transfer, ultimately leading to skin hyperpigmentation. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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14 pages, 2022 KiB  
Article
AMPK-Mediated Phosphorylation of Nrf2 at S374/S408/S433 Favors Its βTrCP2-Mediated Degradation in KEAP1-Deficient Cells
by Eleni Petsouki, Sylvia Ender, Shara Natalia Sosa Cabrera and Elke H. Heiss
Antioxidants 2023, 12(8), 1586; https://doi.org/10.3390/antiox12081586 - 09 Aug 2023
Cited by 1 | Viewed by 2901
Abstract
Nrf2 is a transcription factor facilitating cells’ resilience against redox and various other forms of stress. In the absence of stressors, KEAP1 and/or βTrCP mediate the ubiquitination of Nrf2 and prevent Nrf2-dependent gene expression and detoxification. AMPK regulates cellular energy homeostasis and redox [...] Read more.
Nrf2 is a transcription factor facilitating cells’ resilience against redox and various other forms of stress. In the absence of stressors, KEAP1 and/or βTrCP mediate the ubiquitination of Nrf2 and prevent Nrf2-dependent gene expression and detoxification. AMPK regulates cellular energy homeostasis and redox balance. Previous studies indicated a potential Nrf2-AMPK cooperativity. In line with this, our lab had previously identified three AMPK-dependent phosphorylation sites (S374/408/433) in Nrf2. Given their localization in or near the Neh6 domain, known to regulate βTrCP-mediated degradation, we examined whether they may influence the βTrCP-driven degradation of Nrf2. By employing expression plasmids for WT and triple mutant (TM)-Nrf2 (Nrf2S374/408/433→A), (co)immunoprecipitation, proximity ligation, protein half-life, knockdown, ubiquitination experiments, and qPCR in Keap1-null mouse embryonic fibroblasts, we show that TM-Nrf2S→A374/408/433 had enhanced stability due to impeded interaction with βTrCP2 and reduced ubiquitination in comparison to WT-Nrf2. In addition, TM-Nrf2 elicited higher expression of the Nrf2 target gene Gclc, potentiated in the presence of a pharmacological AMPK activator. Overall, we propose that AMPK-dependent phospho-sites of Nrf2 can favor its βTrCP2-mediated degradation and dampen the extent of Nrf2 target gene expression. Therefore, targeting AMPK might be able to diminish Nrf2-mediated responses in cells with overactive Nrf2 due to KEAP1 deficiency. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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24 pages, 6300 KiB  
Article
Nrf2 as a Therapeutic Target in the Resistance to Targeted Therapies in Melanoma
by Marie Angèle Cucci, Margherita Grattarola, Chiara Monge, Antonella Roetto, Giuseppina Barrera, Emilia Caputo, Chiara Dianzani and Stefania Pizzimenti
Antioxidants 2023, 12(6), 1313; https://doi.org/10.3390/antiox12061313 - 20 Jun 2023
Cited by 1 | Viewed by 2805
Abstract
The use of specific inhibitors towards mutant BRAF (BRAFi) and MEK (MEKi) in BRAF-mutated patients has significantly improved progression-free and overall survival of metastatic melanoma patients. Nevertheless, half of the patients still develop resistance within the first year of therapy. Therefore, understanding the [...] Read more.
The use of specific inhibitors towards mutant BRAF (BRAFi) and MEK (MEKi) in BRAF-mutated patients has significantly improved progression-free and overall survival of metastatic melanoma patients. Nevertheless, half of the patients still develop resistance within the first year of therapy. Therefore, understanding the mechanisms of BRAFi/MEKi-acquired resistance has become a priority for researchers. Among others, oxidative stress-related mechanisms have emerged as a major force. The aim of this study was to evaluate the contribution of Nrf2, the master regulator of the cytoprotective and antioxidant response, in the BRAFi/MEKi acquired resistance of melanoma. Moreover, we investigated the mechanisms of its activity regulation and the possible cooperation with the oncogene YAP, which is also involved in chemoresistance. Taking advantage of established in vitro melanoma models resistant to BRAFi, MEKi, or dual resistance to BRAFi/MEKi, we demonstrated that Nrf2 was upregulated in melanoma cells resistant to targeted therapy at the post-translational level and that the deubiquitinase DUB3 participated in the control of the Nrf2 protein stability. Furthermore, we found that Nrf2 controlled the expression of YAP. Importantly, the inhibition of Nrf2, directly or through inhibition of DUB3, reverted the resistance to targeted therapies. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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20 pages, 9994 KiB  
Article
CD38-Induced Metabolic Dysfunction Primes Multiple Myeloma Cells for NAD+-Lowering Agents
by Pamela Becherini, Debora Soncini, Silvia Ravera, Elisa Gelli, Claudia Martinuzzi, Giulia Giorgetti, Antonia Cagnetta, Fabio Guolo, Federico Ivaldi, Maurizio Miglino, Sara Aquino, Katia Todoerti, Antonino Neri, Andrea Benzi, Mario Passalacqua, Alessio Nencioni, Ida Perrotta, Maria Eugenia Gallo Cantafio, Nicola Amodio, Antonio De Flora, Santina Bruzzone, Roberto M. Lemoli and Michele Ceaadd Show full author list remove Hide full author list
Antioxidants 2023, 12(2), 494; https://doi.org/10.3390/antiox12020494 - 15 Feb 2023
Viewed by 2191
Abstract
Cancer cells fuel growth and energy demands by increasing their NAD+ biosynthesis dependency, which therefore represents an exploitable vulnerability for anti-cancer strategies. CD38 is a NAD+-degrading enzyme that has become crucial for anti-MM therapies since anti-CD38 monoclonal antibodies represent the [...] Read more.
Cancer cells fuel growth and energy demands by increasing their NAD+ biosynthesis dependency, which therefore represents an exploitable vulnerability for anti-cancer strategies. CD38 is a NAD+-degrading enzyme that has become crucial for anti-MM therapies since anti-CD38 monoclonal antibodies represent the backbone for treatment of newly diagnosed and relapsed multiple myeloma patients. Nevertheless, further steps are needed to enable a full exploitation of these strategies, including deeper insights of the mechanisms by which CD38 promotes tumorigenesis and its metabolic additions that could be selectively targeted by therapeutic strategies. Here, we present evidence that CD38 upregulation produces a pervasive intracellular-NAD+ depletion, which impairs mitochondrial fitness and enhances oxidative stress; as result, genetic or pharmacologic approaches that aim to modify CD38 surface-level prime MM cells to NAD+-lowering agents. The molecular mechanism underlying this event is an alteration in mitochondrial dynamics, which decreases mitochondria efficiency and triggers energetic remodeling. Overall, we found that CD38 handling represents an innovative strategy to improve the outcomes of NAD+-lowering agents and provides the rationale for testing these very promising agents in clinical studies involving MM patients. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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Review

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27 pages, 2696 KiB  
Review
The Multifaceted Roles of NRF2 in Cancer: Friend or Foe?
by Christophe Glorieux, Cinthya Enríquez, Constanza González, Gabriela Aguirre-Martínez and Pedro Buc Calderon
Antioxidants 2024, 13(1), 70; https://doi.org/10.3390/antiox13010070 - 02 Jan 2024
Cited by 1 | Viewed by 2079
Abstract
Physiological concentrations of reactive oxygen species (ROS) play vital roles in various normal cellular processes, whereas excessive ROS generation is central to disease pathogenesis. The nuclear factor erythroid 2-related factor 2 (NRF2) is a critical transcription factor that regulates the cellular antioxidant systems [...] Read more.
Physiological concentrations of reactive oxygen species (ROS) play vital roles in various normal cellular processes, whereas excessive ROS generation is central to disease pathogenesis. The nuclear factor erythroid 2-related factor 2 (NRF2) is a critical transcription factor that regulates the cellular antioxidant systems in response to oxidative stress by governing the expression of genes encoding antioxidant enzymes that shield cells from diverse oxidative alterations. NRF2 and its negative regulator Kelch-like ECH-associated protein 1 (KEAP1) have been the focus of numerous investigations in elucidating whether NRF2 suppresses tumor promotion or conversely exerts pro-oncogenic effects. NRF2 has been found to participate in various pathological processes, including dysregulated cell proliferation, metabolic remodeling, and resistance to apoptosis. Herein, this review article will examine the intriguing role of phase separation in activating the NRF2 transcriptional activity and explore the NRF2 dual impacts on tumor immunology, cancer stem cells, metastasis, and long non-coding RNAs (LncRNAs). Taken together, this review aims to discuss the NRF2 multifaceted roles in both cancer prevention and promotion while also addressing the advantages, disadvantages, and limitations associated with modulating NRF2 therapeutically in cancer treatment. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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20 pages, 1513 KiB  
Review
Targeting Nrf2 Signaling Pathway in Cancer Prevention and Treatment: The Role of Cannabis Compounds
by Anna Rybarczyk, Aleksandra Majchrzak-Celińska and Violetta Krajka-Kuźniak
Antioxidants 2023, 12(12), 2052; https://doi.org/10.3390/antiox12122052 - 28 Nov 2023
Cited by 2 | Viewed by 1597
Abstract
The development and progression of cancer are associated with the dysregulation of multiple pathways involved in cell proliferation and survival, as well as dysfunction in redox balance, immune response, and inflammation. The master antioxidant pathway, known as the nuclear factor erythroid 2-related factor [...] Read more.
The development and progression of cancer are associated with the dysregulation of multiple pathways involved in cell proliferation and survival, as well as dysfunction in redox balance, immune response, and inflammation. The master antioxidant pathway, known as the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, regulates the cellular defense against oxidative stress and inflammation, making it a promising cancer prevention and treatment target. Cannabinoids have demonstrated anti-tumor and anti-inflammatory properties, affecting signaling pathways, including Nrf2. Increased oxidative stress following exposure to anti-cancer therapy prompts cancer cells to activate antioxidant mechanisms. This indicates the dual effect of Nrf2 in cancer cells—influencing proliferation and apoptotic processes and protecting against the toxicity of anti-cancer therapy. Therefore, understanding the complex role of cannabinoids in modulating Nrf2 might shed light on its potential implementation as an anti-cancer support. In this review, we aim to highlight the impact of cannabinoids on Nrf2-related factors, with a focus on cancer prevention and treatment. Additionally, we have presented the results of several research studies that combined cannabidiol (CBD) with other compounds targeting Nrf2. Further studies should be directed toward exploring the anti-inflammatory effects of cannabinoids in the context of cancer prevention and therapy. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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32 pages, 2108 KiB  
Review
Roles of Oxidative Stress and Nrf2 Signaling in Pathogenic and Non-Pathogenic Cells: A Possible General Mechanism of Resistance to Therapy
by Mira Hammad, Mohammad Raftari, Rute Cesário, Rima Salma, Paulo Godoy, S. Noushin Emami and Siamak Haghdoost
Antioxidants 2023, 12(7), 1371; https://doi.org/10.3390/antiox12071371 - 30 Jun 2023
Cited by 13 | Viewed by 4995
Abstract
The coordinating role of nuclear factor erythroid-2-related factor 2 (Nrf2) in cellular function is undeniable. Evidence indicates that this transcription factor exerts massive regulatory functions in multiple signaling pathways concerning redox homeostasis and xenobiotics, macromolecules, and iron metabolism. Being the master regulator of [...] Read more.
The coordinating role of nuclear factor erythroid-2-related factor 2 (Nrf2) in cellular function is undeniable. Evidence indicates that this transcription factor exerts massive regulatory functions in multiple signaling pathways concerning redox homeostasis and xenobiotics, macromolecules, and iron metabolism. Being the master regulator of antioxidant system, Nrf2 controls cellular fate, influencing cell proliferation, differentiation, apoptosis, resistance to therapy, and senescence processes, as well as infection disease success. Because Nrf2 is the key coordinator of cell defence mechanisms, dysregulation of its signaling has been associated with carcinogenic phenomena and infectious and age-related diseases. Deregulation of this cytoprotective system may also interfere with immune response. Oxidative burst, one of the main microbicidal mechanisms, could be impaired during the initial phagocytosis of pathogens, which could lead to the successful establishment of infection and promote susceptibility to infectious diseases. There is still a knowledge gap to fill regarding the molecular mechanisms by which Nrf2 orchestrates such complex networks involving multiple pathways. This review describes the role of Nrf2 in non-pathogenic and pathogenic cells. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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Other

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18 pages, 2146 KiB  
Systematic Review
Ozone Exposure Controls Oxidative Stress and the Inflammatory Process of Hepatocytes in Murine Models
by Silvania Mol Pelinsari, Mariáurea Matias Sarandy, Emerson Ferreira Vilela, Rômulo Dias Novaes, Jade Schlamb and Reggiani Vilela Gonçalves
Antioxidants 2024, 13(2), 212; https://doi.org/10.3390/antiox13020212 - 08 Feb 2024
Viewed by 935
Abstract
(1) Background: Ozone exposure is a promising tool for treating liver damage since it is known to control the release of free radicals and increase the expression of antioxidant enzymes. The objective is to investigate the main intracellular pathways activated after exposure to [...] Read more.
(1) Background: Ozone exposure is a promising tool for treating liver damage since it is known to control the release of free radicals and increase the expression of antioxidant enzymes. The objective is to investigate the main intracellular pathways activated after exposure to ozone, considering the dosage of antioxidant enzymes and markers of oxidative stress. (2) Methods: This systematic review was performed based on the PRISMA guidelines and using a structured search in MEDLINE (PubMed), Scopus, and Web of Science. Bias analysis and methodological quality assessments were examined using the SYRCLE Risk of Bias tool. (3) Results: Nineteen studies were selected. The results showed that the exposure to ozone has a protective effect on liver tissue, promoting a decrease in inflammatory markers and a reduction in oxidative stress in liver tissue. In addition, ozone exposure also promoted an increase in antioxidant enzymes. The morphological consequences of controlling these intracellular pathways were reducing the tissue inflammatory process and reducing areas of degeneration and necrosis. (4) Conclusions: Ozone exposure has a beneficial effect on models of liver injury through the decrease in oxidative stress in tissue and inflammatory markers. In addition, it regulates the Nrf2/ARE antioxidant pathway and blocks the NF-κB inflammatory pathway. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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23 pages, 1327 KiB  
Systematic Review
Docosahexaenoic Acid as Master Regulator of Cellular Antioxidant Defenses: A Systematic Review
by Sara Margherita Borgonovi, Stefania Iametti and Mattia Di Nunzio
Antioxidants 2023, 12(6), 1283; https://doi.org/10.3390/antiox12061283 - 15 Jun 2023
Cited by 1 | Viewed by 1718
Abstract
Docosahexaenoic acid (DHA) is a polyunsaturated fatty acid that benefits the prevention of chronic diseases. Due to its high unsaturation, DHA is vulnerable to free radical oxidation, resulting in several unfavorable effects, including producing hazardous metabolites. However, in vitro and in vivo investigations [...] Read more.
Docosahexaenoic acid (DHA) is a polyunsaturated fatty acid that benefits the prevention of chronic diseases. Due to its high unsaturation, DHA is vulnerable to free radical oxidation, resulting in several unfavorable effects, including producing hazardous metabolites. However, in vitro and in vivo investigations suggest that the relationship between the chemical structure of DHA and its susceptibility to oxidation may not be as clear-cut as previously thought. Organisms have developed a balanced system of antioxidants to counteract the overproduction of oxidants, and the nuclear factor erythroid 2-related factor 2 (Nrf2) is the key transcription factor identified for transmitting the inducer signal to the antioxidant response element. Thus, DHA might preserve the cellular redox status promoting the transcriptional regulation of cellular antioxidants through Nrf2 activation. Here, we systematically summarize the research on the possible role of DHA in controlling cellular antioxidant enzymes. After the screening process, 43 records were selected and included in this review. Specifically, 29 studies related to the effects of DHA in cell cultures and 15 studies concerned the effects of consumption or treatment with DHA in animal. Despite DHA’s promising and encouraging effects at modulating the cellular antioxidant response in vitro/in vivo, some differences observed among the reviewed studies may be accounted for by the different experimental conditions adopted, including the time of supplementation/treatment, DHA concentration, and cell culture/tissue model. Moreover, this review offers potential molecular explanations for how DHA controls cellular antioxidant defenses, including involvement of transcription factors and the redox signaling pathway. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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