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Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2019) | Viewed by 75495

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Prof. Dr. Sergio Di Meo

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Department of Biology, University of Naples Federico II, Monte Sant’Angelo Via Cinthia, Naples, Italy
Interests: ROS; oxidative stress; antioxidants; exercise; hyperthyroidism; diabetes; mitochondria
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Dr. Paola Venditti

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Department of Biology, University of Naples Federico II, Monte Sant’Angelo Via Cinthia, 80126 Naples, Italy
Interests: ROS; oxidative stress; mitochondria; antioxidants; ischemia–reperfusion; functional and experimental hyperthyroidism; exercise; hyperthyroidism; diabetes
Special Issues, Collections and Topics in MDPI journals

Dr. Gaetana Napolitano

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Guest Editor

Department of Sciences and Technology, University of Naples Parthenope, Via Acton 38, 80133 Naples, Italy
Interests: oxidative stress; fish physiology; endurance; ROS; environmental pollution; mitochondria
Special Issues, Collections and Topics in MDPI journals

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Dear colleagues,

ROS were long considered one of the key players in tissue injury. Indeed, overproduction of ROS results in oxidative stress, a process leading to the development of many pathological conditions for whose treatment the use of antioxidants was proposed.

Over time, it was shown that ROS at low concentrations act as signaling molecules leading to the regulation of physiological functions. Moreover, several interventions that increase ROS generation activate stress-adaptive responses that extend lifespan. It was also shown that excessive use of antioxidants can counter the beneficial effects of ROS.

Currently, much progress has been made in understanding the role of ROS in human diseases and ageing as well as in the regulation of physiological functions, and in identifying the signaling pathways involved in ROS. However, much remains to be understood about the mutual interactions among signaling pathways underlying organism-adaptive responses, their modifications (which occur during ageing), and some disease states. For this reason, we invite you to submit original research articles and reviews that address the effects of ROS production and antioxidant treatment in living organisms, focusing on their impact on health, diseases, and ageing.

Prof. Dr. Sergio Di Meo
Prof. Dr. Paola Venditti
Dr. Gaetana Napolitano
Guest Editors

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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

ROS
Antioxidants
Health
Disease
Aging
Redox homeostasis
Redox signaling
Antioxidant supplementation.

Related Special Issue

Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment 2.0 in International Journal of Molecular Sciences (9 articles)

Published Papers (12 papers)

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Editorial

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3 pages, 164 KiB

Open AccessEditorial

Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment

by Sergio Di Meo, Gaetana Napolitano and Paola Venditti

Int. J. Mol. Sci. 2019, 20(19), 4810; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20194810 - 27 Sep 2019

Cited by 13 | Viewed by 2326

Abstract

From their discovery in biological systems, reactive oxygen species (ROS) have been considered key players in tissue injury for their capacity to oxidize biological macromolecules [...] Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

Research

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23 pages, 7469 KiB

Open AccessArticle

Carbon Monoxide Releasing Molecule-2-Upregulated ROS-Dependent Heme Oxygenase-1 Axis Suppresses Lipopolysaccharide-Induced Airway Inflammation

by Chih-Chung Lin, Li-Der Hsiao, Rou-Ling Cho and Chuen-Mao Yang

Int. J. Mol. Sci. 2019, 20(13), 3157; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20133157 - 28 Jun 2019

Cited by 29 | Viewed by 3766

Abstract

The up-regulation of heme oxygenase-1 (HO-1) is mediated through nicotinamaide adenine dinucleotide phosphate (NADPH) oxidases (Nox) and reactive oxygen species (ROS) generation, which could provide cytoprotection against inflammation. However, the molecular mechanisms of carbon monoxide-releasing molecule (CORM)-2-induced HO-1 expression in human tracheal smooth muscle cells (HTSMCs) remain unknown. Here, we found that pretreatment with CORM-2 attenuated the lipopolysaccharide (LPS)-induced intercellular adhesion molecule (ICAM-1) expression and leukocyte count through the up-regulation of HO-1 in mice, which was revealed by immunohistochemistrical staining, Western blot, real-time PCR, and cell count. The inhibitory effects of HO-1 by CORM-2 were reversed by transfection with HO-1 siRNA. Next, Western blot, real-time PCR, and promoter activity assay were performed to examine the HO-1 induction in HTSMCs. We found that CORM-2 induced HO-1 expression via the activation of protein kinase C (PKC)α and proline-rich tyrosine kinase (Pyk2), which was mediated through Nox-derived ROS generation using pharmacological inhibitors or small interfering ribonucleic acids (siRNAs). CORM-2-induced HO-1 expression was mediated through Nox-(1, 2, 4) or p47^phox, which was confirmed by transfection with their own siRNAs. The Nox-derived ROS signals promoted the activities of extracellular signal-regulated kinase 1/2 (ERK1/2). Subsequently, c-Fos and c-Jun—activator protein-1 (AP-1) subunits—were up-regulated by activated ERK1/2, which turned on transcription of the HO-1 gene by regulating the HO-1 promoter. These results suggested that in HTSMCs, CORM-2 activates PKCα/Pyk2-dependent Nox/ROS/ERK1/2/AP-1, leading to HO-1 up-regulation, which suppresses the lipopolysaccharide (LPS)-induced airway inflammation. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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13 pages, 2363 KiB

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Trimethylamine N-Oxide Does Not Impact Viability, ROS Production, and Mitochondrial Membrane Potential of Adult Rat Cardiomyocytes

by Giulia Querio, Susanna Antoniotti, Renzo Levi and Maria Pia Gallo

Int. J. Mol. Sci. 2019, 20(12), 3045; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20123045 - 21 Jun 2019

Cited by 19 | Viewed by 3535

Abstract

Trimethylamine N-oxide (TMAO) is an organic compound derived from dietary choline and L-carnitine. It behaves as an osmolyte, a protein stabilizer, and an electron acceptor, showing different biological functions in different animals. Recent works point out that, in humans, high circulating levels of TMAO are related to the progression of atherosclerosis and other cardiovascular diseases. However, studies on a direct role of TMAO in cardiomyocyte parameters are still limited. The purpose of this work is to study the effects of TMAO on isolated adult rat cardiomyocytes. TMAO in both 100 µM and 10 mM concentrations, from 1 to 24 h of treatment, does not affect cell viability, sarcomere length, intracellular ROS, and mitochondrial membrane potential. Furthermore, the simultaneous treatment with TMAO and known cardiac insults, such as H₂O₂ or doxorubicin, does not affect the treatment’s effect. In conclusion, TMAO cannot be considered a direct cause or an exacerbating risk factor of cardiac damage at the cellular level in acute conditions. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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16 pages, 3036 KiB

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Sphingomyelin Synthase 2 Promotes Endothelial Dysfunction by Inducing Endoplasmic Reticulum Stress

by Lingyue Hua, Na Wu, Ruilin Zhao, Xuanhong He, Qian Liu, Xiatian Li, Zhiqiang He, Lehan Yu and Nianlong Yan

Int. J. Mol. Sci. 2019, 20(12), 2861; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20122861 - 12 Jun 2019

Cited by 14 | Viewed by 3606

Abstract

Endothelial dysfunction (ED) is an important contributor to atherosclerotic cardiovascular disease. Our previous study demonstrated that sphingomyelin synthase 2 (SMS2) promotes ED. Moreover, endoplasmic reticulum (ER) stress can lead to ED. However, whether there is a correlation between SMS2 and ER stress is unclear. To examine their correlation and determine the detailed mechanism of this process, we constructed a human umbilical vein endothelial cell (HUVEC) model with SMS2 overexpression. These cells were treated with 4-PBA or simvastatin and with LiCl and salinomycin alone. The results showed that SMS2 can promote the phosphorylation of lipoprotein receptor-related protein 6 (LRP6) and activate the Wnt/β-catenin pathway and that activation or inhibition of the Wnt/β-catenin pathway can induce or block ER stress, respectively. However, inhibition of ER stress by 4-PBA can decrease ER stress and ED. Furthermore, when the biosynthesis of cholesterol is inhibited by simvastatin, the reduction in intracellular cholesterol coincides with a decrease in ER stress and ED. Collectively, our results demonstrate that SMS2 can activate the Wnt/β-catenin pathway and promote intracellular cholesterol accumulation, both of which can contribute to the induction of ER stress and finally lead to ED. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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15 pages, 3197 KiB

Open AccessArticle

Artemisinin Attenuated Hydrogen Peroxide (H₂O₂)-Induced Oxidative Injury in SH-SY5Y and Hippocampal Neurons via the Activation of AMPK Pathway

by Xia Zhao, Jiankang Fang, Shuai Li, Uma Gaur, Xingan Xing, Huan Wang and Wenhua Zheng

Int. J. Mol. Sci. 2019, 20(11), 2680; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20112680 - 31 May 2019

Cited by 57 | Viewed by 6477

Abstract

Oxidative stress is believed to be one of the main causes of neurodegenerative diseases such as Alzheimer’s disease (AD). The pathogenesis of AD is still not elucidated clearly but oxidative stress is one of the key hypotheses. Here, we found that artemisinin, an anti-malarial Chinese medicine, possesses neuroprotective effects. However, the antioxidative effects of artemisinin remain to be explored. In this study, we found that artemisinin rescued SH-SY5Y and hippocampal neuronal cells from hydrogen peroxide (H₂O₂)-induced cell death at clinically relevant doses in a concentration-dependent manner. Further studies showed that artemisinin significantly restored the nuclear morphology, improved the abnormal changes in intracellular reactive oxygen species (ROS), reduced the mitochondrial membrane potential, and caspase-3 activation, thereby attenuating apoptosis. Artemisinin also stimulated the phosphorylation of the adenosine monophosphate -activated protein kinase (AMPK) pathway in SH-SY5Y cells in a time- and concentration-dependent manner. Inhibition of the AMPK pathway attenuated the protective effect of artemisinin. These data put together suggested that artemisinin has the potential to protect neuronal cells. Similar results were obtained in primary cultured hippocampal neurons. Cumulatively, these results indicated that artemisinin protected neuronal cells from oxidative damage, at least in part through the activation of AMPK. Our findings support the role of artemisinin as a potential therapeutic agent for neurodegenerative diseases. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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14 pages, 11977 KiB

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Key Role of Reactive Oxygen Species (ROS) in Indirubin Derivative-Induced Cell Death in Cutaneous T-Cell Lymphoma Cells

by Marwa Y. Soltan, Uly Sumarni, Chalid Assaf, Peter Langer, Ulrich Reidel and Jürgen Eberle

Int. J. Mol. Sci. 2019, 20(5), 1158; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20051158 - 07 Mar 2019

Cited by 16 | Viewed by 3702

Abstract

Cutaneous T-cell lymphoma (CTCL) may develop a highly malignant phenotype in its late phase, and patients may profit from innovative therapies. The plant extract indirubin and its chemical derivatives represent new and promising antitumor strategies. This first report on the effects of an indirubin derivative in CTCL cells shows a strong decrease of cell proliferation and cell viability as well as an induction of apoptosis, suggesting indirubin derivatives for therapy of CTCL. As concerning the mode of activity, the indirubin derivative DKP-071 activated the extrinsic apoptosis cascade via caspase-8 and caspase-3 through downregulation of the caspase antagonistic proteins c-FLIP and XIAP. Importantly, a strong increase of reactive oxygen species (ROS) was observed as an immediate early effect in response to DKP-071 treatment. The use of antioxidative pre-treatment proved the decisive role of ROS, which turned out upstream of all other proapoptotic effects monitored. Thus, reactive oxygen species appear as a highly active proapoptotic pathway in CTCL, which may be promising for therapeutic intervention. This pathway can be efficiently activated by an indirubin derivative. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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Review

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23 pages, 1900 KiB

Open AccessReview

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

by Tayaba Ismail, Youni Kim, Hongchan Lee, Dong-Seok Lee and Hyun-Shik Lee

Int. J. Mol. Sci. 2019, 20(18), 4407; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20184407 - 07 Sep 2019

Cited by 80 | Viewed by 10054

Abstract

Mitochondria are multifunctional cellular organelles that are major producers of reactive oxygen species (ROS) in eukaryotes; to maintain the redox balance, they are supplemented with different ROS scavengers, including mitochondrial peroxiredoxins (Prdxs). Mitochondrial Prdxs have physiological and pathological significance and are associated with the initiation and progression of various cancer types. In this review, we have focused on signaling involving ROS and mitochondrial Prdxs that is associated with cancer development and progression. An upregulated expression of Prdx3 and Prdx5 has been reported in different cancer types, such as breast, ovarian, endometrial, and lung cancers, as well as in Hodgkin’s lymphoma and hepatocellular carcinoma. The expression of Prdx3 and Prdx5 in different types of malignancies involves their association with different factors, such as transcription factors, micro RNAs, tumor suppressors, response elements, and oncogenic genes. The microenvironment of mitochondrial Prdxs plays an important role in cancer development, as cancerous cells are equipped with a high level of antioxidants to overcome excessive ROS production. However, an increased production of Prdx3 and Prdx5 is associated with the development of chemoresistance in certain types of cancers and it leads to further complications in cancer treatment. Understanding the interplay between mitochondrial Prdxs and ROS in carcinogenesis can be useful in the development of anticancer drugs with better proficiency and decreased resistance. However, more targeted studies are required for exploring the tumor microenvironment in association with mitochondrial Prdxs to improve the existing cancer therapies and drug development. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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18 pages, 2367 KiB

Open AccessReview

Causative Links between Protein Aggregation and Oxidative Stress: A Review

by Elise Lévy, Nadine El Banna, Dorothée Baïlle, Amélie Heneman-Masurel, Sandrine Truchet, Human Rezaei, Meng-Er Huang, Vincent Béringue, Davy Martin and Laurence Vernis

Int. J. Mol. Sci. 2019, 20(16), 3896; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20163896 - 09 Aug 2019

Cited by 110 | Viewed by 9765

Abstract

Compelling evidence supports a tight link between oxidative stress and protein aggregation processes, which are noticeably involved in the development of proteinopathies, such as Alzheimer’s disease, Parkinson’s disease, and prion disease. The literature is tremendously rich in studies that establish a functional link between both processes, revealing that oxidative stress can be either causative, or consecutive, to protein aggregation. Because oxidative stress monitoring is highly challenging and may often lead to artefactual results, cutting-edge technical tools have been developed recently in the redox field, improving the ability to measure oxidative perturbations in biological systems. This review aims at providing an update of the previously known functional links between oxidative stress and protein aggregation, thereby revisiting the long-established relationship between both processes. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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18 pages, 642 KiB

Open AccessReview

Dual Role of Reactive Oxygen Species in Muscle Function: Can Antioxidant Dietary Supplements Counteract Age-Related Sarcopenia?

by Simona Damiano, Espedita Muscariello, Giuliana La Rosa, Martina Di Maro, Paolo Mondola and Mariarosaria Santillo

Int. J. Mol. Sci. 2019, 20(15), 3815; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20153815 - 05 Aug 2019

Cited by 65 | Viewed by 7117

Abstract

Sarcopenia is characterized by the progressive loss of skeletal muscle mass and strength. In older people, malnutrition and physical inactivity are often associated with sarcopenia, and, therefore, dietary interventions and exercise must be considered to prevent, delay, or treat it. Among the pathophysiological mechanisms leading to sarcopenia, a key role is played by an increase in reactive oxygen and nitrogen species (ROS/RNS) levels and a decrease in enzymatic antioxidant protection leading to oxidative stress. Many studies have evaluated, in addition to the effects of exercise, the effects of antioxidant dietary supplements in limiting age-related muscle mass and performance, but the data which have been reported are conflicting. In skeletal muscle, ROS/RNS have a dual function: at low levels they increase muscle force and adaptation to exercise, while at high levels they lead to a decline of muscle performance. Controversial results obtained with antioxidant supplementation in older persons could in part reflect the lack of univocal effects of ROS on muscle mass and function. The purpose of this review is to examine the molecular mechanisms underlying the dual effects of ROS in skeletal muscle function and the analysis of literature data on dietary antioxidant supplementation associated with exercise in normal and sarcopenic subjects. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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20 pages, 1027 KiB

Open AccessReview

Glutathione Metabolism in Renal Cell Carcinoma Progression and Implications for Therapies

by Yi Xiao and David Meierhofer

Int. J. Mol. Sci. 2019, 20(15), 3672; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20153672 - 26 Jul 2019

Cited by 59 | Viewed by 11358

Abstract

A significantly increased level of the reactive oxygen species (ROS) scavenger glutathione (GSH) has been identified as a hallmark of renal cell carcinoma (RCC). The proposed mechanism for increased GSH levels is to counteract damaging ROS to sustain the viability and growth of the malignancy. Here, we review the current knowledge about the three main RCC subtypes, namely clear cell RCC (ccRCC), papillary RCC (pRCC), and chromophobe RCC (chRCC), at the genetic, transcript, protein, and metabolite level and highlight their mutual influence on GSH metabolism. A further discussion addresses the question of how the manipulation of GSH levels can be exploited as a potential treatment strategy for RCC. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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19 pages, 937 KiB

Open AccessReview

Evolution Shapes the Gene Expression Response to Oxidative Stress

by Rima Siauciunaite, Nicholas S. Foulkes, Viola Calabrò and Daniela Vallone

Int. J. Mol. Sci. 2019, 20(12), 3040; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20123040 - 21 Jun 2019

Cited by 36 | Viewed by 5565

Abstract

Reactive oxygen species (ROS) play a key role in cell physiology and function. ROS represents a potential source of damage for many macromolecules including DNA. It is thought that daily changes in oxidative stress levels were an important early factor driving evolution of the circadian clock which enables organisms to predict changes in ROS levels before they actually occur and thereby optimally coordinate survival strategies. It is clear that ROS, at relatively low levels, can serve as an important signaling molecule and also serves as a key regulator of gene expression. Therefore, the mechanisms that have evolved to survive or harness these effects of ROS are ancient evolutionary adaptations that are tightly interconnected with most aspects of cellular physiology. Our understanding of these mechanisms has been mainly based on studies using a relatively small group of genetic models. However, we know comparatively little about how these mechanisms are conserved or have adapted during evolution under different environmental conditions. In this review, we describe recent work that has revealed significant species-specific differences in the gene expression response to ROS by exploring diverse organisms. This evidence supports the notion that during evolution, rather than being highly conserved, there is inherent plasticity in the molecular mechanisms responding to oxidative stress. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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38 pages, 1426 KiB

Open AccessReview

Mediators of Physical Activity Protection against ROS-Linked Skeletal Muscle Damage

by Sergio Di Meo, Gaetana Napolitano and Paola Venditti

Int. J. Mol. Sci. 2019, 20(12), 3024; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20123024 - 20 Jun 2019

Cited by 75 | Viewed by 7214

Abstract

Unaccustomed and/or exhaustive exercise generates excessive free radicals and reactive oxygen and nitrogen species leading to muscle oxidative stress-related damage and impaired contractility. Conversely, a moderate level of free radicals induces the body’s adaptive responses. Thus, a low oxidant level in resting muscle is essential for normal force production, and the production of oxidants during each session of physical training increases the body’s antioxidant defenses. Mitochondria, NADPH oxidases and xanthine oxidases have been identified as sources of free radicals during muscle contraction, but the exact mechanisms underlying exercise-induced harmful or beneficial effects yet remain elusive. However, it is clear that redox signaling influences numerous transcriptional activators, which regulate the expression of genes involved in changes in muscle phenotype. The mitogen-activated protein kinase family is one of the main links between cellular oxidant levels and skeletal muscle adaptation. The family components phosphorylate and modulate the activities of hundreds of substrates, including transcription factors involved in cell response to oxidative stress elicited by exercise in skeletal muscle. To elucidate the complex role of ROS in exercise, here we reviewed the literature dealing on sources of ROS production and concerning the most important redox signaling pathways, including MAPKs that are involved in the responses to acute and chronic exercise in the muscle, particularly those involved in the induction of antioxidant enzymes. Full article

(This article belongs to the Special Issue Physiological and Pathological Role of ROS: Benefits and Limitations of Antioxidant Treatment)

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