Special Issue "Mitochondria-Targeted Antioxidants"

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (15 April 2019)

Special Issue Editors

Guest Editor
Prof. Dr. Dmitry B. Zorov

A.N. Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia
Website | E-Mail
Guest Editor
Prof. Dr. Egor Yu. Plotnikov

A.N. Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia
Website | E-Mail

Special Issue Information

Dear Colleagues,

Mitochondria are believed to be the main reactive oxygen species (ROS) source in a wide spectrum of diseases and pathologies, from cardiovascular conditions like stroke and myocardiac infarction to Parkinson’s disease, Alzheimer’s disease, diabetes, and even cancer. This makes them promising targets for pharmaceutical intervention. Furthermore, ROS are essential signaling molecules needed for normal cell physiology, while excessive amounts of ROS should be targeted and neutralized.

Mitochondria-targeted antioxidants provide one of the means to at least partially solve this problem. Since they are directed to the major site of cellular ROS production, their side effects on “signaling ROS” are noticeably reduced, and their therapeutic concentrations could be much lower than those of general antioxidants.

Recently, several types of mitochondria-targeted antioxidants have been developed. Many of them are permeable ions which carry a lipophilic delocalized positive charge, while others have an SS-type mitochondria-targeting peptide, and some use channel-forming compounds to permeabilize the mitochondrial membrane. An antioxidant moiety is also different among these substances: they can carry ROS-scavenging compounds, iron chelators, and mitochondria-targeted antioxidant enzymes such as catalase.

Mitochondria-targeted antioxidants have already been shown to bear a therapeutic effect on Parkinson's and Alzheimer's diseases, type 2 diabetes, hypertension, sepsis, acute bacterial infection as well as diseases caused by xenobiotics, toxic chemicals or irradiation. However, we still need to clarify a number of issues: Should we specifically target mitochondria or not? Do we want to target the mitochondrial matrix or the membrane? What principle of ROS neutralization should be used? Whether we should target chemical or signaling effect of ROS. The purpose of this Special Issue is to bring together our current knowledge of the impact of mitochondria-targeted antioxidants on treatment of different pathologies and diseases. We would like to highlight on the future perspectives and challenges for such antioxidants to overcome their limitations in clinical practice as one of the most universal and promising approaches for treatment of diseases without hiding their adverse effects.

The editors of this Special Issue invite researchers in the field to contribute original research papers and review articles on the subject to this ambitious task.

Prof. Dr. Dmitry B. Zorov
Prof. Dr. Egor Yu. Plotnikov
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 papers will be 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 550 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

  • mitochondria
  • reactive oxygen species
  • oxidative stress
  • aging
  • ischemia
  • inflammation

Published Papers (2 papers)

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Research

Open AccessArticle Protective Effect of Glutathione against Oxidative Stress-induced Cytotoxicity in RAW 264.7 Macrophages through Activating the Nuclear Factor Erythroid 2-Related Factor-2/Heme Oxygenase-1 Pathway
Antioxidants 2019, 8(4), 82; https://doi.org/10.3390/antiox8040082
Received: 18 February 2019 / Revised: 26 March 2019 / Accepted: 27 March 2019 / Published: 1 April 2019
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Abstract
Reactive oxygen species (ROS), products of oxidative stress, contribute to the initiation and progression of the pathogenesis of various diseases. Glutathione is a major antioxidant that can help prevent the process through the removal of ROS. The aim of this study was to [...] Read more.
Reactive oxygen species (ROS), products of oxidative stress, contribute to the initiation and progression of the pathogenesis of various diseases. Glutathione is a major antioxidant that can help prevent the process through the removal of ROS. The aim of this study was to evaluate the protective effect of glutathione on ROS-mediated DNA damage and apoptosis caused by hydrogen peroxide, H2O2, in RAW 264.7 macrophages and to investigate the role of the nuclear factor erythroid 2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. The results showed that the decrease in the survival rate of RAW 264.7 cells treated with H2O2 was due to the induction of DNA damage and apoptosis accompanied by the increased production of ROS. However, H2O2-induced cytotoxicity and ROS generation were significantly reversed by glutathione. In addition, the H2O2-induced loss of mitochondrial membrane potential was related to a decrease in adenosine triphosphate (ATP) levels, and these changes were also significantly attenuated in the presence of glutathione. These protective actions were accompanied by a increase in the expression rate of B-cell lymphoma-2 (Bcl-2)/Bcl-2-associated X protein (Bax) and poly(ADP-ribose) polymerase cleavage by the inactivation of caspase-3. Moreover, glutathione-mediated cytoprotective properties were associated with an increased activation of Nrf2 and expression of HO-1; however, the inhibition of the HO-1 function using an HO-1 specific inhibitor, zinc protoporphyrin IX, significantly weakened the cytoprotective effects of glutathione. Collectively, the results demonstrate that the exogenous administration of glutathione is able to protect RAW 264.7 cells against oxidative stress-induced mitochondria-mediated apoptosis along with the activity of the Nrf2/HO-1 signaling pathway. Full article
(This article belongs to the Special Issue Mitochondria-Targeted Antioxidants)
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Open AccessArticle Suppression of Light-Induced Oxidative Stress in the Retina by Mitochondria-Targeted Antioxidant
Antioxidants 2019, 8(1), 3; https://doi.org/10.3390/antiox8010003
Received: 22 October 2018 / Revised: 3 December 2018 / Accepted: 13 December 2018 / Published: 21 December 2018
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Abstract
Light-induced oxidation of lipids and proteins provokes retinal injuries and results in progression of degenerative retinal diseases, such as, for instance, iatrogenic photic maculopathies. Having accumulated over years retinal injuries contribute to development of age-related macular degeneration (AMD). Antioxidant treatment is regarded as [...] Read more.
Light-induced oxidation of lipids and proteins provokes retinal injuries and results in progression of degenerative retinal diseases, such as, for instance, iatrogenic photic maculopathies. Having accumulated over years retinal injuries contribute to development of age-related macular degeneration (AMD). Antioxidant treatment is regarded as a promising approach to protecting the retina from light damage and AMD. Here, we examine oxidative processes induced in rabbit retina by excessive light illumination with or without premedication using mitochondria-targeted antioxidant SkQ1 (10-(6’-plastoquinonyl)decyltriphenyl-phosphonium). The retinal extracts obtained from animals euthanized within 1–7 days post exposure were analyzed for H2O2, malondialdehyde (MDA), total antioxidant activity (AOA), and activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) using colorimetric and luminescence assays. Oxidation of visual arrestin was monitored by immunoblotting. The light exposure induced lipid peroxidation and H2O2 accumulation in the retinal cells. Unexpectedly, it prominently upregulated AOA in retinal extracts although SOD and GPx activities were compromised. These alterations were accompanied by accumulation of disulfide dimers of arrestin revealing oxidative stress in the photoreceptors. Premedication of the eyes with SkQ1 accelerated normalization of H2O2 levels and redox-status of lipids and proteins, contemporarily enhancing AOA and, likely, sustaining normal activity of GPx. Thus, SkQ1 protects the retina from light-induced oxidative stress and could be employed to suppress oxidative damage of proteins and lipids contributing to AMD. Full article
(This article belongs to the Special Issue Mitochondria-Targeted Antioxidants)
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