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Recent Advances in the Reactive Oxygen Species Production and Handling...
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Recent Advances in the Reactive Oxygen Species Production and Handling by Biological Systems

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Bioorganic Chemistry".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 19377

Special Issue Editor

Dr. Alejandro Samhan-Arias

E-Mail Website1 Website2
Guest Editor
Departamento de Bioquímica, Universidad Autónoma de Madrid (UAM), C/Arturo Duperier 4, 28029-Madrid, Spain
Interests: free radical biology; reactive oxygen species; reactive nitrogen species; peroxidases; NADH oxidases; lipidomics; intrinsically disordered proteins; neurodegenerative diseases; redox biomedicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The reduction of O2 by natural or artificial means transforms molecular O2 into ROS. The superoxide anion radical has attracted the attention of many scientists due to its role in life and disease. The mechanisms of its production and detoxification has been the focus of study for many researchers in the last 50 years. Drs. JoeMcCord and Fridovich discovered the activity of superoxide dismutase early on—a key protein implicated in the detoxification and protection against superoxide anion radical that can be generated by old and recently described mammalian enzymes producing this radical. Moreover, some microorganisms present a different class of enzymes named the superoxide reductases, which are implicated in the detoxification of superoxide anion and protection during infection. This Special Issue is focused on the review of the latest advances in this field.

Dr. Alejandro K. Samhan-Arias
Guest Editor

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Keywords

  • superoxide anion radical
  • superoxide reductases
  • superoxide dismutases
  • antioxidants
  • detection
  • infectivity
  • nitration
  • phosphorylation
  • glutathionylation
  • glycation

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Published Papers (4 papers)

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Research

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17 pages, 3942 KiB  
Article
Molecular Evidence of the Inhibitory Potential of Melatonin against NaAsO2-Induced Aging in Male Rats
by Maryam Baeeri, Tina Didari, Madiha Khalid, Solmaz Mohammadi-Nejad, Seyed Mojtaba Daghighi, Ramtin Farhadi, Mahban Rahimifard, Zahra Bayrami, Hamed Haghi-Aminjan, Roham Foroumadi, Mahdi Gholami and Mohammad Abdollahi
Molecules 2021, 26(21), 6603; https://doi.org/10.3390/molecules26216603 - 31 Oct 2021
Cited by 9 | Viewed by 2881
Abstract
Arsenic (As) poisoning is widespread due to exposure to pollution. The toxic level of (As) causes oxidative stress-induced aging and tissue damage. Since melatonin (MLT) has anti-oxidant and anti-aging properties, we aimed to evaluate the protective effect of MLT against the toxicity of [...] Read more.
Arsenic (As) poisoning is widespread due to exposure to pollution. The toxic level of (As) causes oxidative stress-induced aging and tissue damage. Since melatonin (MLT) has anti-oxidant and anti-aging properties, we aimed to evaluate the protective effect of MLT against the toxicity of sodium arsenite (NaAsO2). Healthy male NMRI mice were divided into eight different groups. The control group received a standard regular diet. Other groups were treated with varying diets, including MLT alone, NaAsO2, and NaAsO2 plus MLT. After one month of treatment, biochemical and pathological tests were performed on blood, heart, and lung tissue samples. NaAsO2 increased the levels of TNF-α, 8-hydroxy-2-deoxy guanosine (8OHdG), malondialdehyde (MDA), reactive oxygen species (ROS), and high mobility group box 1 (HMGB1), increased the expression of TNF receptor type 1-associated death domain (TRADD) mRNA and telomerase reverse transcriptase, and decreased the expression of Klotho (KL) mRNA in both plasma and tissues. In contrast, MLT reduced MDA, ROS, HMGB1, lactate, and TNF-α enhanced the mRNA expression of KL, and suppressed the mRNA expression of the TERT and TRADD genes. Thus, MLT confers potent protection against NaAsO2- induced tissue injury and oxidative stress. Full article
(This article belongs to the Special Issue Recent Advances in the Reactive Oxygen Species Production and Handling by Biological Systems)
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12 pages, 1725 KiB  
Article
The Short-Term Exposure to SDHI Fungicides Boscalid and Bixafen Induces a Mitochondrial Dysfunction in Selective Human Cell Lines
by Donatienne d’Hose, Pauline Isenborghs, Davide Brusa, Bénédicte F. Jordan and Bernard Gallez
Molecules 2021, 26(19), 5842; https://doi.org/10.3390/molecules26195842 - 26 Sep 2021
Cited by 17 | Viewed by 4215
Abstract
Fungicides are used to suppress the growth of fungi for crop protection. The most widely used fungicides are succinate dehydrogenase inhibitors (SDHIs) that act by blocking succinate dehydrogenase, the complex II of the mitochondrial electron transport chain. As recent reports suggested that SDHI-fungicides [...] Read more.
Fungicides are used to suppress the growth of fungi for crop protection. The most widely used fungicides are succinate dehydrogenase inhibitors (SDHIs) that act by blocking succinate dehydrogenase, the complex II of the mitochondrial electron transport chain. As recent reports suggested that SDHI-fungicides could not be selective for their fungi targets, we tested the mitochondrial function of human cells (Peripheral Blood Mononuclear Cells or PBMCs, HepG2 liver cells, and BJ-fibroblasts) after exposure for a short time to Boscalid and Bixafen, the two most used SDHIs. Electron Paramagnetic Resonance (EPR) spectroscopy was used to assess the oxygen consumption rate (OCR) and the level of mitochondrial superoxide radical. The OCR was significantly decreased in the three cell lines after exposure to both SDHIs. The level of mitochondrial superoxide increased in HepG2 after Boscalid and Bixafen exposure. In BJ-fibroblasts, mitochondrial superoxide was increased after Bixafen exposure, but not after Boscalid. No significant increase in mitochondrial superoxide was observed in PBMCs. Flow cytometry revealed an increase in the number of early apoptotic cells in HepG2 exposed to both SDHIs, but not in PBMCs and BJ-fibroblasts, results consistent with the high level of mitochondrial superoxide found in HepG2 cells after exposure. In conclusion, short-term exposure to Boscalid and Bixafen induces a mitochondrial dysfunction in human cells. Full article
(This article belongs to the Special Issue Recent Advances in the Reactive Oxygen Species Production and Handling by Biological Systems)
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14 pages, 1174 KiB  
Article
Compensatory Neuroprotective Response of Thioredoxin Reductase against Oxidative-Nitrosative Stress Induced by Experimental Autoimmune Encephalomyelitis in Rats: Modulation by Theta Burst Stimulation
by Ivana Stevanovic, Milica Ninkovic, Bojana Mancic, Marija Milivojevic, Ivana Stojanovic, Tihomir Ilic, Maja Vujovic and Mirjana Djukic
Molecules 2020, 25(17), 3922; https://doi.org/10.3390/molecules25173922 - 27 Aug 2020
Cited by 10 | Viewed by 2513
Abstract
Cortical theta burst stimulation (TBS) structured as intermittent (iTBS) and continuous (cTBS) could prevent the progression of the experimental autoimmune encephalomyelitis (EAE). The interplay of brain antioxidant defense systems against free radicals (FRs) overproduction induced by EAE, as well as during iTBS or [...] Read more.
Cortical theta burst stimulation (TBS) structured as intermittent (iTBS) and continuous (cTBS) could prevent the progression of the experimental autoimmune encephalomyelitis (EAE). The interplay of brain antioxidant defense systems against free radicals (FRs) overproduction induced by EAE, as well as during iTBS or cTBS, have not been entirely investigated. This study aimed to examine whether oxidative-nitrogen stress (ONS) is one of the underlying pathophysiological mechanisms of EAE, which may be changed in terms of health improvement by iTBS or cTBS. Dark Agouti strain female rats were tested for the effects of EAE and TBS. The rats were randomly divided into the control group, rats specifically immunized for EAE and nonspecifically immuno-stimulated with Complete Freund’s adjuvant. TBS or sham TBS was applied to EAE rats from 14th–24th post-immunization day. Superoxide dismutase activity, levels of superoxide anion (O2•–), lipid peroxidation, glutathione (GSH), nicotinamide adenine dinucleotide phosphate (NADPH), and thioredoxin reductase (TrxR) activity were analyzed in rat spinal cords homogenates. The severity of EAE clinical coincided with the climax of ONS. The most critical result refers to TrxR, which immensely responded against the applied stressors of the central nervous system (CNS), including immunization and TBS. We found that the compensatory neuroprotective role of TrxR upregulation is a positive feedback mechanism that reduces the harmfulness of ONS. iTBS and cTBS both modulate the biochemical environment against ONS at a distance from the area of stimulation, alleviating symptoms of EAE. The results of our study increase the understanding of FRs’ interplay and the role of Trx/TrxR in ONS-associated neuroinflammatory diseases, such as EAE. Also, our results might help the development of new ideas for designing more effective medical treatment, combining neuropsychological with noninvasive neurostimulation–neuromodulation techniques to patients living with MS. Full article
(This article belongs to the Special Issue Recent Advances in the Reactive Oxygen Species Production and Handling by Biological Systems)
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Review

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20 pages, 1215 KiB  
Review
Free Radicals as a Double-Edged Sword: The Cancer Preventive and Therapeutic Roles of Curcumin
by Nehal Gupta, Kshitij Verma, Sarath Nalla, Alok Kulshreshtha, Rajiv Lall and Sahdeo Prasad
Molecules 2020, 25(22), 5390; https://doi.org/10.3390/molecules25225390 - 18 Nov 2020
Cited by 97 | Viewed by 8737
Abstract
Free radicals, generally composed of reactive oxygen species (ROS) and reactive nitrogen species (RNS), are generated in the body by various endogenous and exogenous systems. The overproduction of free radicals is known to cause several chronic diseases including cancer. However, increased production of [...] Read more.
Free radicals, generally composed of reactive oxygen species (ROS) and reactive nitrogen species (RNS), are generated in the body by various endogenous and exogenous systems. The overproduction of free radicals is known to cause several chronic diseases including cancer. However, increased production of free radicals by chemotherapeutic drugs is also associated with apoptosis in cancer cells, indicating the dual nature of free radicals. Among various natural compounds, curcumin manifests as an antioxidant in normal cells that helps in the prevention of carcinogenesis. It also acts as a prooxidant in cancer cells and is associated with inducing apoptosis. Curcumin quenches free radicals, induces antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), and upregulates antioxidative protein markers–Nrf2 and HO-1 that lead to the suppression of cellular oxidative stress. In cancer cells, curcumin aggressively increases ROS that results in DNA damage and subsequently cancer cell death. It also sensitizes drug-resistant cancer cells and increases the anticancer effects of chemotherapeutic drugs. Thus, curcumin shows beneficial effects in prevention, treatment and chemosensitization of cancer cells. In this review, we will discuss the dual role of free radicals as well as the chemopreventive and chemotherapeutic effects of curcumin and its analogues against cancer. Full article
(This article belongs to the Special Issue Recent Advances in the Reactive Oxygen Species Production and Handling by Biological Systems)
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