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Molecular Research on Free Radicals and Oxidative Stress
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Molecular Research on Free Radicals and Oxidative Stress

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 1 May 2025 | Viewed by 17663

Special Issue Editor

Dr. Mosharraf Sarker

E-Mail Website
Guest Editor
Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK
Interests: oxidative stress; reactive oxygen species (ROS); free radicals; inflammation; microcirculation; blood–brain barrier
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is a condition characterized by an imbalance between unstable reactive oxygen species (ROS) production and the body's antioxidant defense mechanisms. Free radicals, which include superoxide radicals (O2•−), hydroxyl radicals (•OH), and peroxyl radicals (ROO•), as well as reactive nitrogen species (RNS) like nitric oxide (•NO) and nitrogen dioxide (•NO2), are highly reactive molecules with unpaired electrons that play a pivotal role in oxidative stress by damaging cellular components, such as lipids, proteins, and DNA.

Various environmental factors, such as radiation exposure, obesity, smoking, pollution, alcohol consumption, dietary habits, and lifestyle, contribute to the generation of free radicals, exacerbating oxidative stress and disrupting the physiological antioxidant defense system. While some free radicals play important roles in physiological processes, like cell signaling and immune responses, their excessive accumulation can lead to oxidative stress and damage to the cellular components, contributing to various diseases and aging processes, including neurodegenerative diseases, cancer, atherosclerosis, diabetes, infertility, and fibrosis.

At the molecular level, the mechanisms driving oxidative-induced cellular dysfunction are complex and include mitochondrial damage, autophagy, mitophagy, endoplasmic reticulum stress, and apoptosis. However, the intricate interactions among these mechanisms, especially in metabolic diseases, are not fully understood.

This Special Issue invites the submission of original research articles and reviews elucidating the role of oxidative stress and unravelling the underlying molecular mechanisms. We hope to advance our understanding of oxidative stress-related pathologies and pave the way for innovative therapeutic strategies.

Dr. Mosharraf Sarker
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. Current Issues in Molecular Biology 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 2200 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
  • free radicals
  • reactive oxygen species (ROS)
  • gene regulation
  • antioxidants
  • mitochondrial dysfunction
  • insulin resistance
  • inflammation
  • autophagy

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Published Papers (8 papers)

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Research

Jump to: Review

13 pages, 1944 KiB  
Article
Antioxidant Mechanisms of the Protective Action of Selenase in Experimental Chronic Generalized Periodontitis
by Valeriy Salnykov, Igor Belenichev, Lyudmyla Makyeyeva, Dmytro Skoryna, Valentyn Oksenych and Oleksandr Kamyshnyi
Curr. Issues Mol. Biol. 2025, 47(3), 186; https://doi.org/10.3390/cimb47030186 - 12 Mar 2025
Viewed by 550
Abstract
Inflammatory periodontal diseases, despite all the efforts of modern dentistry, remain an important predictor of tooth loss worldwide. Oxidative stress plays a crucial role in the pathogenesis of periodontitis, making the use of antioxidants an attractive option for its treatment. Our attention was [...] Read more.
Inflammatory periodontal diseases, despite all the efforts of modern dentistry, remain an important predictor of tooth loss worldwide. Oxidative stress plays a crucial role in the pathogenesis of periodontitis, making the use of antioxidants an attractive option for its treatment. Our attention was drawn to the selenium compound Selenase as an antioxidant therapeutic agent. In this study, we modeled a calcium-deficient prooxidant chronic generalized periodontitis (CGP) model in white non-linear rats. Then, after 14 days, Selenase (50 μg/kg) and Mexidol (250 mg/kg) were administered intragastrically. Blood samples from the animals were analyzed using ELISA and biochemical methods to determine Cu-Zn SOD, nitrotyrosine, GPX-4, iNOS, NOx, GSH, and GSSG levels. The CGP model led to the typical clinical signs of periodontitis, including hyperemia, edema, gingival pocket formation, bleeding, tooth mobility, as well as an increase in molecular–biochemical markers of nitrosative stress and a reduction of endogenous antioxidants in the blood. Selenase resulted in a decrease in the clinical manifestations of CGP, reduced iNOS, nitrotyrosine, and NOx levels, and an increase in Cu-Zn SOD and GPX-4 compared to the control group (p < 0.05). Mexidol had a less pronounced effect on these markers compared to Selenase (p < 0.05). Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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13 pages, 664 KiB  
Article
Comparative Effects of Vitamin D Supplementation on Oxidative Stress in Relapsing–Remitting Multiple Sclerosis
by Martyna Lis, Natalia Niedziela, Jowita Adamczyk-Zostawa, Jolanta Zalejska-Fiolka, Jarosław Szczygieł, Agata Sowa, Agata Świętek and Monika Adamczyk-Sowa
Curr. Issues Mol. Biol. 2024, 46(12), 14119-14131; https://doi.org/10.3390/cimb46120845 - 14 Dec 2024
Viewed by 1004
Abstract
Studies suggest that vitamin D (VitD) may reduce oxidative stress (OS) in multiple sclerosis (MS) patients. This study aimed to compare the effects of various VitD doses on OS in relapsing–remitting MS (RRMS). A 6-month supplementation was introduced using two doses of VitD: [...] Read more.
Studies suggest that vitamin D (VitD) may reduce oxidative stress (OS) in multiple sclerosis (MS) patients. This study aimed to compare the effects of various VitD doses on OS in relapsing–remitting MS (RRMS). A 6-month supplementation was introduced using two doses of VitD: 2000 IU/day in the high-dose group (HD, n = 23) and 15,960 IU/month in the low-dose group (LD, n = 29). Significant differences in body weight, height, and age were found between groups. A significant increase in the level of VitD (25(OH)D) was noted in both groups (p < 0.01). A significant increase was observed in the levels of LF and MDA (p < 0.01) and a significant decrease in the concentrations of PSH (p < 0.01), CuZnSOD (p = 0.02), and TOS (p < 0.01). A significant positive correlation was observed between serum VitD and SOD (R = 0.38, p < 0.01) and MnSOD (R = 0.31, p < 0.05), as well as a significant negative correlation between serum VitD and MDA (R = −0.31, p = 0.05) at the beginning of the study. At the end of the study, a significant positive correlation was observed between serum VitD and SOD (R = 0.34, p < 0.05) and CuZnSOD (R = 0.51, p < 0.01). In RRMS patients, the VitD doses are probably insufficient to induce a beneficial effect on the pro- and antioxidant balance. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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14 pages, 1415 KiB  
Article
Algal Oil Mitigates Sodium Taurocholate-Induced Pancreatitis by Alleviating Calcium Overload, Oxidative Stress, and NF-κB Activation in Pancreatic Acinar Cells
by Yi Fang, Sung-Yen Lin, Chung-Hwan Chen and Hui-Chen Lo
Curr. Issues Mol. Biol. 2024, 46(5), 4403-4416; https://doi.org/10.3390/cimb46050267 - 7 May 2024
Viewed by 1300
Abstract
Acute pancreatitis (AP) is characterized by elevated intracellular Ca2+ concentrations, mitochondrial dysfunction, and oxidative stress in pancreatic acinar cells. Algal oil (AO) has demonstrated antioxidant and anti-inflammatory properties. This study aims to explore the effects of algal oil on the microenvironment of [...] Read more.
Acute pancreatitis (AP) is characterized by elevated intracellular Ca2+ concentrations, mitochondrial dysfunction, and oxidative stress in pancreatic acinar cells. Algal oil (AO) has demonstrated antioxidant and anti-inflammatory properties. This study aims to explore the effects of algal oil on the microenvironment of AP. Rat pancreatic acinar AR42J cells were pretreated with AO containing 0, 50, 100, or 150 μM of docosahexaenoic acid (DHA) 2 h prior to AP induction using sodium taurocholate (STC). After 1 h of STC treatment, AR42J cells exhibited a significant increase in intracellular Ca2+ concentration and the production of amylase, lipase, reactive oxygen species, and pro-inflammatory mediators, including tumor necrosis factor-α and interleukin-6. These STC-induced increases were markedly reduced in cells pretreated with AO. In comparison to cells without AO, those treated with a high dose of AO before STC exposure demonstrated a significant increase in mitochondrial membrane potential and a decrease in lipid peroxidation. Furthermore, STC-activated nuclear factor kappa-B (NF-κB) was attenuated in AO-pretreated cells, as evidenced by a significant decrease in activated NF-κB. In conclusion, AO may prevent damage to pancreatic acinar cells by alleviating intracellular Ca2+ overload, mitigating mitochondrial dysfunction, reducing oxidative stress, and attenuating NF-κB-targeted inflammation. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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Review

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14 pages, 2650 KiB  
Review
Liposomes as Imaging Agents of Inflammation and Oxidative Stress in Bone Implants
by Delia Danila, Patricia S. Pardo, R. Devesh Kumar Misra and Aladin M. Boriek
Curr. Issues Mol. Biol. 2025, 47(5), 295; https://doi.org/10.3390/cimb47050295 - 22 Apr 2025
Viewed by 240
Abstract
Liposomes are tiny, spherical vesicles made from cholesterol and natural phospholipids that are promising imaging agents for detecting medical complications. They can carry fluorescent markers or other imaging agents, making them effective for medical imaging. Furthermore, liposomes can target specific cells involved in [...] Read more.
Liposomes are tiny, spherical vesicles made from cholesterol and natural phospholipids that are promising imaging agents for detecting medical complications. They can carry fluorescent markers or other imaging agents, making them effective for medical imaging. Furthermore, liposomes can target specific cells involved in inflammation, such as macrophages, and accumulate at inflammation sites when injected. Additionally, liposomes can be designed to respond to oxidative stress, which is often associated with bone implant complications. By detecting areas of stress, liposomes provide valuable information about implant health. However, challenges such as rapid clearance from the body, precise targeting, immune reactions, and high production costs must be addressed. Research is ongoing to improve the design and functionality of liposomes. They can potentially monitor bone implants as non-invasive imaging agents, enabling early detection of complications and timely interventions. This approach can enhance patient outcomes and extend the longevity of implants, making it a promising strategy for better patient care and implant success. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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22 pages, 7092 KiB  
Review
ROS Chronicles in HIV Infection: Genesis of Oxidative Stress, Associated Pathologies, and Therapeutic Strategies
by R Harshithkumar, Prachibahen Shah, Pratiksha Jadaun and Anupam Mukherjee
Curr. Issues Mol. Biol. 2024, 46(8), 8852-8873; https://doi.org/10.3390/cimb46080523 - 14 Aug 2024
Cited by 4 | Viewed by 2767
Abstract
Reactive oxygen species (ROS) are widely regarded as signaling molecules and play essential roles in various cellular processes, but when present in excess, they can lead to oxidative stress (OS). Growing evidence suggests that the OS plays a critical role in the pathogenesis [...] Read more.
Reactive oxygen species (ROS) are widely regarded as signaling molecules and play essential roles in various cellular processes, but when present in excess, they can lead to oxidative stress (OS). Growing evidence suggests that the OS plays a critical role in the pathogenesis of HIV infection and is associated with several comorbidities in HIV-infected individuals. ROS, generated both naturally during mitochondrial oxidative metabolism and as a response to various cellular processes, can trigger host antiviral responses but can also promote viral replication. While the multifaceted roles of ROS in HIV pathophysiology clearly need more investigation, this review paper unravels the mechanisms of OS generation in the context of HIV infections, offering insights into HIV viral protein-mediated and antiretroviral therapy-generated OS. Though the viral protein Tat is significantly attributed to the endogenous cellular increase in ROS post HIV infection, this paper sums up the contribution of other viral proteins in HIV-mediated elicitation of ROS. Given the investigations recognizing the significant role of ROS in the onset and progression of diverse pathologies, the paper also explores the critical function of ROS in the mediation of an of array of pathologies associated with HIV infection and retroviral therapy. HIV patients are observed with disruption to the antioxidant defense system, the antioxidant therapy is gaining focus as a potential therapeutic intervention and is well discussed. While ROS play a significant role in the HIV scenario, further exploratory studies are imperative to identifying alternative therapeutic strategies that could mitigate the toxicities and pathologies associated with ART-induced OS. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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28 pages, 2008 KiB  
Review
Oxidative Stress and Erectile Dysfunction: Pathophysiology, Impacts, and Potential Treatments
by Aris Kaltsas, Athanasios Zikopoulos, Fotios Dimitriadis, Danja Sheshi, Magdalena Politis, Efthalia Moustakli, Evangelos N. Symeonidis, Michael Chrisofos, Nikolaos Sofikitis and Athanasios Zachariou
Curr. Issues Mol. Biol. 2024, 46(8), 8807-8834; https://doi.org/10.3390/cimb46080521 - 14 Aug 2024
Cited by 18 | Viewed by 5664
Abstract
Erectile dysfunction (ED) is a prevalent condition affecting men’s sexual health, with oxidative stress (OS) having recently been identified as a significant contributing causative factor. This narrative review aims to elucidate the role of OS in the pathophysiology of ED, focusing on impact, [...] Read more.
Erectile dysfunction (ED) is a prevalent condition affecting men’s sexual health, with oxidative stress (OS) having recently been identified as a significant contributing causative factor. This narrative review aims to elucidate the role of OS in the pathophysiology of ED, focusing on impact, mechanisms, and potential therapeutic interventions. Key findings indicate that OS disrupts endothelial function and nitric oxide (NO) signaling, crucial for erectile function. Various sources of reactive oxygen species (ROS) and their detrimental effects on penile tissue are discussed, including aging, diabetes mellitus, hypertension, hyperlipidemia, smoking, obesity, alcohol consumption, psychological stress, hyperhomocysteinemia, chronic kidney disease, and sickle cell disease. Major sources of ROS, such as NADPH oxidase, xanthine oxidase, uncoupled endothelial NO synthase (eNOS), and mitochondrial electron transport, are identified. NO is scavenged by these ROS, leading to endothelial dysfunction characterized by reduced NO availability, impaired vasodilation, increased vascular tone, and inflammation. This ultimately results in ED due to decreased blood flow to penile tissue and the inability to achieve or maintain an erection. Furthermore, ROS impact the transmission of nitrergic neurotransmitters by causing the death of nitrergic neurons and reducing the signaling of neuronal NO synthase (nNOS), exacerbating ED. Therapeutic approaches targeting OS, including antioxidants and lifestyle modifications, show promise in ameliorating ED symptoms. The review underscores the need for further research to develop effective treatments, emphasizing the interplay between OS and vascular health in ED. Integrating pharmacological and non-pharmacological strategies could enhance clinical outcomes for ED patients, advocating for OS management in ED treatment protocols to improve patient quality of life. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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17 pages, 2548 KiB  
Review
MicroRNAs as Regulators of Radiation-Induced Oxidative Stress
by Branislav Kura, Patricia Pavelkova, Barbora Kalocayova, Margita Pobijakova and Jan Slezak
Curr. Issues Mol. Biol. 2024, 46(7), 7097-7113; https://doi.org/10.3390/cimb46070423 - 6 Jul 2024
Cited by 1 | Viewed by 2072
Abstract
microRNAs (miRNAs) represent small RNA molecules involved in the regulation of gene expression. They are implicated in the regulation of diverse cellular processes ranging from cellular homeostasis to stress responses. Unintended irradiation of the cells and tissues, e.g., during medical uses, induces various [...] Read more.
microRNAs (miRNAs) represent small RNA molecules involved in the regulation of gene expression. They are implicated in the regulation of diverse cellular processes ranging from cellular homeostasis to stress responses. Unintended irradiation of the cells and tissues, e.g., during medical uses, induces various pathological conditions, including oxidative stress. miRNAs may regulate the expression of transcription factors (e.g., nuclear factor erythroid 2 related factor 2 (Nrf2), nuclear factor kappa B (NF-κB), tumor suppressor protein p53) and other redox-sensitive genes (e.g., mitogen-activated protein kinase (MAPKs), sirtuins (SIRTs)), which trigger and modulate cellular redox signaling. During irradiation, miRNAs mainly act with reactive oxygen species (ROS) to regulate the cell fate. Depending on the pathway involved and the extent of oxidative stress, this may lead to cell survival or cell death. In the context of radiation-induced oxidative stress, miRNA-21 and miRNA-34a are among the best-studied miRNAs. miRNA-21 has been shown to directly target superoxide dismutase (SOD), or NF-κB, whereas miRNA-34a is a direct regulator of NADPH oxidase (NOX), SIRT1, or p53. Understanding the mechanisms underlying radiation-induced injury including the involvement of redox-responsive miRNAs may help to develop novel approaches for modulating the cellular response to radiation exposure. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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39 pages, 4172 KiB  
Review
Comparing Redox and Intracellular Signalling Responses to Cold Plasma in Wound Healing and Cancer
by Adrian I. Abdo and Zlatko Kopecki
Curr. Issues Mol. Biol. 2024, 46(5), 4885-4923; https://doi.org/10.3390/cimb46050294 - 17 May 2024
Cited by 4 | Viewed by 2969
Abstract
Cold plasma (CP) is an ionised gas containing excited molecules and ions, radicals, and free electrons, and which emits electric fields and UV radiation. CP is potently antimicrobial, and can be applied safely to biological tissue, birthing the field of plasma medicine. Reactive [...] Read more.
Cold plasma (CP) is an ionised gas containing excited molecules and ions, radicals, and free electrons, and which emits electric fields and UV radiation. CP is potently antimicrobial, and can be applied safely to biological tissue, birthing the field of plasma medicine. Reactive oxygen and nitrogen species (RONS) produced by CP affect biological processes directly or indirectly via the modification of cellular lipids, proteins, DNA, and intracellular signalling pathways. CP can be applied at lower levels for oxidative eustress to activate cell proliferation, motility, migration, and antioxidant production in normal cells, mainly potentiated by the unfolded protein response, the nuclear factor-erythroid factor 2-related factor 2 (Nrf2)-activated antioxidant response element, and the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, which also activates nuclear factor-kappa B (NFκB). At higher CP exposures, inactivation, apoptosis, and autophagy of malignant cells can occur via the degradation of the PI3K/Akt and mitogen-activated protein kinase (MAPK)-dependent and -independent activation of the master tumour suppressor p53, leading to caspase-mediated cell death. These opposing responses validate a hormesis approach to plasma medicine. Clinical applications of CP are becoming increasingly realised in wound healing, while clinical effectiveness in tumours is currently coming to light. This review will outline advances in plasma medicine and compare the main redox and intracellular signalling responses to CP in wound healing and cancer. Full article
(This article belongs to the Special Issue Molecular Research on Free Radicals and Oxidative Stress)
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