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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: 30 September 2024 | Viewed by 1263

Special Issue Editor


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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

Published Papers (2 papers)

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Research

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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
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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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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
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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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