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Oxidative Stress and Inflammation in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 4811

Special Issue Editors


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Guest Editor
Department of Farmacy and Biotechnology, University of Bologna, 40126 Bologna, Italy
Interests: antioxidants; oxidative stress-related diseases; electronic cigarette toxicity; co-carcinogenesis pathways; DNA repair and mutagenesis; drug metabolism

E-Mail Website
Guest Editor
Department of Farmacy and Biotechnology, University of Bologna, 40126 Bologna, Italy
Interests: oxidative stress status; inflammation; oxidative and post-oxidative markers; antioxidant employment; prevention of chronic diseases; in vitro and in vivo toxicity; biomarkers of exposure; electronic cigarette toxicity

Special Issue Information

Dear Colleagues,

Oxidative stress and systemic inflammation are connected processes that can influence and amplify each other. Oxidative stress can activate immune cells to release pro-inflammatory molecules and to generate reactive oxygen species, as part of their defense mechanisms. In turn, pro-inflammatory cytokines can trigger the generation of more radicals, creating a vicious cycle that sustains chronic inflammation and leads to tissue damage in various organs.

This Special Issue aims to highlight the current understanding of the bidirectional relationship between inflammation and oxidative stress and their role in the development and progression of various diseases and conditions such as cardiovascular and respiratory diseases, neurodegenerative and reproductive system disorders, diabetes and obesity, and cancer. Moreover, studies on how lifestyle factors (environmental exposures, antioxidant adjuvant treatments, diet, etc.) can contribute to the reduction or increase in the risk of these chronic conditions are welcome.

This Special Issue will accept original articles and reviews dealing with the molecular aspects of oxidative stress and systemic inflammation.

Dr. Fabio Vivarelli
Dr. Donatella Canistro
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 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

  • oxidative stress
  • inflammation
  • chronic diseases
  • risk factors
  • prevention

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Published Papers (4 papers)

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14 pages, 1666 KiB  
Article
Correlations between Gut Microbiota and Hematological, Inflammatory, Biochemical and Oxidative Stress Parameters in Treatment-Naïve Psoriasis Patients
by Elena Codruța Cozma, Ionela Avram, Vlad Mihai Voiculescu, Mara Mădălina Mihai and Amelia Maria Găman
Int. J. Mol. Sci. 2024, 25(12), 6649; https://doi.org/10.3390/ijms25126649 - 17 Jun 2024
Viewed by 1164
Abstract
Psoriasis is an inflammatory dermatosis with a complex pathogenesis, significantly impacting the quality of life of patients. The role of oxidative stress and gut microbiota in the pathogenesis of this disease is increasingly studied, appearing to underlie the comorbidities associated with this condition. [...] Read more.
Psoriasis is an inflammatory dermatosis with a complex pathogenesis, significantly impacting the quality of life of patients. The role of oxidative stress and gut microbiota in the pathogenesis of this disease is increasingly studied, appearing to underlie the comorbidities associated with this condition. We present the first prospective observational study conducted in Romania evaluating the interrelationship between gut microbiota and hematological, inflammatory, biochemical, and oxidative stress parameters in treatment-naïve psoriasis patients. Significant differences were observed in terms of microbiota composition, with lower levels of Firmicutes and Enterobacteriaceae in the psoriasis group compared to the control group. Moreover, a negative correlation was found between the serum triglyceride levels in patients with psoriasis and the Enterobacteriaceae family (p = 0.018, r = −0.722), and a positive correlation was found between the serum glucose levels and the Firmicutes/Bacteroides ratio (p = 0.03, r = 0.682). Regarding the oxidant–antioxidant status, a significant correlation was found between the FORT level and Lactobacillus (p = 0.034, r = 0.669). Lastly, the Firmicutes level negatively correlated with the DLQI level, independent of the clinical severity of the disease (p = 0.02, r = −0.685). In conclusion, even though the number of included patients is small, these results may serve as a starting point for future research into the involvement of the microbiota–inflammation–oxidative stress axis in psoriasis development. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Health and Disease)
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15 pages, 964 KiB  
Review
Purslane Ameliorates Inflammation and Oxidative Stress in Diabetes Mellitus: A Systematic Review
by Zikho Nkhumeleni, Wendy N. Phoswa and Kabelo Mokgalaboni
Int. J. Mol. Sci. 2024, 25(22), 12276; https://doi.org/10.3390/ijms252212276 - 15 Nov 2024
Cited by 1 | Viewed by 1383
Abstract
Type 2 diabetes (T2D) is characterised by insulin resistance and leads to hyperglycaemia. Its prevalence and associated complications continue to rise exponentially, despite the existence of pharmaceutical drugs, and this has prompted research into exploring safer herbal remedies. Portulaca oleracea (purslane) has been [...] Read more.
Type 2 diabetes (T2D) is characterised by insulin resistance and leads to hyperglycaemia. Its prevalence and associated complications continue to rise exponentially, despite the existence of pharmaceutical drugs, and this has prompted research into exploring safer herbal remedies. Portulaca oleracea (purslane) has been investigated in animal and clinical trials to explore its effects on diabetes, yielding conflicting results. This study aimed to evaluate the effects of purslane on inflammation and oxidative stress in diabetes mellitus. We conducted a comprehensive literature search on Scopus PubMed, and through a manual bibliographical search to find relevant studies from inception to 13 September 2024. The search terms included purslane, portulaca oleracea, and type 2 diabetes mellitus. Of the 38 retrieved studies, 12 were considered relevant and underwent critical review. Evidence from rodent studies showed decreased inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), nuclear factor kappa-beta (NF-κβ), and C-reactive (CRP), while interleukin-10 (IL-10) was increased after intervention with purslane. The markers of oxidative stress such as superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) levels increased, thiobarbituric acid reactive substances (TBARS), reactive oxygen species (ROS) and malondialdehyde (MDA) decreased. Notably, the evidence from clinical trials showed a significant reduction in NF-κβ and CRP after purslane treatment; however, no effect was observed on MDA and TAC. The evidence gathered in this study suggests that purslane exerts anti-inflammatory properties by downregulating NF-κβ, thus suppressing the production of associated pro-inflammatory cytokines. Therefore, purslane may be used as an antioxidant and inflammatory agent for diabetes. However, further clinical evidence with a broader population is required to validate the therapeutic properties of purslane in diabetes. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Health and Disease)
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25 pages, 2033 KiB  
Article
Expression of Neuronal Nicotinic Acetylcholine Receptor and Early Oxidative DNA Damage in Aging Rat Brain—The Effects of Memantine
by Małgorzata Anna Lewandowska, Agata Różycka, Teresa Grzelak, Bartosz Kempisty, Paweł Piotr Jagodziński, Margarita Lianeri and Jolanta Dorszewska
Int. J. Mol. Sci. 2025, 26(4), 1634; https://doi.org/10.3390/ijms26041634 - 14 Feb 2025
Viewed by 697
Abstract
Aging and age-related neurodegenerative disorders are characterized by the dysfunction or loss of brain nicotinic acetylcholine receptors (nAChRs), and these changes may be related to other senescence markers, such as oxidative stress and DNA repair dysfunction. However, the mechanism of nAChR loss in [...] Read more.
Aging and age-related neurodegenerative disorders are characterized by the dysfunction or loss of brain nicotinic acetylcholine receptors (nAChRs), and these changes may be related to other senescence markers, such as oxidative stress and DNA repair dysfunction. However, the mechanism of nAChR loss in the aging brain and the modification of this process by drugs (e.g., memantine, Mem) are not yet fully understood. To study whether the differences in nAChR expression in the rat brain occur due to aging or oxidative stress and are modulated by Mem, we analyzed nAChR subunits (at RNA and protein levels) and other biomarkers by real-time quantitative polymerase chain reaction (RQ-PCR) and Western blot validation. Twenty-one female Wistar rats were divided into four groups, depending on age, and the oldest group received injections of Mem or water with the use of intragastric catheters. We studied the cerebral grey matter (CGM), subcortical white matter (SCWM), and cerebellum (Ce). Results showed an age-related decrease of α7 nAChR mRNA level in SCWM. The α7 nAChR mRNA loss was accompanied by reduced expression of 8-oxoguanine DNA glycosylase 1 (OGG1) and an increased tumor necrosis factor alpha (TNFα) level. In the water group, we observed a higher level of α7 nAChR protein in the SCWM and Ce. Biomarker levels changed, but to a different extent depending on the brain area. Importantly, the dysfunction in antioxidative status was stopped and even regressed under Mem treatment. After two weeks of treatment, an increase in TP53 protein level and a decrease in 8-oxo-2′deoxyguanosine (8-oxo-2′dG) level were observed. We conclude that Mem administration may be protective against the senescence process by antioxidative mechanisms. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Health and Disease)
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25 pages, 2009 KiB  
Review
Erectile Dysfunction and Oxidative Stress: A Narrative Review
by Dake Zhu, Quan Minh Pham, Chunlin Wang, Elena Colonnello, Dimitri Yannas, Bac Hoai Nguyen, Yan Zhang, Emmanuele A. Jannini and Andrea Sansone
Int. J. Mol. Sci. 2025, 26(7), 3073; https://doi.org/10.3390/ijms26073073 - 27 Mar 2025
Viewed by 1205
Abstract
Erectile dysfunction (ED) is a prevalent condition affecting male sexual health, characterized by the inability to achieve or maintain satisfactory erections. ED has a multifactorial pathogenesis in which psychological, hormonal, neurologic, cardiovascular, and lifestyle factors all contribute to a progressive decline of erectile [...] Read more.
Erectile dysfunction (ED) is a prevalent condition affecting male sexual health, characterized by the inability to achieve or maintain satisfactory erections. ED has a multifactorial pathogenesis in which psychological, hormonal, neurologic, cardiovascular, and lifestyle factors all contribute to a progressive decline of erectile function. A critical underlying mechanism involves oxidative stress (OS), an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, which disrupts endothelial function, reduces nitric oxide (NO) bioavailability, and contributes to vascular dysfunction. This narrative review explores the interplay between OS and ED, focusing on the roles of ROS sources such as NADPH oxidase, xanthine oxidase, uncoupled nitric oxide synthase, and mitochondrial dysfunction. It examines the impact of OS on chronic conditions like hypertension, diabetes mellitus, hyperlipidemia, hypogonadism, and lifestyle factors like smoking and obesity, which exacerbate ED through endothelial and systemic effects. Emerging research underscores the potential of antioxidant therapies and lifestyle interventions to restore redox balance, improve endothelial function, and mitigate ED’s progression. This review also highlights gaps in understanding the molecular pathways linking ROS to ED, emphasizing the need for further research to develop targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Health and Disease)
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