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Targeting Oxidative Stress for Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 2348

Special Issue Editors

Department of Animal Physiology, Faculty of Science, University of Zagreb, Rooseveltov trg 6, 10000 Zagreb, Croatia
Interests: oxidative stress-induced diseases; natural products; chemoprevention and tumor therapy; bee products and health; radioprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) represents the metabolic state of the organism induced by an increase in the amount of reactive oxygen species (ROS). It is most often associated with neurological diseases but also contributes to the pathogenesis of a number of seemingly unrelated disorders, including type 2 diabetes, cancer, aging, heart and acute renal failure, hypertension, preeclampsia, atherosclerosis and coronary disease, asthma, chronic obstructive pulmonary disease, rheumatoid arthritis, glaucoma, osteoporosis, and sexual dysfunction, among others.

This Special Issue aims to provide a comprehensive insight into the understanding of the role of ROS-mediated effects in the physiological, and especially in the pathological processes of diseases’ development. We would like to highlight the possibilities of exploiting OS as a therapeutic approach in the treatment of cancer.

We cordially invite authors to contribute original articles as well as review papers that present advances on the potential of the most relevant dietary antioxidants on redox biology. These include their antioxidant capacity that may affect biomarkers of oxidative stress and inflammation, as well as their role in the regulation of mitochondrial function, cell signaling proteins, ion channels and transporters, and the ubiquitination/proteasome system, preventing the occurrence of numerous pathological processes.

Prof. Dr. Nada Orsolic
Dr. Maja Jazvinšćak Jembrek
Guest Editors

Manuscript Submission Information

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Keywords

  • oxidants and free radical production
  • physiological activities of free radicals
  • detrimental effects of free radicals on human health
  • ROS and ROS-mediated cellular signaling
  • pathophysiology of oxidative stress
  • biomarkers of oxidative stress
  • chronic degenerative diseases
  • therapeutic approaches targeting oxidative stress
  • biochemical/molecular targets of chronic diseases
  • exogenous antioxidants and human health
  • flavonoids and redox biology in the pathophysiology of diseases
  • pro-oxidative role of antioxidants: double-sided sword
  • prooxidant agents in therapy

Published Papers (3 papers)

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Research

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20 pages, 12760 KiB  
Article
Hepatic Alterations in a BTBR T + Itpr3tf/J Mouse Model of Autism and Improvement Using Melatonin via Mitigation Oxidative Stress, Inflammation and Ferroptosis
Int. J. Mol. Sci. 2024, 25(2), 1086; https://doi.org/10.3390/ijms25021086 - 16 Jan 2024
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Abstract
Autism spectrum disorder (ASD) is a complicated neurodevelopmental disorder, and its etiology is not well understood. It is known that genetic and nongenetic factors determine alterations in several organs, such as the liver, in individuals with this disorder. The aims of the present [...] Read more.
Autism spectrum disorder (ASD) is a complicated neurodevelopmental disorder, and its etiology is not well understood. It is known that genetic and nongenetic factors determine alterations in several organs, such as the liver, in individuals with this disorder. The aims of the present study were to analyze morphological and biological alterations in the liver of an autistic mouse model, BTBR T + Itpr3tf/J (BTBR) mice, and to identify therapeutic strategies for alleviating hepatic impairments using melatonin administration. We studied hepatic cytoarchitecture, oxidative stress, inflammation and ferroptosis in BTBR mice and used C57BL6/J mice as healthy control subjects. The mice were divided into four groups and then treated and not treated with melatonin, respectively. BTBR mice showed (a) a retarded development of livers and (b) iron accumulation and elevated oxidative stress and inflammation. We demonstrated that the expression of ferroptosis markers, the transcription factor nuclear factor erythroid-related factor 2 (NFR2), was upregulated, and the Kelch-like ECH-associated protein 1 (KEAP1) was downregulated in BTBR mice. Then, we evaluated the effects of melatonin on the hepatic alterations of BTBR mice; melatonin has a positive effect on liver cytoarchitecture and metabolic functions. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress for Disease)
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9 pages, 1442 KiB  
Article
Comparative Analysis of Anticonvulsant Activity of Trans and Cis 5,5′-Diphenylhydantoin Schiff Bases
Int. J. Mol. Sci. 2023, 24(22), 16071; https://doi.org/10.3390/ijms242216071 - 08 Nov 2023
Cited by 1 | Viewed by 549
Abstract
Recently, the four 5,5′-diphenylhydantoin Schiff bases, possessing different aromatic species (SB1-Ph, SB2-Ph, SB3-Ph and SB4-Ph) were synthesized, characterized, and evaluated for anticonvulsant activity in combination with phenytoin. In the present study, the SB1-Ph and SB4-Ph compounds were selected, based on their [...] Read more.
Recently, the four 5,5′-diphenylhydantoin Schiff bases, possessing different aromatic species (SB1-Ph, SB2-Ph, SB3-Ph and SB4-Ph) were synthesized, characterized, and evaluated for anticonvulsant activity in combination with phenytoin. In the present study, the SB1-Ph and SB4-Ph compounds were selected, based on their anticonvulsant potency, and compared with their cis isomers, prepared after a one-hour exposure to the UV source, for their anticonvulsant potency in the maximal electroshock (MES) test and the kainate (KA)-induced status epilepticus (SE) test in mice. In the MES test, the cis SB1-Ph compound exhibited superior to phenytoin and trans isomer activity in the three tested doses, while the cis SB4-Ph compound entirely suppressed the electroshock-induced seizure spread at the highest dose of 40 mg/kg. Pretreatment with the cis SB1-Ph compound and the cis SB4-Ph at the doses of 40 mg/kg, respectively, for seven days, significantly attenuated the severity of KA SE compared to the matched control group pretreated with a vehicle, while phenytoin was ineffective in this test. The cis SB4-Ph but not the cis SB1-Ph demonstrated an antioxidant effect against the KA-induced SE in the hippocampus. Our results suggest that trans–cis conversion of 5,5′-diphenylhydantoin Schiff bases has potential against seizure spread in the MES test and mitigated the KA-induced SE. The antioxidant potency of cis SB4-Ph might be associated with its efficacy in mitigating the SE. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress for Disease)
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Review

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16 pages, 3234 KiB  
Review
Oxidative Mechanisms and Cardiovascular Abnormalities of Cirrhosis and Portal Hypertension
Int. J. Mol. Sci. 2023, 24(23), 16805; https://doi.org/10.3390/ijms242316805 - 27 Nov 2023
Viewed by 760
Abstract
In patients with portal hypertension, there are many complications including cardiovascular abnormalities, hepatorenal syndrome, ascites, variceal bleeding, and hepatic encephalopathy. The underlying mechanisms are not yet completely clarified. It is well known that portal hypertension causes mesenteric congestion which produces reactive oxygen species [...] Read more.
In patients with portal hypertension, there are many complications including cardiovascular abnormalities, hepatorenal syndrome, ascites, variceal bleeding, and hepatic encephalopathy. The underlying mechanisms are not yet completely clarified. It is well known that portal hypertension causes mesenteric congestion which produces reactive oxygen species (ROS). ROS has been associated with intestinal mucosal injury, increased intestinal permeability, enhanced gut bacterial overgrowth, and translocation; all these changes result in increased endotoxin and inflammation. Portal hypertension also results in the development of collateral circulation and reduces liver mass resulting in an overall increase in endotoxin/bacteria bypassing detoxication and immune clearance in the liver. Endotoxemia can in turn aggravate oxidative stress and inflammation, leading to a cycle of gut barrier dysfunction → endotoxemia → organ injury. The phenotype of cardiovascular abnormalities includes hyperdynamic circulation and cirrhotic cardiomyopathy. Oxidative stress is often accompanied by inflammation; thus, blocking oxidative stress can minimize the systemic inflammatory response and alleviate the severity of cardiovascular diseases. The present review aims to elucidate the role of oxidative stress in cirrhosis-associated cardiovascular abnormalities and discusses possible therapeutic effects of antioxidants on cardiovascular complications of cirrhosis including hyperdynamic circulation, cirrhotic cardiomyopathy, and hepatorenal syndrome. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress for Disease)
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