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Special Issue "Oxidative Stress: Focusing on New Therapeutic Approaches and Biochemical Markers"

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

Deadline for manuscript submissions: closed (30 April 2021).

Special Issue Editors

Prof. Dr. Daniela Impellizzeri
E-Mail Website
Guest Editor
Department of Chemical Biological, Pharmaceutical and Environmental Sciences, Università degli Studi di Messina, Messina, Italy
Interests: inflammation; oxidative stress; biochemistry; pharmacology; molecular biology
Special Issues and Collections in MDPI journals
Dr. Roberta Fusco
E-Mail Website
Guest Editor
Department of Chemical biological,pharmaceutical and environmental sciences, Università degli Studi di Messina, Messina, Italy
Interests: biochemistry; molecular biology; inflammation; oxidative stress; pharmacology
Special Issues and Collections in MDPI journals
Dr. Rosalba Siracusa
E-Mail Website
Guest Editor
Department of Chemical biological,pharmaceutical and environmental sciences, Università degli Studi di Messina, Messina, Italy
Interests: Biochemistry; Molecular Biology; Inflammation; Oxidative stress; Pathology; Pharmacology

Special Issue Information

Dear Colleagues,

A free radical can be defined as any molecular species capable of independent existence that contains an unpaired electron in an atomic orbital. Many abiotic stresses induce the overproduction of reactive oxygen species (ROS) in humans and animals. As highly reactive and toxic species, they cause damage to DNA, proteins, carbohydrates, and lipids, thus leading to oxidative stress. This oxidative stress induces damage to cells and tissues, resulting in a large number of diseases. Several compounds with antioxidant properties could neutralize the effects of ROS and prevent the development of many inflammatory pathologies. A number of scientific studies report the varied health benefits of antioxidant supplementation in processes such as inflammation, stress, aging, apoptosis and neurological diseases.

This Special Issue will focus on the role of the antioxidant therapy on different human diseases and possible molecular pathways involved. Moreover, the Special Issue will welcome reviews and original studies providing evidence of the effect of antioxidants factors wellbeing.

Prof. Dr. Daniela Impellizzeri
Dr. Roberta Fusco
Dr. Rosalba Siracusa
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 papers will be 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

  • antioxidant
  • biochemical marker
  • one health
  • wellbeing
  • nutrition
  • animal model
  • in vitro study

Published Papers (2 papers)

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Research

Open AccessArticle
Validation of a Gas Chromatography-Mass Spectrometry Method for the Measurement of the Redox State Metabolic Ratios Lactate/Pyruvate and β-Hydroxybutyrate/Acetoacetate in Biological Samples
Int. J. Mol. Sci. 2021, 22(9), 4752; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094752 - 30 Apr 2021
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Abstract
The metabolic ratios lactate/pyruvate and β-hydroxybutyrate/acetoacetate are considered valuable tools to evaluate the in vivo redox cellular state by estimating the free NAD+/NADH in cytoplasm and mitochondria, respectively. The aim of the current study was to validate a gas-chromatography mass spectrometry method for [...] Read more.
The metabolic ratios lactate/pyruvate and β-hydroxybutyrate/acetoacetate are considered valuable tools to evaluate the in vivo redox cellular state by estimating the free NAD+/NADH in cytoplasm and mitochondria, respectively. The aim of the current study was to validate a gas-chromatography mass spectrometry method for simultaneous determination of the four metabolites in plasma and liver tissue. The procedure included an o-phenylenediamine microwave-assisted derivatization, followed by liquid-liquid extraction with ethyl acetate and silylation with bis(trimethylsilyl)trifluoroacetamide:trimethylchlorosilane 99:1. The calibration curves presented acceptable linearity, with a limit of quantification of 0.001 mM for pyruvate, β-hydroxybutyrate and acetoacetate and of 0.01 mM for lactate. The intra-day and inter-day accuracy and precision were within the European Medicines Agency’s Guideline specifications. No significant differences were observed in the slope coefficient of three-point standard metabolite-spiked curves in plasma or liver and water, and acceptable recoveries were obtained in the metabolite-spiked samples. Applicability of the method was tested in precision-cut liver rat slices and also in HepG2 cells incubated under different experimental conditions challenging the redox state. In conclusion, the validated method presented good sensitivity, specificity and reproducibility in the quantification of lactate/pyruvate and β-hydroxybutyrate/acetate metabolites and may be useful in the evaluation of in vivo redox states. Full article
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Open AccessArticle
The Methyl Ester of 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic Acid Reduces Endometrial Lesions Development by Modulating the NFkB and Nrf2 Pathways
Int. J. Mol. Sci. 2021, 22(8), 3991; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083991 - 13 Apr 2021
Viewed by 259
Abstract
Endometriosis is a common gynecological disease. Here, we aimed to investigate the anti-fibrotic, anti-inflammatory, and anti-oxidative role of the methyl ester of 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO-Me) on endometriosis. An endometriosis rat model was constructed by intraperitoneally injecting recipient rats with an equivalent of tissue [...] Read more.
Endometriosis is a common gynecological disease. Here, we aimed to investigate the anti-fibrotic, anti-inflammatory, and anti-oxidative role of the methyl ester of 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO-Me) on endometriosis. An endometriosis rat model was constructed by intraperitoneally injecting recipient rats with an equivalent of tissue from the uterus of a donor animal. Endometriosis was allowed to develop for seven days. CDDO-Me was administered on the 7th day and for the next 7 days. On day 14, rats were sacrificed, and peritoneal fluid and endometriotic implants were collected. CDDO-Me displayed antioxidant activity by activating the Nfr2 pathway and the expression of antioxidant mediators such as NQO-1 and HO-1. Moreover, it reduced lipid peroxidation and increased glutathione (GSH) levels and superoxide dismutase (SOD) activity. CDDO-Me also showed anti-inflammatory activity by decreasing the expression of pro-inflammatory cytokines in peritoneal fluids and NFkB activation. It, in turn, reduced cyclooxygenase-2 (COX-2) expression in the endometriotic loci and prostaglandin E2 (PGE2) levels in the peritoneal fluids, leading to increased apoptosis and reduced angiogenesis. The reduced oxidative stress and pro-inflammatory microenvironment decreased implants diameter, area, and volume. In particular, CDDO-Me administration reduced the histopathological signs of endometriosis and inflammatory cells recruitment into the lesions, as shown by toluidine blue staining and myeloperoxidase (MPO) activity. CDDO-Me strongly suppressed α-SMA and fibronectin expression and collagen deposition, reducing endometriosis-associated fibrosis. In conclusion, CDDO-Me treatment resulted in a coordinated and effective suppression of endometriosis by modulating the Nrf2 and NFkB pathways. Full article
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