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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 (28 February 2022) | Viewed by 19377

Special Issue Editors


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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: biochemistry; molecular mechanism; oxidative stress; endometriosis
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: clinical biochemistry; molecular biology; biomarkers
Special Issues, Collections and Topics in MDPI journals

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.

Dr. Daniela Impellizzeri
Dr. Roberta Fusco
Dr. Rosalba Siracusa
Guest Editors

Manuscript Submission Information

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Keywords

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

Published Papers (6 papers)

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Research

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10 pages, 2026 KiB  
Article
Telmisartan Attenuates Kanamycin-Induced Ototoxicity in Rats
by Chang Ho Lee, So Min Lee and So Young Kim
Int. J. Mol. Sci. 2021, 22(23), 12716; https://doi.org/10.3390/ijms222312716 - 24 Nov 2021
Cited by 3 | Viewed by 1793
Abstract
Telmisartan (TM) has been proposed to relieve inflammatory responses by modulating peroxisome proliferator activator receptor-γ (PPARγ) signaling. This study aimed to investigate the protective effects of TM on kanamycin(KM)-induced ototoxicity in rats. Forty-eight, 8-week-old female Sprague Dawley rats were divided into four groups: [...] Read more.
Telmisartan (TM) has been proposed to relieve inflammatory responses by modulating peroxisome proliferator activator receptor-γ (PPARγ) signaling. This study aimed to investigate the protective effects of TM on kanamycin(KM)-induced ototoxicity in rats. Forty-eight, 8-week-old female Sprague Dawley rats were divided into four groups: (1) control group, (2) TM group, (3) KM group, and (4) TM + KM group. Auditory brainstem response was measured. The histology of the cochlea was examined. The protein expression levels of angiotensin-converting enzyme 2 (ACE2), HO1, and PPARγ were measured by Western blotting. The auditory threshold shifts at 4, 8, 16, and 32 kHz were lower in the TM + KM group than in the KM group (all p < 0.05). The loss of cochlear outer hair cells and spiral ganglial cells was lower in the TM + KM group than in the KM group. The protein expression levels of ACE2, PPARγ, and HO1 were higher in the KM group than in the control group (all p < 0.05). The TM + KM group showed lower expression levels of PPARγ and HO1 than the KM group.TM protected the cochlea from KM-induced injuries in rats. TM preserved hearing levels and attenuated the increase in PPARγ and HO1 expression levels in KM-exposed rat cochleae. Full article
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12 pages, 2972 KiB  
Article
Effects of Androgen Receptor Inhibition on Kanamycin-Induced Hearing Loss in Rats
by Kyung-Ju Chun, Chang-Ho Lee, Kyung-Woon Kim, So-Min Lee and So-Young Kim
Int. J. Mol. Sci. 2021, 22(10), 5307; https://doi.org/10.3390/ijms22105307 - 18 May 2021
Cited by 8 | Viewed by 1833
Abstract
Megalin has been proposed as an endocytic receptor for aminoglycosides as well as estrogen and androgen. We aimed to investigate the otoprotective effects of antiandrogens (flutamide, FM) on kanamycin (KM)-induced hearing loss in rats. Rats were divided into four groups. The KM group [...] Read more.
Megalin has been proposed as an endocytic receptor for aminoglycosides as well as estrogen and androgen. We aimed to investigate the otoprotective effects of antiandrogens (flutamide, FM) on kanamycin (KM)-induced hearing loss in rats. Rats were divided into four groups. The KM group was administered KM (20 mg/kg/day) for 5 days, while the FM group received FM (15 mg/kg/day) for 10 days. In the KM + FM group, KM and FM (15 mg/kg/day) were simultaneously injected for 5 days and then FM was injected for 5 days. Auditory brainstem responses were measured. Western blotting and/or quantitative reverse transcriptase-polymerase chain reaction were performed for megalin, cytochrome P450 1A1 (Cyp1a1), Cyp1b1, metallothionein 1A (MT1A), MT2A, tumor necrosis factor (TNF)-α, caspase 3, and cleaved caspase 3. The FM + KM group showed attenuated auditory thresholds when compared with the KM group at 4, 8, 16, and 32 kHz (all p < 0.05). The KM + FM group showed lower megalin and Cyp1b1 levels than the KM group (all p < 0.05). The KM + FM group revealed lower MT1A, TNFα, and caspase 3 protein levels, compared with those in the KM group (all p < 0.05). Androgen receptor inhibition protects against cochlear injuries in KM-induced hearing loss rats by attenuating megalin expression, revealing anti-inflammatory and anti-apoptotic effects. Full article
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14 pages, 1335 KiB  
Article
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
by Robin Wijngaard, Meritxell Perramón, Marina Parra-Robert, Susana Hidalgo, Gina Butrico, Manuel Morales-Ruiz, Muling Zeng, Eudald Casals, Wladimiro Jiménez, Guillermo Fernández-Varo, Gerald I. Shulman, Gary W. Cline and Gregori Casals
Int. J. Mol. Sci. 2021, 22(9), 4752; https://doi.org/10.3390/ijms22094752 - 30 Apr 2021
Cited by 7 | Viewed by 2517
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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13 pages, 2386 KiB  
Article
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
by Rosalba Siracusa, Ramona D’Amico, Marika Cordaro, Alessio Filippo Peritore, Tiziana Genovese, Enrico Gugliandolo, Rosalia Crupi, Daniela Impellizzeri, Salvatore Cuzzocrea, Roberta Fusco and Rosanna Di Paola
Int. J. Mol. Sci. 2021, 22(8), 3991; https://doi.org/10.3390/ijms22083991 - 13 Apr 2021
Cited by 24 | Viewed by 5283
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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Review

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19 pages, 1472 KiB  
Review
Low Psychological Resilience in Older Individuals: An Association with Increased Inflammation, Oxidative Stress and the Presence of Chronic Medical Conditions
by Ljiljana Trtica Majnarić, Zvonimir Bosnić, Silva Guljaš, Domagoj Vučić, Tomislav Kurevija, Mile Volarić, Ivo Martinović and Thomas Wittlinger
Int. J. Mol. Sci. 2021, 22(16), 8970; https://doi.org/10.3390/ijms22168970 - 20 Aug 2021
Cited by 23 | Viewed by 4110
Abstract
The term resilience, which has been present in science for almost half a century, stands for the capacity of some system needed to overcome an amount of disturbance from the environment in order to avoid a change to another stable state. In medicine, [...] Read more.
The term resilience, which has been present in science for almost half a century, stands for the capacity of some system needed to overcome an amount of disturbance from the environment in order to avoid a change to another stable state. In medicine, the concept of resilience means the ability to deal with daily stress and disturbance to our homeostasis with the intention of protecting it from disturbance. With aging, the organism becomes more sensitive to environmental impacts and more susceptible to changes. Mental disturbances and a decline in psychological resilience in older people are potentiated with many social and environmental factors along with a subjective perception of decreasing health. Distinct from findings in younger age groups, mental and physical medical conditions in older people are closely associated with each other, sharing common mechanisms and potentiating each other’s development. Increased inflammation and oxidative stress have been recognized as the main driving mechanisms in the development of aging diseases. This paper aims to reveal, through a translational approach, physiological and molecular mechanisms of emotional distress and low psychological resilience in older individuals as driving mechanisms for the accelerated development of chronic aging diseases, and to systematize the available information sources on strategies for mitigation of low resilience in order to prevent chronic diseases. Full article
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17 pages, 1055 KiB  
Review
Implications of SGLT Inhibition on Redox Signalling in Atrial Fibrillation
by David Bode, Lukas Semmler, Christian U. Oeing, Alessio Alogna, Gabriele G. Schiattarella, Burkert M. Pieske, Frank R. Heinzel and Felix Hohendanner
Int. J. Mol. Sci. 2021, 22(11), 5937; https://doi.org/10.3390/ijms22115937 - 31 May 2021
Cited by 8 | Viewed by 2901
Abstract
Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have [...] Read more.
Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have shown that treatment with sodium-glucose linked transporter inhibitors (SGLTi) improves mortality and hospitalisation in heart failure patients independent of the presence of diabetes. Post hoc analysis of the DECLARE-TIMI 58 trial showed a 19% reduction in AF in patients with diabetes mellitus (hazard ratio, 0.81 (95% confidence interval: 0.68–0.95), n = 17.160) upon treatment with SGLTi, regardless of pre-existing AF or heart failure and independent from blood pressure or renal function. Accordingly, ongoing experimental work suggests that SGLTi not only positively impact heart failure but also counteract cellular ROS production in cardiomyocytes, thereby potentially altering atrial remodelling and reducing AF burden. In this article, we review recent studies investigating the effect of SGLTi on cellular processes closely interlinked with redox balance and their potential effects on the onset and progression of AF. Despite promising insight into SGLTi effect on Ca2+ cycling, Na+ balance, inflammatory and fibrotic signalling, mitochondrial function and energy balance and their potential effect on AF, the data are not yet conclusive and the importance of individual pathways for human AF remains to be established. Lastly, an overview of clinical studies investigating SGLTi in the context of AF is provided. Full article
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