Special Issue "Oxidative Stress and Antioxidants in Aging"

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 28 February 2023 | Viewed by 8529

Special Issue Editors

Dr. Angela Marino
E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale F. Stagno D’Alcontres 31, 98166 Messina, Italy
Interests: physiology; toxicology
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Dossena
E-Mail Website
Guest Editor
Institute of Pharmacology and Toxicology, Paracelsus Medical University, 5020 Salzburg, Austria
Interests: hearing loss; gene analysis; SLC26A4/pendrin; Pendred syndrome; Enlarged Vestibular Aqueduct (EVA); ion transport; functional testing; ion channels; ion exchangers; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The process of aging implies various pathophysiological alterations that progressively result in failure of cell and tissue function and may lead to the onset of chronic diseases. The increase in life expectancy over the past century and the global aging of the population pose a challenging medical problem of ensuring healthy aging. As a consequence, understanding the impact of aging on a cellular and molecular level is of utmost importance. The process of aging is tightly connected to oxidative stress. Therefore, the aim of this Special Issue is to collect the most recent research on the mechanisms underlying the impact of oxidative stress during aging on cells and cellular components, including DNA, organelles, membrane ion transport systems, and the cell redox system. In this context, the beneficial effects of antioxidants against age-related detrimental consequences and possible mechanisms of cell adaptation to age-related conditions will be worthy of note. Research articles collecting data from both cell and animal models, as well as review articles, are welcome. Possible topics include but are not limited to:

  • Erythrocyte aging;
  • Molecular mechanisms in age-related hearing loss;
  • Ion channels and solute transporters in aging;
  • Molecular mechanisms of chronic kidney disease in aging;
  • Antioxidants in aging-associated diseases.

Dr. Angela Marino
Dr. Silvia Dossena
Guest Editors

Manuscript Submission Information

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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. Antioxidants 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 2400 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
  • aging
  • antioxidants
  • cellular components

Published Papers (7 papers)

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Research

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Article
Astaxanthin Induces Transcriptomic Responses Associated with Lifespan Extension in Caenorhabditis elegans
by and
Antioxidants 2022, 11(11), 2115; https://doi.org/10.3390/antiox11112115 - 27 Oct 2022
Viewed by 913
Abstract
Astaxanthin is a marine xanthophyll carotenoid which effectively prevents intracellular oxidative stress and has beneficial effects against various human diseases. It has been shown that astaxanthin protects Caenorhabditis elegans (C. elegans) from oxidative damages and extends the lifespan of C. elegans [...] Read more.
Astaxanthin is a marine xanthophyll carotenoid which effectively prevents intracellular oxidative stress and has beneficial effects against various human diseases. It has been shown that astaxanthin protects Caenorhabditis elegans (C. elegans) from oxidative damages and extends the lifespan of C. elegans possibly by modulating genes involved in insulin/insulin-like growth factor (IGF) signaling (IIS) and the oxidoreductase system, although the exact mechanisms remain elusive. In this study, RNA sequencing analyses were employed to identify the differentially expressed genes in C. elegans in response to astaxanthin treatment. A total of 190 mRNAs and 6 microRNAs (miRNAs) were significantly changed by astaxanthin treatment in C. elegans. Gene ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that the mRNAs and miRNAs significantly altered by astaxanthin mainly function in innate immunity, lipid metabolism and stress responses, a significant portion of which are related to lifespan regulation in C. elegans. The study revealed novel mRNA and miRNA targets of astaxanthin, providing new insights for understanding the anti-aging mechanisms and the biological function of astaxanthin. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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Article
Anti-Oxidant and Anti-Aging Effects of Phlorizin Are Mediated by DAF-16-Induced Stress Response and Autophagy in Caenorhabditis elegans
Antioxidants 2022, 11(10), 1996; https://doi.org/10.3390/antiox11101996 - 08 Oct 2022
Cited by 3 | Viewed by 842
Abstract
Phlorizin (phloridzin) is a polyphenolic phytochemical primarily found in unripe Malus (apple). It is a glucoside of phloretin and acts as an inhibitor of renal glucose transport, thus lowering blood glucose. The objective of this study was to determine effects of dietary supplementation [...] Read more.
Phlorizin (phloridzin) is a polyphenolic phytochemical primarily found in unripe Malus (apple). It is a glucoside of phloretin and acts as an inhibitor of renal glucose transport, thus lowering blood glucose. The objective of this study was to determine effects of dietary supplementation with phlorizin on stress response, aging, and age-related diseases using Caenorhabditis elegans as a model system. Survival after oxidative stress or ultraviolet irradiation was significantly increased by pre-treatment of phlorizin. Dietary supplementation with phlorizin also significantly extended lifespans without reducing fertility. Age-related decline of muscle function was delayed by supplementation with phlorizin. Phlorizin induced the expression of stress-responsive genes hsp-16.2 and sod-3 and nuclear localization of DAF-16, a FOXO transcription factor modulating stress response and lifespan in C. elegans. Amyloid-beta-induced toxicity was significantly reduced by phlorizin. This effect was dependent on DAF-16 and SKN-1. Increased mortality induced with a high-glucose diet was partially prevented by phlorizin via SKN-1. Inactivation of dopaminergic neurons observed in a Parkinson’s disease model was completely recovered by supplementation with phlorizin. Genetic analysis suggests that lifespan extension by phlorizin is mediated through oxidative stress response and autophagy. Taken together, these data suggest that phlorizin has strong anti-oxidant and anti-aging activities with potential to be developed as a novel anti-oxidant nutraceutical against aging and age-related diseases. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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Article
Preventive Effect of Cocoa Flavonoids via Suppression of Oxidative Stress-Induced Apoptosis in Auditory Senescent Cells
Antioxidants 2022, 11(8), 1450; https://doi.org/10.3390/antiox11081450 - 26 Jul 2022
Cited by 2 | Viewed by 980
Abstract
Presbycusis or Age-related hearing loss (ARHL) is a sensorineural hearing loss that affects communication, leading to depression and social isolation. Currently, there are no effective treatments against ARHL. It is known that cocoa products have high levels of polyphenol content (mainly flavonoids), that [...] Read more.
Presbycusis or Age-related hearing loss (ARHL) is a sensorineural hearing loss that affects communication, leading to depression and social isolation. Currently, there are no effective treatments against ARHL. It is known that cocoa products have high levels of polyphenol content (mainly flavonoids), that are potent anti-inflammatory and antioxidant agents with proven benefits for health. The objective is to determine the protective effect of cocoa at the cellular and molecular levels in Presbycusis. For in vitro study, we used House Ear Institute-Organ of Corti 1 (HEI-OC1), stria vascularis (SV-k1), and organ of Corti (OC-k3) cells (derived from the auditory organ of a transgenic mouse). Each cell line was divided into a control group (CTR) and an H2O2 group (induction of senescence by an oxygen radical). Additionally, every group of every cell line was treated with the cocoa polyphenolic extract (CPE), measuring different markers of apoptosis, viability, the activity of antioxidant enzymes, and oxidative/nitrosative stress. The data show an increase of reactive oxidative and nitrogen species (ROS and RNS, respectively) in senescent cells compared to control ones. CPE treatment effectively reduced these high levels and correlated with a significant reduction in apoptosis cells by inhibiting the mitochondrial-apoptotic pathway. Furthermore, in senescence cells, the activity of antioxidant enzymes (Superoxide dismutase, SOD; Catalase, CAT; and Glutathione peroxidase, GPx) was recovered after CPE treatment. Administration of CPE also decreased oxidative DNA damage in the auditory senescent cells. In conclusion, CPE inhibits the activation of senescence-related apoptotic signaling by decreasing oxidative stress in auditory senescent cells. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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Article
SOD3 Suppresses the Expression of MMP-1 and Increases the Integrity of Extracellular Matrix in Fibroblasts
Antioxidants 2022, 11(5), 928; https://doi.org/10.3390/antiox11050928 - 09 May 2022
Cited by 6 | Viewed by 1178
Abstract
The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3). In this study, we examined the potential roles of SOD family members in [...] Read more.
The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3). In this study, we examined the potential roles of SOD family members in skin aging. We found that SOD3 expression levels were significantly more reduced in the skin tissues of old mice and humans than in young counterparts, but SOD1 and SOD2 expression levels remained unchanged with aging. Accordingly, we analyzed the effects of SOD3 on intracellular ROS levels and the integrity of the extracellular matrix in fibroblasts. The treatment of foreskin fibroblasts with recombinant SOD3 reduced the intracellular ROS levels and secretion of MMP-1 while increasing the secretion of type I collagen. The effects of SOD3 were greater in fibroblasts treated with the TNF-α. SOD3 treatment also decreased the mRNA levels and promoter activity of MMP-1 while increasing the mRNA levels and promoter activities of COL1A1 and COL1A2. SOD3 treatment reduced the phosphorylation of NF-κB, p38 MAPK, ERK, and JNK, which are essential for MMP-1 transactivation. In a three-dimensional culture of fibroblasts, SOD3 decreased the amount of type I collagen fragments produced by MMP-1 and increased the amount of nascent type I procollagen. These results demonstrate that SOD3 reduces intracellular ROS levels, suppresses MMP-1 expression, and induces type I collagen expression in fibroblasts. Therefore, SOD3 may play a role in delaying or preventing skin aging. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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Article
Angiotensin Type-1 Receptor Inhibition Reduces NLRP3 Inflammasome Upregulation Induced by Aging and Neurodegeneration in the Substantia Nigra of Male Rodents and Primary Mesencephalic Cultures
Antioxidants 2022, 11(2), 329; https://doi.org/10.3390/antiox11020329 - 08 Feb 2022
Cited by 2 | Viewed by 1155
Abstract
The tissue renin–angiotensin system (RAS) has been shown to be involved in prooxidative and proinflammatory changes observed in aging and aging-related diseases such as dopaminergic degeneration in Parkinson’s disease (PD). We studied the activation of the NLRP3 inflammasome in the substantia nigra with [...] Read more.
The tissue renin–angiotensin system (RAS) has been shown to be involved in prooxidative and proinflammatory changes observed in aging and aging-related diseases such as dopaminergic degeneration in Parkinson’s disease (PD). We studied the activation of the NLRP3 inflammasome in the substantia nigra with aging and early stages of dopaminergic degeneration in PD models and, particularly, if the brain RAS, via its prooxidative proinflammatory angiotensin II (AngII) type 1 (AT1) receptors, mediates the inflammasome activation. Nigras from aged rats and mice and 6-hydroxydopamine PD models showed upregulation in transcription of inflammasome-related components (NLRP3, pro-IL1β and pro-IL18) and IL1β and IL18 protein levels, which was inhibited by the AT1 receptor antagonist candesartan. The role of the AngII/AT1 axis in inflammasome activation was further confirmed in rats intraventricularly injected with AngII, and in primary mesencephalic cultures treated with 6-hydroxydopamine, which showed inflammasome activation that was blocked by candesartan. Observations in the nigra of young and aged AT1 and AT2 knockout mice confirmed the major role of AT1 receptors in nigral inflammasome activation. In conclusion, the inflammasome is upregulated by aging and dopaminergic degeneration in the substantia nigra, possibly related with a decrease in dopamine levels, and it is mediated by the AngII/AT1 axis. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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Article
Na/H Exchange Regulatory Factor 1 Deficient Mice Show Evidence of Oxidative Stress and Altered Cisplatin Pharmacokinetics
Antioxidants 2021, 10(7), 1036; https://doi.org/10.3390/antiox10071036 - 28 Jun 2021
Cited by 1 | Viewed by 1393
Abstract
(1) Background: One third of patients who receive cisplatin develop an acute kidney injury. We previously demonstrated the Na/H Exchange Regulatory Factor 1 (NHERF1) loss resulted in increased kidney enzyme activity of the pentose phosphate pathway and was associated with more severe cisplatin [...] Read more.
(1) Background: One third of patients who receive cisplatin develop an acute kidney injury. We previously demonstrated the Na/H Exchange Regulatory Factor 1 (NHERF1) loss resulted in increased kidney enzyme activity of the pentose phosphate pathway and was associated with more severe cisplatin nephrotoxicity. We hypothesized that changes in proximal tubule biochemical pathways associated with NHERF1 loss alters renal metabolism of cisplatin or response to cisplatin, resulting in exacerbated nephrotoxicity. (2) Methods: 2–4 month-old male wild-type and NHERF1 knock out littermate mice were treated with either vehicle or cisplatin (20 mg/kg dose IP), with samples taken at either 4, 24, or 72 h. Kidney injury was determined by urinary neutrophil gelatinase-associated lipocalin and histology. Glutathione metabolites were measured by HPLC and genes involved in glutathione synthesis were measured by qPCR. Kidney handling of cisplatin was assessed by a kidney cortex measurement of γ-glutamyl transferase activity, Western blot for γ-glutamyl transferase and cysteine S-conjugate beta lyase, and ICP-MS for platinum content. (3) Results: At 24 h knock out kidneys show evidence of greater tubular injury after cisplatin and exhibit a decreased reduced/oxidized glutathione ratio under baseline conditions in comparison to wild-type. KO kidneys fail to show an increase in γ-glutamyl transferase activity and experience a more rapid decline in tissue platinum when compared to wild-type. (4) Conclusions: Knock out kidneys show evidence of greater oxidative stress than wild-type accompanied by a greater degree of early injury in response to cisplatin. NHERF1 loss has no effect on the initial accumulation of cisplatin in the kidney cortex but is associated with an altered redox status which may alter the activity of enzymes involved in cisplatin metabolism. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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Review

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Review
Redox Mechanisms of Platelet Activation in Aging
Antioxidants 2022, 11(5), 995; https://doi.org/10.3390/antiox11050995 - 19 May 2022
Viewed by 1017
Abstract
Aging is intrinsically linked with physiologic decline and is a major risk factor for a broad range of diseases. The deleterious effects of advancing age on the vascular system are evidenced by the high incidence and prevalence of cardiovascular disease in the elderly. [...] Read more.
Aging is intrinsically linked with physiologic decline and is a major risk factor for a broad range of diseases. The deleterious effects of advancing age on the vascular system are evidenced by the high incidence and prevalence of cardiovascular disease in the elderly. Reactive oxygen species are critical mediators of normal vascular physiology and have been shown to gradually increase in the vasculature with age. There is a growing appreciation for the complexity of oxidant and antioxidant systems at the cellular and molecular levels, and accumulating evidence indicates a causal association between oxidative stress and age-related vascular disease. Herein, we review the current understanding of mechanistic links between oxidative stress and thrombotic vascular disease and the changes that occur with aging. While several vascular cells are key contributors, we focus on oxidative changes that occur in platelets and their mediation in disease progression. Additionally, we discuss the impact of comorbid conditions (i.e., diabetes, atherosclerosis, obesity, cancer, etc.) that have been associated with platelet redox dysregulation and vascular disease pathogenesis. As we continue to unravel the fundamental redox mechanisms of the vascular system, we will be able to develop more targeted therapeutic strategies for the prevention and management of age-associated vascular disease. Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)
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