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Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related...
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Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases

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: 31 July 2024 | Viewed by 7657

Special Issue Editors

Prof. Dr. Jean Paul Jay-Gerin

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Guest Editor
Département de Médecine Nucléaire et de Radiobiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC J1H 5N4, Canada
Interests: radiation chemistry; water radiolysis; early events in radiobiology; free radicals; radioprotectors/antioxidants; FLASH radiobiology; Monte Carlo track chemistry simulations
Prof. Dr. Edouard I. Azzam

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Guest Editor
1. Department of Radiology, Rutgers New Jersey Medical School, Newark, NJ, USA
2. Radiobiology and Health Branch, Canadian Nuclear Laboratories, Chalk River, ON, Canada
3. Department of Nuclear Medicine and Radiobiology, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada
Interests: molecular and cellular mechanisms of the targeted and non-targeted effects (i.e., bystander effects, genomic instability, adaptive/protective responses, oxidative metabolism) of ionizing radiation in normal and cancerous human cells and tissues
Prof. Dr. Abdelouahed Khalil

E-Mail Website
Guest Editor
Research Centre on Aging, Department of Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada
Interests: aging; atherosclerosis; lipoproteins; inflammation; antioxidants
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive oxygen species, or ROS, are reactive molecules or free radicals derived from O2 and involved both in the maintenance of homeostasis and as the main inducer of oxidative damage to plasma and cellular components (lipids, proteins and DNA). Oxidative stress, which is defined as an imbalance between ROS and the available antioxidant system, is involved in different physiological and physio-pathological processes.

While the free-radical theory of aging, first proposed by Denham Harman in the 1950s-60s, explains the aging process as an accumulation of ROS-induced oxidative damage, several age-related diseases such as diabetes, neurodegenerative disorders, and cardiovascular diseases are also the consequence of ROS damage. Indeed, cellular senescence is activated by multiple intrinsic and extrinsic stimuli, including telomere shortening, DNA damaging agents, oncogene hyperactivation, and inflammatory and development signals, among others. Interventions with antioxidants have shown a beneficial effect in inhibiting or reducing the incidence of different age-related diseases.

ROS are produced naturally by aerobic organisms through the process of respiration, but are also produced by environmental insults such as tobacco smoke, air pollution, and exposure to oxidizing agents, including ionizing radiation.

The purpose of this Special Issue is to review the current state of our knowledge regarding the effect of free radicals on the aging process and age-related diseases. Particular attention will be given to studies on the effect of antioxidants in reducing the damage induced by ROS and in preventing the development of certain physio-pathological alterations.

Prof. Dr. Jean-Paul Jay-Gerin
Prof. Dr. Edouard I. Azzam
Prof. Dr. Abdelouahed Khalil
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. 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 2900 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

  • free radicals/reactive oxygen species (ROS)
  • oxidative stress/oxidative damage
  • oxidative metabolism
  • ROS-induced damage
  • antioxidants
  • cellular senescence
  • aging
  • age-related diseases: diabetes, neurodegenerative disorders, cardiovascular diseases

Published Papers (7 papers)

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Research

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19 pages, 7583 KiB  
Article
S-Allylmercapto-N-Acetylcysteine (ASSNAC) Attenuates Osteoporosis in Ovariectomized (OVX) Mice
by Itay Bleichman, Sahar Hiram-Bab, Yankel Gabet and Naphtali Savion
Antioxidants 2024, 13(4), 474; https://doi.org/10.3390/antiox13040474 - 17 Apr 2024
Viewed by 332
Abstract
Osteoporosis is a bone-debilitating disease, demonstrating a higher prevalence in post-menopausal women due to estrogen deprivation. One of the main mechanisms underlying menopause-related bone loss is oxidative stress. S-allylmercapto-N-acetylcysteine (ASSNAC) is a nuclear factor erythroid 2-related factor 2 (Nrf2) activator [...] Read more.
Osteoporosis is a bone-debilitating disease, demonstrating a higher prevalence in post-menopausal women due to estrogen deprivation. One of the main mechanisms underlying menopause-related bone loss is oxidative stress. S-allylmercapto-N-acetylcysteine (ASSNAC) is a nuclear factor erythroid 2-related factor 2 (Nrf2) activator and cysteine supplier, previously shown to have anti-oxidation protective effects in cultured cells and animal models. Here, we studied the therapeutic potential of ASSNAC with and without Alendronate in ovariectomized (OVX) female mice. The experimental outcome included (i) femur and L3 lumbar vertebra morphometry via Micro-Computed Tomography (μCT); (ii) bone remodeling (formation vs. resorption); and (iii) oxidative stress markers in bone marrow (BM) cells. Four weeks after OVX, there was a significant bone loss that remained evident after 8 weeks, as demonstrated via µCT in the femur (cortical and trabecular bone compartments) and vertebra (trabecular bone). ASSNAC at a dose of 50 mg/Kg/day prevented bone loss after the four-week treatment but had no significant effect after 8 weeks, while ASSNAC at a dose of 20 mg/Kg/day significantly protected against bone loss after 8 weeks of treatment. Alendronate prevented ovariectomy-induced bone loss, and combining it with ASSNAC further augmented this effect. OVX mice demonstrated high serum levels of both C-terminal cross-linked telopeptides of type I collagen (CTX) (bone resorption) and procollagen I N-terminal propeptide (P1NP) (bone formation) after 2 weeks, and these returned to control levels after 8 weeks. Alendronate, ASSNAC and their combination decreased CTX and increased P1NP. Alendronate induced oxidative stress as reflected by decreased glutathione and increased malondialdehyde (MDA) levels, and combining it with ASSNAC partially attenuated these changes. These results portray the therapeutic potential of ASSNAC for the management of post-menopausal osteoporosis. Furthermore, ASSNAC ameliorates the Alendronate-associated oxidative stress, suggesting its potential to prevent Alendronate side effects as well as improve its bone-protective effect. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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21 pages, 5814 KiB  
Article
Evaluation of Antioxidant Effects of Pumpkin (Cucurbita pepo L.) Seed Extract on Aging- and Menopause-Related Diseases Using Saos-2 Cells and Ovariectomized Rats
by Joohee Oh, Sookyeong Hong, Seong-Hee Ko and Hyun-Sook Kim
Antioxidants 2024, 13(2), 241; https://doi.org/10.3390/antiox13020241 - 16 Feb 2024
Viewed by 1204
Abstract
Aging and menopause are associated with oxidative stress and inflammation. Here, we evaluated the antioxidant properties of pumpkin (Cucurbita pepo L.) seed extract and assessed its ameliorative effects on aging- and menopause-related diseases using Saos-2 cells and ovariectomized rats. The seed extract [...] Read more.
Aging and menopause are associated with oxidative stress and inflammation. Here, we evaluated the antioxidant properties of pumpkin (Cucurbita pepo L.) seed extract and assessed its ameliorative effects on aging- and menopause-related diseases using Saos-2 cells and ovariectomized rats. The seed extract had bioactive components that exhibited antioxidant activity. The extract increased the alkaline phosphatase (ALP) activity of Saos-2 cells. The oral administration of the extract to ovariectomized rats for 12 weeks decreased their body weight, fat weight, and cardiac risk indices. It also contributed to reductions in the levels of reactive oxygen species, oxidative stress, and inflammation, as assessed by measuring the serum levels of malondialdehyde and analyzing gene expression in rats. Furthermore, the administration of the extract also promoted an enhancement of the transcription of nuclear factor erythroid 2-related factor (Nrf2), heme oxygenase-1 (Ho-1), and catalase (Cat), involved in antioxidant activity; endothelial nitric oxide synthase (eNos), involved in vasculoprotective activity; and PR/SET domain 16 (Prdm16) and peroxisome proliferator-activated receptor-gamma coactivator (Pgc1α), involved in brown adipogenesis and thermogenesis. Our results using ovariectomized rats show that pumpkin seed extract may have ameliorative effects on menopause-related diseases by increasing ALP activity, evaluating the antioxidant system, ameliorating oxidative stress and thermogenesis, and enhancing lipid profiles. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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14 pages, 2397 KiB  
Article
High Tyrosol and Hydroxytyrosol Intake Reduces Arterial Inflammation and Atherosclerotic Lesion Microcalcification in Healthy Older Populations
by Nada Zoubdane, Redha-Alla Abdo, Michel Nguyen, M’hamed Bentourkia, Eric E. Turcotte, Hicham Berrougui, Tamas Fulop and Abdelouahed Khalil
Antioxidants 2024, 13(1), 130; https://doi.org/10.3390/antiox13010130 - 22 Jan 2024
Cited by 2 | Viewed by 1162
Abstract
Aging is an important risk factor for cardiovascular diseases and convincing data have shown that chronic low-grade inflammation, which develops with advanced age, contributes significantly to cardiovascular risk. The present study aimed to use 18F-FDG/18F-NaF-PET/CT imaging to, respectively, gauge arterial [...] Read more.
Aging is an important risk factor for cardiovascular diseases and convincing data have shown that chronic low-grade inflammation, which develops with advanced age, contributes significantly to cardiovascular risk. The present study aimed to use 18F-FDG/18F-NaF-PET/CT imaging to, respectively, gauge arterial inflammation and microcalcification in a healthy elderly population and to assess the potential benefits of a tyrosol- and hydroxytyrosol-rich diet on these two markers of atherosclerotic plaque fragility. Eleven healthy participants (mean age 75 ± 5.67 years) were supplemented for 6 months with high polyphenol-rich extra virgin olive oil (HP-EVOO), extra virgin olive oil (EVOO), or refined olive oil (ROO). The participants underwent PET/CT imaging with 18F-FDG and 18F-NaF radiotracers at baseline and after 6 months. 18F-FDG and 18F-NaF uptakes were quantified using standardized uptake values (SUV) and were categorized based on artery calcification and olive oil type. A total of 324 slices of the aortas of the imaged participants were analyzed for arterial inflammation and 327 slices were analyzed for microcalcification. 18F-FDG uptake was significantly higher in the non-calcified segments than in the calcified segments (SUVmax = 2.70 ± 0.62 and SUVmax = 2.54 ± 0.44, respectively, p < 0.042). Conversely, the non-calcified segments displayed significantly lower 18F-NaF uptake than the calcified segments (SUVmax = 1.90 ± 0.37 and 2.09 ± 0.24, respectively, p < 0.0001). The 6-month supplementation with HP-EVOO induced a significant reduction in 18F-FDG uptake in both the non-calcified (2.93 ± 0.23 to 2.75 ± 0.38, p < 0.004) and calcified segments of the aortas (2.25 ± 0.29 to 2.15 ± 0.19, p < 0.02). 18F-NaF uptake was also significantly lower in patients supplemented with HP-EVOO (SUVmax = 1.98 ± 0.33 at baseline compared to 1.85 ± 0.28, after the 6-month supplementation, p < 0.004), whereas no significant effect was observed with EVOO. Conversely, participants supplemented with ROO displayed a significant increase in 18F-NaF uptake (SUVmax = 1.78 ± 0.34 to 1.95 ± 0.34, p < 0.0001). The present study confirmed that a phenolic-compound-rich diet reduces both arterial inflammation and atherosclerotic lesion microcalcification and demonstrated that 18F-FDG/18F-NaF-PET/CT imaging is a valuable approach for assessing age-related arterial damage. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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18 pages, 9646 KiB  
Article
Vutiglabridin Alleviates Cellular Senescence with Metabolic Regulation and Circadian Clock in Human Dermal Fibroblasts
by Jin-Woong Heo, Hye-Eun Lee, Jimin Lee, Leo Sungwong Choi, Jaejin Shin, Ji-Young Mun, Hyung-Soon Park, Sang-Chul Park and Chang-Hoon Nam
Antioxidants 2024, 13(1), 109; https://doi.org/10.3390/antiox13010109 - 16 Jan 2024
Viewed by 1164
Abstract
The process of cellular senescence, which is characterized by stable cell cycle arrest, is strongly associated with dysfunctional cellular metabolism and circadian rhythmicity, both of which are reported to result from and also be causal to cellular senescence. As a result, modifying any [...] Read more.
The process of cellular senescence, which is characterized by stable cell cycle arrest, is strongly associated with dysfunctional cellular metabolism and circadian rhythmicity, both of which are reported to result from and also be causal to cellular senescence. As a result, modifying any of them—senescence, metabolism, or the circadian clock—may affect all three simultaneously. Obesity accelerates aging by disrupting the homeostasis of reactive oxygen species (ROS) via an increased mitochondrial burden of fatty acid oxidation. As a result, if senescence, metabolism, and circadian rhythm are all linked, anti-obesity treatments may improve metabolic regulation while also alleviating senescence and circadian rhythm. Vutiglabridin is a small molecule in clinical trials that improves obesity by enhancing mitochondrial function. We found that chronic treatment of senescent primary human dermal fibroblasts (HDFs) with vutiglabridin alleviates all investigated markers of cellular senescence (SA-β-gal, CDKN1A, CDKN2A) and dysfunctional cellular circadian rhythm (BMAL1) while remarkably preventing the alterations of mitochondrial function and structure that occur during the process of cellular senescence. Our results demonstrate the significant senescence-alleviating effects of vutiglabridin, specifically with the restoration of cellular circadian rhythmicity and metabolic regulation. These data support the potential development of vutiglabridin against aging-associated diseases and corroborate the intricate link between cellular senescence, metabolism, and the circadian clock. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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13 pages, 4299 KiB  
Article
Indian Almond (Terminalia catappa Linn.) Leaf Extract Extends Lifespan by Improving Lipid Metabolism and Antioxidant Activity Dependent on AMPK Signaling Pathway in Caenorhabditis elegans under High-Glucose-Diet Conditions
by Yebin Kim, Seul-bi Lee, Myogyeong Cho, Soojin Choe and Miran Jang
Antioxidants 2024, 13(1), 14; https://doi.org/10.3390/antiox13010014 - 20 Dec 2023
Cited by 2 | Viewed by 1170
Abstract
This study aimed to evaluate the antioxidant and antiaging effects of Indian almond (Terminalia catappa Linn.) leaf extract (TCE) on high-glucose (GLU)-induced obese Caenorhabditis elegans. Since TCE contains high contents of flavonoids and phenolics, strong radical scavenging activity was confirmed in [...] Read more.
This study aimed to evaluate the antioxidant and antiaging effects of Indian almond (Terminalia catappa Linn.) leaf extract (TCE) on high-glucose (GLU)-induced obese Caenorhabditis elegans. Since TCE contains high contents of flavonoids and phenolics, strong radical scavenging activity was confirmed in vitro. The stress-resistance effect of TCE was confirmed under thermal and oxidative stress conditions at nontoxic tested concentrations (6.25, 12.5, and 25 μg/mL). GLU at 2% caused lipid and reactive oxygen species (ROS) accumulation in C. elegans, and TCE inhibited lipid and ROS accumulation under both normal and 2% GLU conditions in a concentration-dependent manner. In addition, TCE proved to be effective in prolonging the lifespan of C. elegans under normal and 2% GLU conditions. The ROS reduction effect of TCE was abolished in mutants deficient in daf-16/FOXO and skn-1/Nrf-2. In addition, the lifespan-extending effect of TCE in these two mutants disappeared. The lifespan-extending effect was abolished even in atgl-1/ATGL-deficiency mutants. The TCE effect was reduced in aak-1/AMPK-deficient mutants and completely abolished under 2% GLU conditions. Therefore, the effect of prolonging lifespan by inhibiting lipid and ROS accumulation under the high GLU conditions of TCE is considered to be the result of atgl-1, daf-16, and skn-1 being downregulated by aak-1. These results suggest that the physiological potential of TCE contributes to antiaging under metabolic disorders. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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Review

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20 pages, 1509 KiB  
Review
Redox Regulation of Immunometabolism in Microglia Underpinning Diabetic Retinopathy
by Luwei Cai, Mengxue Xia and Fang Zhang
Antioxidants 2024, 13(4), 423; https://doi.org/10.3390/antiox13040423 - 29 Mar 2024
Viewed by 716
Abstract
Diabetic retinopathy (DR) is the leading cause of visual impairment and blindness among the working-age population. Microglia, resident immune cells in the retina, are recognized as crucial drivers in the DR process. Microglia activation is a tightly regulated immunometabolic process. In the early [...] Read more.
Diabetic retinopathy (DR) is the leading cause of visual impairment and blindness among the working-age population. Microglia, resident immune cells in the retina, are recognized as crucial drivers in the DR process. Microglia activation is a tightly regulated immunometabolic process. In the early stages of DR, the M1 phenotype commonly shifts from oxidative phosphorylation to aerobic glycolysis for energy production. Emerging evidence suggests that microglia in DR not only engage specific metabolic pathways but also rearrange their oxidation-reduction (redox) system. This redox adaptation supports metabolic reprogramming and offers potential therapeutic strategies using antioxidants. Here, we provide an overview of recent insights into the involvement of reactive oxygen species and the distinct roles played by key cellular antioxidant pathways, including the NADPH oxidase 2 system, which promotes glycolysis via enhanced glucose transporter 4 translocation to the cell membrane through the AKT/mTOR pathway, as well as the involvement of the thioredoxin and nuclear factor E2-related factor 2 antioxidant systems, which maintain microglia in an anti-inflammatory state. Therefore, we highlight the potential for targeting the modulation of microglial redox metabolism to offer new concepts for DR treatment. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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15 pages, 1004 KiB  
Review
Progress in Understanding Oxidative Stress, Aging, and Aging-Related Diseases
by Jianying Yang, Juyue Luo, Xutong Tian, Yaping Zhao, Yumeng Li and Xin Wu
Antioxidants 2024, 13(4), 394; https://doi.org/10.3390/antiox13040394 - 25 Mar 2024
Viewed by 991
Abstract
Under normal physiological conditions, reactive oxygen species (ROS) are produced through redox reactions as byproducts of respiratory and metabolic activities. However, due to various endogenous and exogenous factors, the body may produce excessive ROS, which leads to oxidative stress (OS). Numerous studies have [...] Read more.
Under normal physiological conditions, reactive oxygen species (ROS) are produced through redox reactions as byproducts of respiratory and metabolic activities. However, due to various endogenous and exogenous factors, the body may produce excessive ROS, which leads to oxidative stress (OS). Numerous studies have shown that OS causes a variety of pathological changes in cells, including mitochondrial dysfunction, DNA damage, telomere shortening, lipid peroxidation, and protein oxidative modification, all of which can trigger apoptosis and senescence. OS also induces a variety of aging-related diseases, such as retinal disease, neurodegenerative disease, osteoarthritis, cardiovascular diseases, cancer, ovarian disease, and prostate disease. In this review, we aim to introduce the multiple internal and external triggers that mediate ROS levels in rodents and humans as well as the relationship between OS, aging, and aging-related diseases. Finally, we present a statistical analysis of effective antioxidant measures currently being developed and applied in the field of aging research. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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