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Antioxidants
Special Issues
Oxidative Stress in Aging and Associated Chronic Diseases
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Oxidative Stress in Aging and Associated Chronic 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: closed (1 August 2021) | Viewed by 38184

Special Issue Editors

Dr. Raquel Rodrigues-Diez

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Guest Editor
1. Department of Pharmacology and Therapeutics, School of Medicine, Universidad Autónoma de Madrid, Calle de Arzobispo Morcillo 4, 28029 Madrid, Spain
2. Center for Biomedical Research Network (CIBER) in Cardiovascular Diseases, Calle de Melchor Fernández Almagro 3, 28029 Madrid, Spain
3. Research Institute University Hospital la Paz (IdIPaz), Calle de Pedro Rico 6, 28029 Madrid, Spain
Interests: vascular diseases; ROS; inflammation; renal diseases; hypertension; aneurysm
Dr. Mª Teresa Barrús Ortiz

E-Mail Website
Guest Editor
Physiology Area, Department of Health Basic Sciences, Faculty of Health Sciences, Universidad Rey Juan Carlos; Avenida de Atenas s/n, 28922 Alcorcón, Madrid, Spain
Interests: hypertension; vascular inflammtion; production of ROS and the ROS-activated signaling transduction pathways contributing to inflammation; pro-inflammatory enzimes; pro-inflammatory citoquines; animal models of hypertension; inflammasome
Dr. Matilde Alique

E-Mail Website
Guest Editor
1. Departamento Biología de Sistemas, Universidad de Alcalá, Alcalá de Henares, Madrid, Spain
2. Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain
Interests: chronic kidney diseases; cardiovascular diseases; extracellular vesicles; senescence; vascular calcification; aging; premature aging; inflammation; age-related diseases; endothelial cells; smooth muscle cells
Prof. Dr. Consuelo Borras

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Medicine, University of Valencia, Avenida Blasco Ibañez 15, 46010 Valencia, Spain
Interests: aging; senescence; stem cells; oxidative stress; sex
Special Issues, Collections and Topics in MDPI journals
Dr. Cristina Mas-Bargues

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Medicine, University of Valencia, Avenida Blasco Ibañez 15, 46010 Valencia, Spain
Interests: stem cells; physioxia; oxidative stress; senescence; apoptosis; autophagy; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging and associated chronic disease incidence, including cardiovascular disease, type 2 diabetes, hypertension, cancer, osteoarthritis, and Alzheimer’s disease, among others, have been increasing in recent years. Although these pathological states are produced by several diverse causes, there is abundant evidence that oxidative stress plays a key role in the development and progression of both aging and chronic diseases. Oxidative stress is defined as a disbalance between reactive oxygen species (ROS) formation and the antioxidant defences that lead to cell damage due to the oxidation of nucleic acids, lipids and proteins.

Currently, numerous experimental and clinical studies have focused their attention on elucidating the role of oxidative stress in the development and progression of aging and chronic disease. While many authors have focused on elucidating the underlying mechanisms and possible signaling pathways, others have attempted to find new therapeutic strategies to slow the development of aging and associated chronic diseases by decreasing oxidative stress.

We encourage scientists and clinicians to contribute with original articles describing novel mechanisms by which oxidative stress contributes to the development of chronic diseases or aging as well as new therapeutic strategies to treat or prevent this pathological status in which oxidative stress might be involved. Reviews that summarize recent findings in both basic and clinical research and discuss current outcome are also welcome.

Dr. Raquel Rodrigues-Diez
Dr. Mª Teresa Barrús Ortiz
Dr. Matilde Alique
Dr. Consuelo Borras
Dr. Cristina Mas Bargues
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

  • oxidative stress
  • aging
  • aging-associated chronic disease

Published Papers (11 papers)

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Editorial

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4 pages, 209 KiB  
Editorial
Special Issue “Oxidative Stress in Aging and Associated Chronic Diseases”
by Cristina Mas-Bargues, Matilde Alique, Mª Teresa Barrús-Ortiz, Consuelo Borrás and Raquel Rodrigues-Díez
Antioxidants 2022, 11(4), 701; https://doi.org/10.3390/antiox11040701 - 02 Apr 2022
Cited by 3 | Viewed by 2128
Abstract
Aging is a risk factor for several diseases, including cardiovascular disease, type 2 diabetes, hypertension, cancer, osteoarthritis, and Alzheimer; oxidative stress is a key player in the development and progression of aging and age-associated diseases [...] Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)

Research

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19 pages, 6493 KiB  
Article
Oxidative Stress and Cellular Senescence Are Involved in the Aging Kidney
by Laura Marquez-Exposito, Lucia Tejedor-Santamaria, Floris A. Valentijn, Antonio Tejera-Muñoz, Sandra Rayego-Mateos, Vanessa Marchant, Raul R. Rodrigues-Diez, Irene Rubio-Soto, Sebastiaan N. Knoppert, Alberto Ortiz, Adrian M. Ramos, Roel Goldschmeding and Marta Ruiz-Ortega
Antioxidants 2022, 11(2), 301; https://doi.org/10.3390/antiox11020301 - 31 Jan 2022
Cited by 23 | Viewed by 4153
Abstract
Chronic kidney disease (CKD) can be considered as a clinical model for premature aging. However, non-invasive biomarkers to detect early kidney damage and the onset of a senescent phenotype are lacking. Most of the preclinical senescence studies in aging have been done in [...] Read more.
Chronic kidney disease (CKD) can be considered as a clinical model for premature aging. However, non-invasive biomarkers to detect early kidney damage and the onset of a senescent phenotype are lacking. Most of the preclinical senescence studies in aging have been done in very old mice. Furthermore, the precise characterization and over-time development of age-related senescence in the kidney remain unclear. To address these limitations, the age-related activation of cellular senescence-associated mechanisms and their correlation with early structural changes in the kidney were investigated in 3- to 18-month-old C57BL6 mice. Inflammatory cell infiltration was observed by 12 months, whereas tubular damage and collagen accumulation occurred later. Early activation of cellular-senescence-associated mechanisms was found in 12-month-old mice, characterized by activation of the DNA-damage-response (DDR), mainly in tubular cells; activation of the antioxidant NRF2 pathway; and klotho downregulation. However, induction of tubular-cell-cycle-arrest (CCA) and overexpression of renal senescent-associated secretory phenotype (SASP) components was only found in 18-month-old mice. In aging mice, both inflammation and oxidative stress (marked by elevated lipid peroxidation and NRF2 inactivation) remained increased. These findings support the hypothesis that prolonged DDR and CCA, loss of nephroprotective factors (klotho), and dysfunctional redox regulatory mechanisms (NRF2/antioxidant defense) can be early drivers of age-related kidney-damage progression. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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20 pages, 3144 KiB  
Article
Aging Induces Hepatic Oxidative Stress and Nuclear Proteomic Remodeling in Liver from Wistar Rats
by Brenda Bárcena, Aurora Salamanca, Cristina Pintado, Lorena Mazuecos, Margarita Villar, Eduardo Moltó, Elena Bonzón-Kulichenko, Jesús Vázquez, Antonio Andrés and Nilda Gallardo
Antioxidants 2021, 10(10), 1535; https://doi.org/10.3390/antiox10101535 - 27 Sep 2021
Cited by 11 | Viewed by 2093
Abstract
Aging is a continuous, universal, and irreversible process that determines progressive loss of adaptability. The liver is a critical organ that supports digestion, metabolism, immunity, detoxification, vitamin storage, and hormone signaling. Nevertheless, the relationship between aging and the development of liver diseases remains [...] Read more.
Aging is a continuous, universal, and irreversible process that determines progressive loss of adaptability. The liver is a critical organ that supports digestion, metabolism, immunity, detoxification, vitamin storage, and hormone signaling. Nevertheless, the relationship between aging and the development of liver diseases remains elusive. In fact, although prolonged fasting in adult rodents and humans delays the onset of the disease and increases longevity, whether prolonged fasting could exert adverse effects in old organisms remains incompletely understood. In this work, we aimed to characterize the oxidative stress and nuclear proteome in the liver of 3-month- and 24-month-old male Wistar rats upon 36 h of fasting and its adaptation in response to 30 min of refeeding. To this end, we analyzed the hepatic lipid peroxidation levels (TBARS) and the expression levels of genes associated with fat metabolism and oxidative stress during aging. In addition, to gain a better insight into the molecular and cellular processes that characterize the liver of old rats, the hepatic nuclear proteome was also evaluated by isobaric tag quantitation (iTRAQ) mass spectrometry-based proteomics. In old rats, aging combined with prolonged fasting had great impact on lipid peroxidation in the liver that was associated with a marked downregulation of antioxidant genes (Sod2, Fmo3, and Cyp2C11) compared to young rats. Besides, our proteomic study revealed that RNA splicing is the hepatic nuclear biological process markedly affected by aging and this modification persists upon refeeding. Our results suggest that aged-induced changes in the nuclear proteome could affect processes associated with the adaptative response to refeeding after prolonged fasting, such as those involved in the defense against oxidative stress. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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23 pages, 4084 KiB  
Article
Hyperphosphatemia-Induced Oxidant/Antioxidant Imbalance Impairs Vascular Relaxation and Induces Inflammation and Fibrosis in Old Mice
by Ana Asenjo-Bueno, Elena Alcalde-Estévez, Mariam El Assar, Gemma Olmos, Patricia Plaza, Patricia Sosa, Patricia Martínez-Miguel, María Piedad Ruiz-Torres and Susana López-Ongil
Antioxidants 2021, 10(8), 1308; https://doi.org/10.3390/antiox10081308 - 19 Aug 2021
Cited by 12 | Viewed by 2273
Abstract
Aging impairs vascular function, but the mechanisms involved are unknown. The aim of this study was to analyze whether aging-related hyperphosphatemia is implied in this effect by elucidating the role of oxidative stress. C57BL6 mice that were aged 5 months (young) and 24 [...] Read more.
Aging impairs vascular function, but the mechanisms involved are unknown. The aim of this study was to analyze whether aging-related hyperphosphatemia is implied in this effect by elucidating the role of oxidative stress. C57BL6 mice that were aged 5 months (young) and 24 months (old), receiving a standard (0.6%) or low-phosphate (0.2%) diet, were used. Isolated mesenteric arteries from old mice showed diminished endothelium-dependent vascular relaxation by the down-regulation of NOS3 expression, increased inflammation and increased fibrosis in isolated aortas, compared to those isolated from young mice. In parallel, increased Nox4 expression and reduced Nrf2, Sod2-Mn and Gpx1 were found in the aortas from old mice, resulting in oxidant/antioxidant imbalance. The low-phosphate diet improved vascular function and oxidant/antioxidant balance in old mice. Mechanisms were analyzed in endothelial (EC) and vascular smooth muscle cells (SMCs) treated with the phosphate donor ß-glycerophosphate (BGP). In EC, BGP increased Nox4 expression and ROS production, which reduced NOS3 expression via NFκB. BGP also increased inflammation in EC. In SMC, BGP increased Collagen I and fibronectin expression by priming ROS production and NFκB activity. In conclusion, hyperphosphatemia reduced endothelium-dependent vascular relaxation and increased inflammation and vascular fibrosis through an impairment of oxidant/antioxidant balance in old mice. A low-phosphate diet achieved improvements in the vascular function in old mice. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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18 pages, 3147 KiB  
Article
Olive Leaf Extract Supplementation to Old Wistar Rats Attenuates Aging-Induced Sarcopenia and Increases Insulin Sensitivity in Adipose Tissue and Skeletal Muscle
by Daniel González-Hedström, Teresa Priego, Sara Amor, María de la Fuente-Fernández, Ana Isabel Martín, Asunción López-Calderón, Antonio Manuel Inarejos-García, Ángel Luís García-Villalón and Miriam Granado
Antioxidants 2021, 10(5), 737; https://doi.org/10.3390/antiox10050737 - 07 May 2021
Cited by 14 | Viewed by 3583
Abstract
Aging is associated with increased visceral adiposity and a decrease in the amount of brown adipose tissue and muscle mass, known as sarcopenia, which results in the development of metabolic alterations such as insulin resistance. In this study, we aimed to analyze whether [...] Read more.
Aging is associated with increased visceral adiposity and a decrease in the amount of brown adipose tissue and muscle mass, known as sarcopenia, which results in the development of metabolic alterations such as insulin resistance. In this study, we aimed to analyze whether 3-week supplementation with a phenolic-rich olive leaf extract (OLE) to 24 months-old male Wistar rats orally (100 mg/kg) attenuated the aging-induced alterations in body composition and insulin resistance. OLE treatment increased brown adipose tissue and attenuated the aging-induced decrease in protein content and gastrocnemius weight. Treatment with OLE prevented the aging-induced increase in the expression of PPAR-γ in visceral and brown adipose tissues, while it significantly increased the expression of PPAR-α in the gastrocnemius of old rats and reduced various markers related to sarcopenia such as myostatin, HDAC-4, myogenin and MyoD. OLE supplementation increased insulin sensitivity in explants of gastrocnemius and epididymal visceral adipose tissue from aged rats through a greater activation of the PI3K/Akt pathway, probably through the attenuation of inflammation in both tissues. In conclusion, supplementation with OLE prevents the loss of muscle mass associated with aging and exerts anti-inflammatory and insulin-sensitizing effects on adipose tissue and skeletal muscle. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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18 pages, 1370 KiB  
Article
The Resistance of Drosophila melanogaster to Oxidative, Genotoxic, Proteotoxic, Osmotic Stress, Infection, and Starvation Depends on Age According to the Stress Factor
by Alexei A. Belyi, Alexey A. Alekseev, Alexander Y. Fedintsev, Stepan N. Balybin, Ekaterina N. Proshkina, Mikhail V. Shaposhnikov and Alexey A. Moskalev
Antioxidants 2020, 9(12), 1239; https://doi.org/10.3390/antiox9121239 - 07 Dec 2020
Cited by 13 | Viewed by 3417
Abstract
We studied how aging affects the ability of Drosophila melanogaster to tolerate various types of stress factors. Data were obtained on the resistance of D. melanogaster to oxidative and genotoxic (separately paraquat, Fe3+, Cu2+, and Zn2+ ions), proteotoxic [...] Read more.
We studied how aging affects the ability of Drosophila melanogaster to tolerate various types of stress factors. Data were obtained on the resistance of D. melanogaster to oxidative and genotoxic (separately paraquat, Fe3+, Cu2+, and Zn2+ ions), proteotoxic (hyperthermia, Cd2+ ions), and osmotic (NaCl) stresses, starvation, and infection with the pathological Beauveria bassiana fungus at different ages. In all cases, we observed a strong negative correlation between age and stress tolerance. The largest change in the age-dependent decline in survival occurred under oxidative and osmotic stress. In most experiments, we observed that young Drosophila females have higher stress resistance than males. We checked whether it is possible to accurately assess the biological age of D. melanogaster based on an assessment of stress tolerance. We have proposed a new approach for assessing a biological age of D. melanogaster using a two-parameter survival curve model. For the model, we used an algorithm that evaluated the quality of age prediction for different age and gender groups. The best predictions were obtained for females who were exposed to CdCl2 and ZnCl2 with an average error of 0.32 days and 0.36 days, respectively. For males, the best results were observed for paraquat and NaCl with an average error of 0.61 and 0.68 days, respectively. The average accuracy for all stresses in our model was 1.73 days. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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Review

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17 pages, 10462 KiB  
Review
NLRP3 Inflammasome in Vascular Disease: A Recurrent Villain to Combat Pharmacologically
by Ainara González-Moro, Inés Valencia, Licia Shamoon, Carlos Félix Sánchez-Ferrer, Concepción Peiró and Fernando de la Cuesta
Antioxidants 2022, 11(2), 269; https://doi.org/10.3390/antiox11020269 - 29 Jan 2022
Cited by 7 | Viewed by 4404
Abstract
Despite the great advances in medicine, mortality from cardiovascular diseases keeps on growing. This tendency is not likely to change considering the pandemic proportions of obesity and diabetes. Besides, the global population is more aged as life expectancy increases, and vascular aging plays [...] Read more.
Despite the great advances in medicine, mortality from cardiovascular diseases keeps on growing. This tendency is not likely to change considering the pandemic proportions of obesity and diabetes. Besides, the global population is more aged as life expectancy increases, and vascular aging plays a key role in the increased risk of vascular disease. In light of recent trials, namely the CANTOS study, showing the enormous potential of anti-inflammatory therapies and in particular those targeted to IL-1β, a change in therapeutical management of cardiovascular diseases is coming about. The NLRP3 inflammasome is a multiprotein complex that assembles to engage the innate immune defense by processing the maturation of pro-inflammatory cytokines IL-1β and IL-18. Substantial evidence has positioned the NLRP3 inflammasome at the center of vascular disease progression, with a particular significance in the context of aging and the low-grade chronic inflammation associated (inflammaging). Therefore, pharmacological blockade of the NLRP3 inflammasome and its end products has arisen as an extremely promising tool to battle vascular disease. In this review, we discuss the mechanisms by which the NLRP3 inflammasome contributes to vascular disease, with particular attention to the consequences of aging, and we enumerate the therapeutic options available to combat this recurrent villain. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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29 pages, 1405 KiB  
Review
Exploring New Kingdoms: The Role of Extracellular Vesicles in Oxi-Inflamm-Aging Related to Cardiorenal Syndrome
by Cristina Mas-Bargues, Matilde Alique, María Teresa Barrús-Ortiz, Consuelo Borrás and Raquel Rodrigues-Díez
Antioxidants 2022, 11(1), 78; https://doi.org/10.3390/antiox11010078 - 29 Dec 2021
Cited by 12 | Viewed by 2873
Abstract
The incidence of age associated chronic diseases has increased in recent years. Although several diverse causes produce these phenomena, abundant evidence shows that oxidative stress plays a central role. In recent years, numerous studies have focused on elucidating the role of oxidative stress [...] Read more.
The incidence of age associated chronic diseases has increased in recent years. Although several diverse causes produce these phenomena, abundant evidence shows that oxidative stress plays a central role. In recent years, numerous studies have focused on elucidating the role of oxidative stress in the development and progression of both aging and chronic diseases, opening the door to the discovery of new underlying mechanisms and signaling pathways. Among them, senolytics and senomorphics, and extracellular vesicles offer new therapeutic strategies to slow the development of aging and its associated chronic diseases by decreasing oxidative stress. In this review, we aim to discuss the role of extracellular vesicles in human cardiorenal syndrome development and their possible role as biomarkers, targets, or vehicles of drugs to treat this syndrome. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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Graphical abstract

19 pages, 1513 KiB  
Review
Oxidative Stress and Energy Metabolism in the Brain: Midlife as a Turning Point
by Volodymyr I. Lushchak, Michael Duszenko, Dmytro V. Gospodaryov and Olga Garaschuk
Antioxidants 2021, 10(11), 1715; https://doi.org/10.3390/antiox10111715 - 28 Oct 2021
Cited by 29 | Viewed by 4384
Abstract
Neural tissue is one of the main oxygen consumers in the mammalian body, and a plentitude of metabolic as well as signaling processes within the brain is accompanied by the generation of reactive oxygen (ROS) and nitrogen (RNS) species. Besides the important signaling [...] Read more.
Neural tissue is one of the main oxygen consumers in the mammalian body, and a plentitude of metabolic as well as signaling processes within the brain is accompanied by the generation of reactive oxygen (ROS) and nitrogen (RNS) species. Besides the important signaling roles, both ROS and RNS can damage/modify the self-derived cellular components thus promoting neuroinflammation and oxidative stress. While previously, the latter processes were thought to progress linearly with age, newer data point to midlife as a critical turning point. Here, we describe (i) the main pathways leading to ROS/RNS generation within the brain, (ii) the main defense systems for their neutralization and (iii) summarize the recent literature about considerable changes in the energy/ROS homeostasis as well as activation state of the brain’s immune system at midlife. Finally, we discuss the role of calorie restriction as a readily available and cost-efficient antiaging and antioxidant lifestyle intervention. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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26 pages, 459 KiB  
Review
Ellagic Acid as a Tool to Limit the Diabetes Burden: Updated Evidence
by Antonio J. Amor, Carmen Gómez-Guerrero, Emilio Ortega, Aleix Sala-Vila and Iolanda Lázaro
Antioxidants 2020, 9(12), 1226; https://doi.org/10.3390/antiox9121226 - 03 Dec 2020
Cited by 40 | Viewed by 3868
Abstract
Oxidative stress contributes not only to the pathogenesis of type 2 diabetes (T2D) but also to diabetic vascular complications. It follows that antioxidants might contribute to limiting the diabetes burden. In this review we focus on ellagic acid (EA), a compound that can [...] Read more.
Oxidative stress contributes not only to the pathogenesis of type 2 diabetes (T2D) but also to diabetic vascular complications. It follows that antioxidants might contribute to limiting the diabetes burden. In this review we focus on ellagic acid (EA), a compound that can be obtained upon intestinal hydrolysis of dietary ellagitannins, a family of polyphenols naturally found in several fruits and seeds. There is increasing research on cardiometabolic effects of ellagitannins, EA, and urolithins (EA metabolites). We updated research conducted on these compounds and (I) glucose metabolism; (II) inflammation, oxidation, and glycation; and (III) diabetic complications. We included studies testing EA in isolation, extracts or preparations enriched in EA, or EA-rich foods (mostly pomegranate juice). Animal research on the topic, entirely conducted in murine models, mostly reported glucose-lowering, antioxidant, anti-inflammatory, and anti-glycation effects, along with prevention of micro- and macrovascular diabetic complications. Clinical research is incipient and mostly involved non-randomized and low-powered studies, which confirmed the antioxidant and anti-inflammatory properties of EA-rich foods, but without conclusive results on glucose control. Overall, EA-related compounds might be potential agents to limit the diabetes burden, but well-designed human randomized controlled trials are needed to fill the existing gap between experimental and clinical research. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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Other

9 pages, 966 KiB  
Brief Report
Female Mice Reaching Exceptionally High Old Age Have Preserved 20S Proteasome Activities
by Irene Martínez de Toda, Suresh I. S. Rattan, Mónica De la Fuente and Lorena Arranz
Antioxidants 2021, 10(9), 1397; https://doi.org/10.3390/antiox10091397 - 31 Aug 2021
Cited by 5 | Viewed by 2630
Abstract
Oxidized, damaged and misfolded proteins accumulate during aging and contribute to impaired cell function and tissue homeodynamics. Damaged proteins are degraded by cellular clearance mechanisms like the 20S proteasome. Aging relates to low 20S proteasome function, whereas long-lived species show high levels. However, [...] Read more.
Oxidized, damaged and misfolded proteins accumulate during aging and contribute to impaired cell function and tissue homeodynamics. Damaged proteins are degraded by cellular clearance mechanisms like the 20S proteasome. Aging relates to low 20S proteasome function, whereas long-lived species show high levels. However, contradictory results exist depending on the tissue or cell type and it is unknown how the 20S proteasome functions in exceptionally old mice. The aim of this study was to investigate two proteasome activities (caspase-like and chymotrypsin-like) in several tissues (lung, heart, axillary lymph nodes, liver, kidney) and cells (peritoneal leukocytes) from adult (28 ± 4 weeks, n = 12), old (76 ± 4 weeks, n = 9) and exceptionally old (128 ± 4 weeks, n = 9) BALB/c female mice. The results show different age-related changes depending on the tissue and the activity considered, so there is no universal decline in proteasome function with age in female mice. Interestingly, exceptionally old mice displayed better maintained proteasome activities, suggesting that preserved 20S proteasome is associated with successful aging. Full article
(This article belongs to the Special Issue Oxidative Stress in Aging and Associated Chronic Diseases)
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