PHYSICAL ACTIVITY AS HEALTHY INTERVENTION AGAINST SEVERE OXIDATIVE STRESS IN ELDERLY POPULATION

2013 ◽  
pp. 1-9
Author(s):  
C. TOMAS-ZAPICO ◽  
E. IGLESIAS-GUTIERREZ ◽  
B. FERNANDEZ-GARCIA ◽  
D. DE GONZALO-CALVO

Severe oxidative stress is a relevant risk factor for major deleterious health-related events in olderpeople and is thought to be an important contributor to age-related disease. Literature has suggested oxidativestress as a therapeutic target for mitigating the biological decline and attenuating the occurrence of adverseclinical events in aged individuals. However, definitive treatments are not known. Regular and moderate physicalactivity has been proposed as possible intervention for slowing age-related decline. This healthy strategy presentsa wide range of beneficial aspects for elderly, from the reduction of morbidity, disability, frailty and mortalityrates to treatment of many age-related disorders. Importantly, the global benefits on health are not shared by anyother strategies. Nevertheless, the physiological basis by which exercise produces its benefits to the organism isnot fully understood. This review summarizes the evidence for the role of physical activity as potential healthyintervention for mitigating the negative aspects of aging through the modulation of the oxidative mechanisms.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rawshan Choudhury ◽  
Nadhim Bayatti ◽  
Richard Scharff ◽  
Ewa Szula ◽  
Viranga Tilakaratna ◽  
...  

AbstractRetinal pigment epithelial (RPE) cells that underlie the neurosensory retina are essential for the maintenance of photoreceptor cells and hence vision. Interactions between the RPE and their basement membrane, i.e. the inner layer of Bruch’s membrane, are essential for RPE cell health and function, but the signals induced by Bruch’s membrane engagement, and their contributions to RPE cell fate determination remain poorly defined. Here, we studied the functional role of the soluble complement regulator and component of Bruch’s membrane, Factor H-like protein 1 (FHL-1). Human primary RPE cells adhered to FHL-1 in a manner that was eliminated by either mutagenesis of the integrin-binding RGD motif in FHL-1 or by using competing antibodies directed against the α5 and β1 integrin subunits. These short-term experiments reveal an immediate protein-integrin interaction that were obtained from primary RPE cells and replicated using the hTERT-RPE1 cell line. Separate, longer term experiments utilising RNAseq analysis of hTERT-RPE1 cells bound to FHL-1, showed an increased expression of the heat-shock protein genes HSPA6, CRYAB, HSPA1A and HSPA1B when compared to cells bound to fibronectin (FN) or laminin (LA). Pathway analysis implicated changes in EIF2 signalling, the unfolded protein response, and mineralocorticoid receptor signalling as putative pathways. Subsequent cell survival assays using H2O2 to induce oxidative stress-induced cell death suggest hTERT-RPE1 cells had significantly greater protection when bound to FHL-1 or LA compared to plastic or FN. These data show a non-canonical role of FHL-1 in protecting RPE cells against oxidative stress and identifies a novel interaction that has implications for ocular diseases such as age-related macular degeneration.


2021 ◽  
Vol 22 (3) ◽  
pp. 1296
Author(s):  
Yue Ruan ◽  
Subao Jiang ◽  
Adrian Gericke

Age-related macular degeneration (AMD) is a common irreversible ocular disease characterized by vision impairment among older people. Many risk factors are related to AMD and interact with each other in its pathogenesis. Notably, oxidative stress and choroidal vascular dysfunction were suggested to be critically involved in AMD pathogenesis. In this review, we give an overview on the factors contributing to the pathophysiology of this multifactorial disease and discuss the role of reactive oxygen species and vascular function in more detail. Moreover, we give an overview on therapeutic strategies for patients suffering from AMD.


2017 ◽  
Vol 63 (2) ◽  
pp. 297-305 ◽  
Author(s):  
Efi Koloverou ◽  
◽  
Konstantinos Tambalis ◽  
Demosthenes B. Panagiotakos ◽  
Ekavi Georgousopoulou ◽  
...  

2021 ◽  
Vol 22 (3) ◽  
pp. 1200
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama

Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.


Blood ◽  
1988 ◽  
Vol 71 (6) ◽  
pp. 1726-1730
Author(s):  
KA Melez ◽  
LF Fries ◽  
BS Bender ◽  
T Quinn ◽  
MM Frank

Decreased immune functions have been suggested as a cause for the increased incidence of autoimmunity, malignancy, and infection in the elderly population. To assess the possible role of changes in macrophage function in the aging process we studied the Fc receptor- mediated clearance of IgG-coated erythrocytes in 56 healthy normal volunteers by following the removal of radiolabeled autologous erythrocytes. An age-related decrease in Fc-mediated clearance rates in both female and male subjects was found, which suggests a physiological decline of this macrophage function in older individuals.


2018 ◽  
Vol 69 (2) ◽  
pp. 16-22
Author(s):  
Milena Kostadinović ◽  
Dejan Nikolić ◽  
Milena Šantrić-Milićević

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Alexander Fidao ◽  
Alysha De Livera ◽  
Tracey Weiland ◽  
George Jelinek ◽  
Sandra Neate ◽  
...  

Abstract Background Fatigue is among the most prevalent symptoms of multiple sclerosis (MS), and significantly detrimental to mental quality of life. We examined the role of depression and physical activity as mediators in the fatigue-QoL relationship in MS. Methods Using an international study cohort measuring a wide range of lifestyle and clinical factors, determinants of fatigue (Fatigue Severity Scale) and mental quality of life (MSQoL-54; QoL) were assessed in 2,104 participants using log-binomial and linear regression, respectively. Structural equation modelling (SEM) was used to assess the mediating role of depression and physical activity between fatigue and mental QoL. Results The median mental QoL score in the sample was 73.8/100. The mean fatigue score was 40.5/63, with 65.6% having clinically significant fatigue. In SEM analyses evaluating depression as a mediator of the fatigue-QoL relationship, mental QoL was 14.17-points lower in those with clinically significant fatigue, of which the indirect effect via depression accounted for over 30.8% (p < 0.001). This mediation effect was most pronounced for the Role Limitations from Emotional Issues (44.9%, p < 0.001) and Emotional Wellbeing (41.6%, p < 0.001) subdomains. Evaluating physical activity as a mediator of the fatigue-QoL relationship, mental QoL was 11.03-points lower in those with clinically significant fatigue, of which the indirect effect via physical activity accounted for only 1.0% (p = 0.001). Conclusions This study provides evidence that depression accounts for a majority of the fatigue-mental QoL relationship, while physical activity only plays a small role. While replication and longitudinal studies are required for validation, our findings may inform the development of treatments for reducing the impacts of fatigue and improving QoL in people with MS. Key messages Fatigue’s negative impact on emotional quality of life in multiple sclerosis is not a function of reduced ambulation but instead its impact on depression. Reducing depression may thus markedly improve quality of life in this population.


2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Bilgen Basgut ◽  
Melissa A. Whidden ◽  
Nataliya Kirichenko ◽  
Mary Woods ◽  
Benedek Erdos ◽  
...  
Keyword(s):  

2020 ◽  
Vol 9 (10) ◽  
pp. 3172 ◽  
Author(s):  
Stefania Vernazza ◽  
Sara Tirendi ◽  
Anna Maria Bassi ◽  
Carlo Enrico Traverso ◽  
Sergio Claudio Saccà

Primary open-angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increasing evidence suggests oxidative damage and immune response defects are key factors contributing to glaucoma onset. Indeed, both the failure of the trabecular meshwork tissue in the conventional outflow pathway and the neuroinflammation process, which drives the neurodegeneration, seem to be linked to the age-related over-production of free radicals (i.e., mitochondrial dysfunction) and to oxidative stress-linked immunostimulatory signaling. Several previous studies have described a wide range of oxidative stress-related makers which are found in glaucomatous patients, including low levels of antioxidant defences, dysfunction/activation of glial cells, the activation of the NF-κB pathway and the up-regulation of pro-inflammatory cytokines, and so on. However, the intraocular pressure is still currently the only risk factor modifiable by medication or glaucoma surgery. This present review aims to summarize the multiple cellular processes, which promote different risk factors in glaucoma including aging, oxidative stress, trabecular meshwork defects, glial activation response, neurodegenerative insults, and the altered regulation of immune response.


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