scholarly journals Deletion of Neuronal CuZnSOD Accelerates Age-Associated Muscle Mitochondria and Calcium Handling Dysfunction That Is Independent of Denervation and Precedes Sarcopenia

2021 ◽  
Vol 22 (19) ◽  
pp. 10735
Author(s):  
Yu Su ◽  
Dennis R. Claflin ◽  
Meixiang Huang ◽  
Carol S. Davis ◽  
Peter C. D. Macpherson ◽  
...  
Keyword(s):  
Old Age ◽  
Mitochondrial Function ◽  
Middle Age ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Calcium Transients ◽  
Calcium Handling ◽  
Muscle Loss ◽  
Mitochondrial Defects ◽  
Loss Of Mass

Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, and mitochondrial dysfunction are all proposed as contributors to age-associated muscle loss, but connections between these factors have not been established. We examined contractility, mitochondrial function, and intracellular calcium transients (ICTs) in muscles of mice throughout the life span to define their sequential relationships. We performed these same measures and analyzed neuromuscular junction (NMJ) morphology in mice with postnatal deletion of neuronal Sod1 (i-mn-Sod1-/- mice), previously shown to display accelerated age-associated muscle loss and exacerbation of denervation in old age, to test relationships between neuronal redox homeostasis, NMJ degeneration and mitochondrial function. In control mice, the amount and rate of the decrease in mitochondrial NADH during contraction was greater in middle than young age although force was not reduced, suggesting decreased efficiency of NADH utilization prior to the onset of weakness. Declines in both the peak of the ICT and force were observed in old age. Muscles of i-mn-Sod1-/- mice showed degeneration of mitochondrial and calcium handling functions in middle-age and a decline in force generation to a level not different from the old control mice, with maintenance of NMJ morphology. Together, the findings support the conclusion that muscle mitochondrial function decreases during aging and in response to altered neuronal redox status prior to NMJ deterioration or loss of mass and force suggesting mitochondrial defects contribute to sarcopenia independent of denervation.

scholarly journals Capsaicin Alleviates the Deteriorative Mitochondrial Function by Upregulating 14-3-3η in Anoxic or Anoxic/Reoxygenated Cardiomyocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-16 ◽  
Author(s):  
Yang Qiao ◽  
Tianhong Hu ◽  
Bin Yang ◽  
Hongwei Li ◽  
Tianpeng Chen ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Complex I ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Neonatal Rat ◽  
Ros Generation ◽  
Consumption Rates ◽  
Vitro Model ◽  
The Impact

Reactive oxygen species (ROS) are byproducts of a defective electron transport chain (ETC). The redox couples, GSH/GSSG and NAD+/NADH, play an essential role in physiology as internal defenses against excessive ROS generation by facilitating intracellular/mitochondrial (mt) redox homeostasis. Anoxia alone and anoxia/reoxygenation (A/R) are dissimilar pathological processes. In this study, we measured the impact of capsaicin (Cap) on these pathological processes using a primary cultured neonatal rat cardiomyocyte in vitro model. The results showed that overproduction of ROS was tightly associated with disturbed GSH/GSSG and NAD+/NADH suppressed mt complex I and III activities, decreased oxygen consumption rates, and elevated extracellular acidification rates. During anoxia or A/R period, these indices interact with each other causing the mitochondrial function to worsen. Cap protected cardiomyocytes against the different stages of A/R injury by rescuing NAD+/NADH, GSH/GSSG, and mt complex I/III activities and cellular energy metabolism. Importantly, Cap-mediated upregulation of 14-3-3η, a protective phosphoserine-binding protein in cardiomyocytes, ameliorated mt function caused by a disruptive redox status and an impaired ETC. In conclusion, redox pair, mt complex I/III, and metabolic equilibrium were significantly different in anoxia alone and A/R injury; Cap through upregulating 14-3-3η plays a protection against the above injury in cardiomyocyte.

Attitude towards Health and Fitness of Middle Age and Old Age Citizens of Gwalior

10.26524/1312 ◽  
2013 ◽  
Vol 2 (1) ◽  
pp. 06-15
Author(s):  
Rajender Singh ◽  
Pradeep Kumar ◽  
Sonu Kumar ◽  
Prabal Pratap Singh
Keyword(s):  
Old Age ◽  
Middle Age ◽  
Health And Fitness

scholarly journals Alterations in glutathione redox homeostasis among adolescents with obesity and anemia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dalal Alkazemi ◽  
Abdur Rahman ◽  
Banan Habra
Keyword(s):  
Defense Mechanism ◽  
Dynamic Balance ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Cross Sectional Study ◽  
Normal Weight ◽  
Overweight And Obesity ◽  
Metabolic Disturbances ◽  
Cross Sectional ◽  
Gpx Activity

AbstractThe reduced (GSH)-to-oxidized (GSSG) glutathione ratio represents a dynamic balance between oxidants and antioxidants. However, redox status in adolescents with obesity and anemia has not been investigated. This study investigated the association of erythrocyte GSH redox status (GSH, GSH:GSSG ratio, and glutathione peroxidase [GPx] activity) with anemia and adiposity in adolescents. This case–control study nested in a cross-sectional study enrolled 524 adolescents (268 boys; 256 girls). The prevalence of anemia in overweight and obesity (OWOB) was 5.2% in boys and 11.7% in girls. The GSH:GSSG ratio and GPx activity were significantly higher in girls than in boys (p < 0.001), in anemic than in non-anemic subjects (p < 0.001), and in OWOB than in normal-weight subjects (p < 0.001). Similarly, significantly higher GSH: GSSG level (p < 0.001) and GPx activity (p < 0.001) were found in subjects with 90th percentile waist circumference than in those with < 90th percentile. GPx and GSH:GSSG were positively associated with anemia after adjusting for age, sex, and body mass index (adjusted odds ratio, adjOR [95% confidence interval, CI] 2.18 [1.44–3.29]) or tertiles (adjOR [95% CI], T3 = 2.49 [1.03–6.01]). A similar association was noted for GSH and GPx. A compensatory increased redox defense mechanism exists in anemia and obesity among adolescents without metabolic disturbances.

scholarly journals Oxidative status in dairy goats: periparturient variation and changes in subclinical hyperketonemia and hypocalcemia

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Yan Huang ◽  
Jing Wen ◽  
Yezi Kong ◽  
Chenxu Zhao ◽  
Siqi Liu ◽  
...  
Keyword(s):  
Milk Yield ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Oxidative Status ◽  
The Body ◽  
Production Performance ◽  
Lactation Period ◽  
Dairy Goats ◽  
Periparturient Period ◽  
Total Antioxidant

Abstract Background A better comprehension of the redox status during the periparturient period may facilitate the development of management and nutritional solutions to prevent subclinical hyperketonemia (SCHK) and subclinical hypocalcemia (SCHC) in dairy goats. We aimed to evaluate the variation in the redox status of dairy goats with SCHK and SCHC during their periparturient periods. Guanzhong dairy goats (n = 30) were assigned to SCHK (n = 10), SCHC (n = 10), and healthy (HEAL, n = 10) groups based on their blood β-hydroxybutyrate (BHBA) and calcium (Ca) concentrations. Blood were withdrawn from goats every week from 3 weeks before the expected parturition date to 3 weeks post-kidding. On the same day, the body condition scores (BCS) were evaluated, and the milk yield was recorded for each goat. The metabolic profile parameters and the indicators of oxidative status were determined by using the standard biochemical techniques. Results In comparison with the HEAL goats, SCHK and SCHC goats presented with a more dramatic decline of BCS post-kidding and a significant decrease in the milk yield at 2- and 3-weeks postpartum, ignoring the obvious increase at 1-week postpartum. The levels of non-esterified fatty acids (NEFA) peaked at parturition, exhibiting significantly higher levels from 1-week prepartum to the parturition day in the SCHK and SCHC groups. The malondialdehyde (MDA) concentration was increased in the SCHK goats from 1-week antepartum until 3-weeks postpartum, with its concentration being significantly higher in the SCHC goats at parturition. The hydrogen peroxide (H2O2) concentration was significantly lower in the SCHK and SCHC goats from 2-weeks antepartum to 1-week post-kidding. The total antioxidant capacity (T-AOC) and the superoxide dismutase (SOD) level were decreased at 1-week antepartum in the SCHK and SCHC goats, respectively. The glutathione peroxidase (GSH-Px) level was increased in the SCHK and SCHC goats during the early lactation period. Conclusions The SCHK and SCHC goats exerted more efforts to maintain their redox homeostasis and to ensure the production performance than the HEAL goats during their periparturient period, probably owing to more intense fat mobilization and lipid peroxidation in the former.

scholarly journals Critical requirement of SOS1 RAS-GEF function for mitochondrial dynamics, metabolism, and redox homeostasis

Oncogene ◽  
2021 ◽  
Author(s):  
Rósula García-Navas ◽  
Pilar Liceras-Boillos ◽  
Carmela Gómez ◽  
Fernando C. Baltanás ◽  
Nuria Calzada ◽  
...  
Keyword(s):  
Mitochondrial Dynamics ◽  
Redox Homeostasis ◽  
Atp Production ◽  
Oxidative Energy Metabolism ◽  
Ras Activation ◽  
Mitochondrial Defects ◽  
Critical Requirement ◽  
Dynamics And Function ◽  
And Function ◽  
And Control

AbstractSOS1 ablation causes specific defective phenotypes in MEFs including increased levels of intracellular ROS. We showed that the mitochondria-targeted antioxidant MitoTEMPO restores normal endogenous ROS levels, suggesting predominant involvement of mitochondria in generation of this defective SOS1-dependent phenotype. The absence of SOS1 caused specific alterations of mitochondrial shape, mass, and dynamics accompanied by higher percentage of dysfunctional mitochondria and lower rates of electron transport in comparison to WT or SOS2-KO counterparts. SOS1-deficient MEFs also exhibited specific alterations of respiratory complexes and their assembly into mitochondrial supercomplexes and consistently reduced rates of respiration, glycolysis, and ATP production, together with distinctive patterns of substrate preference for oxidative energy metabolism and dependence on glucose for survival. RASless cells showed defective respiratory/metabolic phenotypes reminiscent of those of SOS1-deficient MEFs, suggesting that the mitochondrial defects of these cells are mechanistically linked to the absence of SOS1-GEF activity on cellular RAS targets. Our observations provide a direct mechanistic link between SOS1 and control of cellular oxidative stress and suggest that SOS1-mediated RAS activation is required for correct mitochondrial dynamics and function.

Old age support in kind

2009 ◽  
Vol 9 (3) ◽  
pp. 445-472 ◽  
Author(s):  
KAZUTOSHI MIYAZAWA
Keyword(s):  
Economic Growth ◽  
Old Age ◽  
Strategic Behavior ◽  
Middle Age ◽  
Formal Care ◽  
Old Age Support ◽  
Transfer Policy ◽  
Endogenous Growth Model ◽  
Disincentive Effect ◽  
Inter Vivos Transfer

AbstractIt has been argued whether a transfer policy for elderly people should be in kind or in cash. This paper presents a rationale to answer the question in an endogenous growth model with a two-way intrafamily transfer in middle age, education for the child as an inter-vivos transfer, and informal parental care in exchange for a bequest. We have two analytical results. First, a transfer in cash, such as a public pension, prevents economic growth because a strategic behavior concerning caregiving generates a disincentive effect on education. Second, a transfer in kind, such as public formal care, promotes economic growth because the valuation of the service generates an additional benefit of education, which dominates the disincentive effect. Our results show that old age support should be in kind rather than in cash in the context of economic growth and also welfare if bequests are strategic.

Perceptions of Ideal and Typical Middle and Old Age

1979 ◽  
Vol 9 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Nancy C. Sherman ◽  
Joel A. Gold
Keyword(s):  
Old Age ◽  
Undergraduate Students ◽  
Middle Age ◽  
Semantic Differential ◽  
Three Dimensions

An investigation of attitudes toward typical and ideal old age was carried out with seventy-eight undergraduate students. Half of the participants responded to semantic differential scales for typical and ideal old age and half to middle age stimulus objects. The scales were analyzed in terms of three dimensions produced in previous research. No difference was found between the middle and old age conditions for the personal acceptability dimension but differences were found for both the autonomous-dependent and instrumental-ineffective dimensions. The old and middle age objects were rated alike at ideal but the old age object was rated less autonomous and less instrumental at typical.

scholarly journals Mitochondrial Function, Biology, and Role in Disease

2016 ◽  
Vol 118 (12) ◽  
pp. 1960-1991 ◽  
Author(s):  
Elizabeth Murphy ◽  
Hossein Ardehali ◽  
Robert S. Balaban ◽  
Fabio DiLisa ◽  
Gerald W. Dorn ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Function ◽  
The United States ◽  
Therapeutic Interventions ◽  
Therapeutic Approaches ◽  
Mitochondrial Defects ◽  
Exciting Time ◽  
Insight Into ◽  
Novel Therapeutic

Cardiovascular disease is a major leading cause of morbidity and mortality in the United States and elsewhere. Alterations in mitochondrial function are increasingly being recognized as a contributing factor in myocardial infarction and in patients presenting with cardiomyopathy. Recent understanding of the complex interaction of the mitochondria in regulating metabolism and cell death can provide novel insight and therapeutic targets. The purpose of this statement is to better define the potential role of mitochondria in the genesis of cardiovascular disease such as ischemia and heart failure. To accomplish this, we will define the key mitochondrial processes that play a role in cardiovascular disease that are potential targets for novel therapeutic interventions. This is an exciting time in mitochondrial research. The past decade has provided novel insight into the role of mitochondria function and their importance in complex diseases. This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.

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