scholarly journals Reproductive competency and mitochondrial variation in aged Syrian hamster oocytes

2017 ◽  
Vol 29 (7) ◽  
pp. 1384 ◽  
Author(s):  
Fang Li ◽  
Frank J. Castora ◽  
Wentia Ford ◽  
Khalid Alarid ◽  
Howard W. Jones ◽  
...  

The hamster is a useful model of human reproductive biology because its oocytes are similar to those in humans in terms of size and structural stability. In the present study we evaluated fecundity rate, ovarian follicular numbers, ova production, mitochondrial number, structure and function, and cytoplasmic lamellae (CL) in young (2–4 months) and old (12–18 months) Syrian hamsters (Mesocricetus auratus). Young hamsters had higher fertilisation rates and larger litters than old hamsters (100 vs 50% and 9.3 ± 0.6 vs 5.5 ± 0.6, respectively). Ovarian tissue from superovulated animals showed a 46% decrease in preantral follicles in old versus young hamsters. There was a 39% reduction in MII oocyte number in old versus young hamsters. Young ova had no collapsed CL, whereas old ova were replete with areas of collapsed, non-luminal CL. Eighty-nine per cent of young ova were expanded against the zona pellucida with a clear indentation at the polar body, compared with 58.64% for old ova; the remaining old ova had increased perivitelline space with no polar body indentation. Higher reactive oxygen species levels and lower mitochondrial membrane potentials were seen in ova from old versus young hamsters. A significant decrease in mitochondrial number (36%) and lower frequency of clear mitochondria (31%) were observed in MII oocytes from old versus young hamster. In conclusion, the results of the present study support the theory of oocyte depletion during mammalian aging, and suggest that morphological changes of mitochondria and CL in oocytes may be contributing factors in the age-related decline in fertility rates.

2018 ◽  
Vol 43 (12) ◽  
pp. 1215-1223 ◽  
Author(s):  
Camila L.P. Oliveira ◽  
Isabelle J. Dionne ◽  
Carla M. Prado

Aging is characterized by physiological and morphological changes that affect body composition, strength, and function, ultimately leading to sarcopenia. This condition results in physical disability, falls, fractures, poor quality of life, and increased health care costs. Evidence suggests that increased consumption of dietary protein and physical activity levels, especially resistance exercise, can counteract the trajectory of sarcopenia. Canadian guidelines for protein intake and physical activity were last updated in 2005 and 2011, respectively, and new evidence on sarcopenia diagnosis, prevention, and treatment is rapidly evolving. Protein recommendations are set as “one-size-fits-all” for both young and older adults. Recent evidence demonstrates that current recommendations are insufficient to meet the minimum protein requirement to counteract muscle loss and to stimulate hypertrophy in healthy older adults. Beyond quantity, protein quality is also essential to benefit muscle anabolism in older adults. In terms of physical activity, resistance exercise training is a potential strategy to counteract age-related effects, as it can elicit muscle hypertrophic response in addition to increases in muscle strength and function in older adults. Canadian physical activity guidelines lack details on how this modality of training should be performed. Current guidelines for protein intake and physical activity do not reflect recent knowledge on sarcopenia prevention. The gap between guidelines and the latest evidence on the maintenance and promotion of older adult’s health highlight the need for updated protein and physical activity recommendations.


2021 ◽  
Vol 22 (2) ◽  
pp. 697
Author(s):  
Kenneth K. Wu

Cellular senescence contributes to aging and age-related disorders. High glucose (HG) induces mesenchymal stromal/stem cell (MSC) senescence, which hampers cell expansion and impairs MSC function. Intracellular HG triggers metabolic shift from aerobic glycolysis to oxidative phosphorylation, resulting in reactive oxygen species (ROS) overproduction. It causes mitochondrial dysfunction and morphological changes. Tryptophan metabolites such as 5-methoxytryptophan (5-MTP) and melatonin attenuate HG-induced MSC senescence by protecting mitochondrial integrity and function and reducing ROS generation. They upregulate the expression of antioxidant enzymes. Both metabolites inhibit stress-induced MSC senescence by blocking p38 MAPK signaling pathway, NF-κB, and p300 histone acetyltransferase activity. Furthermore, melatonin upregulates SIRT-1, which reduces NF-κB activity by de-acetylation of NF-κB subunits. Melatonin and 5-MTP are a new class of metabolites protecting MSCs against replicative and stress-induced cellular senescence. They provide new strategies to improve the efficiency of MSC-based therapy for diverse human diseases.


2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Cinzia Forni ◽  
Francesco Facchiano ◽  
Manuela Bartoli ◽  
Stefano Pieretti ◽  
Antonio Facchiano ◽  
...  

Aging is related to a number of functional and morphological changes leading to progressive decline of the biological functions of an organism. Reactive Oxygen Species (ROS), released by several endogenous and exogenous processes, may cause important oxidative damage to DNA, proteins, and lipids, leading to important cellular dysfunctions. The imbalance between ROS production and antioxidant defenses brings to oxidative stress conditions and, related to accumulation of ROS, aging-associated diseases. The purpose of this review is to provide an overview of the most relevant data reported in literature on the natural compounds, mainly phytochemicals, with antioxidant activity and their potential protective effects on age-related diseases such as metabolic syndrome, diabetes, cardiovascular disease, cancer, neurodegenerative disease, and chronic inflammation, and possibly lower side effects, when compared to other drugs.


2020 ◽  
Vol 21 (4) ◽  
pp. 475-484 ◽  
Author(s):  
Anastasia Thoma ◽  
Tania Akter-Miah ◽  
Rebecca L. Reade ◽  
Adam P. Lightfoot

2021 ◽  
Vol 31 (2) ◽  
pp. 232-235
Author(s):  
Kostas Stiklioraitis ◽  
Simas Stiklioraitis ◽  
Liveta Sereikaitė ◽  
Monika Jasinskaitė ◽  
Žilvinas Krivickas ◽  
...  

Background. Sarcopenia is an age-related condition, defined by the muscle decline, impaired physical function, and deterioration in muscle tissue quality. The main cause for the interest of Sarcopenia is the apparent association of this disease with patient morbidity, mortality, prolonged hospitalization, and deterioration in the quality of life. The purpose of this review is to present a brief account of some age-related biological changes that may contribute to Sarcopenia. Materials and methods. We reviewed the literature based on data from Medline (PubMed), Google Scholar, Science Direct, and CAIRN. The research was done on articles in English or French, published before the 31st of December 2019. The research was based on the following Mesh headings (Medical Subject Headings): “sarcopenia” AND “aging” OR “muscle loss”. Conclusions. A multitude of etiological factors influences the aging-associated deterioration of muscle mass and function that constitute Sarcopenia, such as imbalanced protein synthesis and degradation, decreasing anabolic hormones, inflammation, and age-related morphological changes, which are described in the review. In the future, research might be conducted for identifying specific biomarkers, which may lead to an opportunity to assess and monitor the disease non-invasively, granting possibilities for a more efficient therapeutic approach.


2019 ◽  
Vol 24 (40) ◽  
pp. 4726-4741 ◽  
Author(s):  
Orathai Tangvarasittichai ◽  
Surapon Tangvarasittichai

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.


Author(s):  
Anietie Francis Udoumoh ◽  
Udensi Maduabuchi Igwebuike ◽  
Chidozie Nwabuisi Okoye ◽  
Ugochukwu Michael Ugwu ◽  
Chike Fidelis Oguejiofor

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Anastasiya Börsch ◽  
Daniel J. Ham ◽  
Nitish Mittal ◽  
Lionel A. Tintignac ◽  
Eugenia Migliavacca ◽  
...  

AbstractSarcopenia, the age-related loss of skeletal muscle mass and function, affects 5–13% of individuals aged over 60 years. While rodents are widely-used model organisms, which aspects of sarcopenia are recapitulated in different animal models is unknown. Here we generated a time series of phenotypic measurements and RNA sequencing data in mouse gastrocnemius muscle and analyzed them alongside analogous data from rats and humans. We found that rodents recapitulate mitochondrial changes observed in human sarcopenia, while inflammatory responses are conserved at pathway but not gene level. Perturbations in the extracellular matrix are shared by rats, while mice recapitulate changes in RNA processing and autophagy. We inferred transcription regulators of early and late transcriptome changes, which could be targeted therapeutically. Our study demonstrates that phenotypic measurements, such as muscle mass, are better indicators of muscle health than chronological age and should be considered when analyzing aging-related molecular data.


Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 373
Author(s):  
Joshua J. Scammahorn ◽  
Isabel T. N. Nguyen ◽  
Eelke M. Bos ◽  
Harry Van Goor ◽  
Jaap A. Joles

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.


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