scholarly journals Increased telomere length and mtDNA copy number induced by multi-walled carbon nanotube exposure in the workplace

2020 ◽  
Vol 394 ◽  
pp. 122569
Author(s):  
Manosij Ghosh ◽  
Lisa Janssen ◽  
Dries S. Martens ◽  
Deniz Öner ◽  
Jelle Vlaanderen ◽  
...  
Keyword(s):  
Carbon Nanotube ◽  
Telomere Length ◽  
Copy Number ◽  
Mtdna Copy Number ◽  
Multi Walled Carbon Nanotube

scholarly journals Born to be young: prenatal thyroid hormones increase early-life telomere length

2020 ◽  
Author(s):  
Antoine Stier ◽  
Bin-Yan Hsu ◽  
Coline Marciau ◽  
Blandine Doligez ◽  
Lars Gustafsson ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Telomere Length ◽  
Early Life ◽  
Copy Number ◽  
Growth Period ◽  
Postnatal Growth ◽  
Mtdna Copy Number ◽  
Underlying Mechanisms ◽  
Growth And Aging ◽  
Positive Effect

AbstractPrenatal environmental conditions can have lifelong consequences on health and aging. The underlying mechanisms remain nonetheless little understood. Thyroid hormones (THs) are important regulators of embryogenesis transferred from the mother to the embryo. In an avian model, we manipulated embryo exposure to maternal THs through egg injection and investigated the consequences on postnatal growth and aging. We first report that mitochondrial DNA (mtDNA) copy number and telomere length significantly decrease from early-life to late adulthood, thus confirming that these two molecular markers are hallmarks of aging in our wild bird model. The experimental elevation of prenatal THs levels had a transient positive effect on postnatal growth. Elevated prenatal THs had no effect on mtDNA copy number but significantly increased telomere length both soon after birth and at the end of the growth period (equivalent to offsetting ca. 4 years of post-growth telomere shortening). These findings suggest that prenatal THs have a key role in setting the ‘biological’ age at birth, and thus might influence longevity.

scholarly journals Born to be young? Prenatal thyroid hormones increase early-life telomere length in wild collared flycatchers

2020 ◽  
Vol 16 (11) ◽  
pp. 20200364
Author(s):  
Antoine Stier ◽  
Bin-Yan Hsu ◽  
Coline Marciau ◽  
Blandine Doligez ◽  
Lars Gustafsson ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Telomere Length ◽  
Early Life ◽  
Copy Number ◽  
Growth Period ◽  
Mtdna Copy Number ◽  
Cross Sectional ◽  
Telomere Shortening ◽  
Underlying Mechanisms ◽  
Age At Birth

The underlying mechanisms of the lifelong consequences of prenatal environmental condition on health and ageing remain little understood. Thyroid hormones (THs) are important regulators of embryogenesis, transferred from the mother to the embryo. Since prenatal THs can accelerate early-life development, we hypothesized that this might occur at the expense of resource allocation in somatic maintenance processes, leading to premature ageing. Therefore, we investigated the consequences of prenatal TH supplementation on potential hallmarks of ageing in a free-living avian model in which we previously demonstrated that experimentally elevated prenatal TH exposure accelerates early-life growth. Using cross-sectional sampling, we first report that mitochondrial DNA (mtDNA) copy number and telomere length significantly decrease from early-life to late adulthood, thus suggesting that these two molecular markers could be hallmarks of ageing in our wild bird model. Elevated prenatal THs had no effect on mtDNA copy number but counterintuitively increased telomere length both soon after birth and at the end of the growth period (equivalent to offsetting ca 4 years of post-growth telomere shortening). These findings suggest that prenatal THs might have a role in setting the ‘biological' age at birth, but raise questions about the nature of the evolutionary costs of prenatal exposure to high TH levels.

Combined Impact of Telomere Length and Mitochondrial DNA Copy Number on Cognitive Function in Community-Dwelling Very Old Adults

2017 ◽  
Vol 44 (3-4) ◽  
pp. 232-243 ◽  
Author(s):  
Jee-Yon Lee ◽  
Jung-Ha Kim ◽  
Duk-Chul Lee
Keyword(s):  
Mitochondrial Dna ◽  
Cognitive Function ◽  
Telomere Length ◽  
Odds Ratio ◽  
Copy Number ◽  
Adjusted Odds Ratio ◽  
Community Dwelling ◽  
Mtdna Copy Number ◽  
Old Adults ◽  
Combined Impact

Background: This study was conducted to investigate the combined impact of telomere length and mitochondrial DNA (mtDNA) copy number on cognitive function in community-dwelling very old adults. Methods: In total, 186 subjects over 75 years participated in this study. Cognitive function was assessed using the Korean Mini-Mental State Examination, and leukocyte telomere length and mtDNA copy number were measured using real-time polymerase chain reaction methods. Results: Both the fourth quartile of telomere length and mtDNA copy number were associated with cognitive dysfunction with an adjusted odds ratio of 0.23 (95% confidence interval (CI), 0.10-0.75) and 0.18 (95% CI, 0.03-0.54), respectively. Participants in the high telomere length/high mtDNA copy number group were more likely to have cognitive dysfunction than participants in the low telomere/low mtDNA copy number group with an adjusted odds ratio of 0.19 (95% CI, 0.07-0.58). Conclusion: Our results collectively suggest that the combination of telomere length and mtDNA copy number may be useful for monitoring cognitive decline in older adults.

scholarly journals Football and Team Handball Training Postpone Cellular Aging in Women

2021 ◽  
Author(s):  
Marie Hagman ◽  
Bjørn Fristrup ◽  
Rémi Michelin ◽  
Peter Krustrup ◽  
Muhammad Asghar
Keyword(s):  
Telomere Length ◽  
Mitochondrial Function ◽  
Copy Number ◽  
Mononuclear Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Cellular Aging ◽  
Elderly Subjects ◽  
Mtdna Copy Number ◽  
Cross Sectional ◽  
Team Handball

Abstract Aims: Several hallmarks of aging have been identified and examined separately in previous exercise studies. For the first time, this study investigates the effect of lifelong regular exercise in humans on two of the central aging hallmarks combined. Methods: This cross-sectional study involved 129 healthy, non-smoking women, including young elite football players (YF, n=29), young untrained controls (YC, n=30), elderly team handball players (EH, n=35) and elderly untrained controls (EC, n=35). From a resting blood sample, mononuclear cells (MNCs) were isolated and sorted into monocytes and lymphocytes. Telomere length, mitochondrial (mtDNA) copy number and mitochondrial function (PGC-1α and PGC-1β expression) were measured using quantitative polymerase chain reaction (qPCR). Results: Overall, young women showed significantly longer telomeres and higher mitochondrial function, but lower mtDNA copy number compared to elderly subjects. A multivariate analysis showed that YF had 22–24% longer telomeres in lymphocytes and MNCs compared to YC. In addition, YF showed 19–20% higher mtDNA copy number in lymphocytes and MNCs compared to YC. The two young groups did not differ in PGC-1α and PGC-1β expression. EH showed 14% lower mtDNA copy number in lymphocytes compared to EC, but 3.4-fold higher lymphocyte PGC-1α expression compared to EC. In MNCs, EH also showed 1.4-1.6- fold higher mitochondrial function. The two elderly groups did not differ in telomere length.Conclusion: Elite football training and lifelong team handball training are associated with anti-aging mechanisms in leukocytes in women, including maintenance of telomere length and upregulation of mitochondrial function.

scholarly journals OR03-04 The Study of Cell Senescence in Cortisol-Producing Adrenocortical Adenomas

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Xin Gao ◽  
Yuto Yamazaki ◽  
Jacopo Pieroni ◽  
Yuta Tezuka ◽  
Kei Omata ◽  
...  
Keyword(s):  
Telomere Length ◽  
Tumor Cells ◽  
Copy Number ◽  
Cell Senescence ◽  
Endocrine Disorders ◽  
Mtdna Copy Number ◽  
Telomere Shortening ◽  
Clear Cells ◽  
Adrenocortical Adenomas ◽  
Mtdna Deletion

Abstract Introduction Aging is associated with the pathogenesis of many endocrine disorders such as cardiovascular diseases and diabetes. Cell senescence has been reported as one of their mechanisms. In addition, stress responsiveness has been reported to be associated with cell senescence. In addition, some genetic abnormalities such as mitochondrial DNA (mtDNA) damages or telomere shortening, have been detected in some endocrine disorders. Cortisol is a well-known stress-induced hormone and closely associated with aging. We previously reported that cortisol-producing adenoma (CPA) more abundantly expressed cell senescent markers such as p16 and p21 than other hormone-producing adrenocortical adenomas. However, the detailed pathophysiology of cell senescence and its association with histological features in CPAs have remained virtually unknown. Therefore, we analyzed cell senescent markers (telomere length, mtDNA copy number, mtDNA deletion and p16 and p21 immunoreactivity) and analyzed their correlation with clinicopathological factors in CPA patients. Methods & Materials Forty CPA cases was immunohistochemically evaluated. Twenty CPA, ten adjacent ZF and six non-functional adenoma (NFA) were examined for mtDNA abnormalities. mtDNA deletion was evaluated by nested-PCR and mtDNA copy number and telomere length were measured using real-time PCR. Results p21 immunoreactivity was significantly higher in CPA than that of adjacent ZF (P=0.0001) and significantly inversely correlated with tumor size (P=0.0004). Telomere length was much longer in CPA than that in adjacent ZF(P=0.0038), and NFA (P=0.0018). mtDNA copy number of NFA was significantly higher than that of CPA and adjacent ZF (P=0.0038). mtDNA copy number of compact cells was significantly higher than that of clear cells (P=0.0432). mtDNA copy number of compact cells was positively correlated with urinary free cortisol (UFC) (P=0.0428) and plasma cortisol (F) (P=0.0609). mtDNA copy number of clear cells were inversely correlated with F (0.0497). 4977 bp mtDNA deletion was more frequently detected in CPA (54%) and in adjacent ZF (50%) than in NFA (17%). Discussion Results of our present study did reveal that CPA harbored more senescent phenotype as demonstrated by abundant p16 and p21, marked telomere shortening, frequent mtDNA 4977bp deletion and relatively low mtDNA copy number, possibly caused by long-term exposure of excessive cortisol in situ compared to NFA. In addition, clear tumor cells could represent more senescent histological phenotype because of their lower mtDNA copy numbers. This is the first study to demonstrate that compact tumor cells were biologically more active than clear tumor cells and could reflect clinical cortisol biosynthesis, resulting in marked functional intratumoral heterogeneity in CPAs.

Telomere length and mtDNA copy number in human cystathionine β-synthase deficiency

2020 ◽  
Vol 160 ◽  
pp. 219-226
Author(s):  
Olga Utyro ◽  
Joanna Perła-Kaján ◽  
Jolanta Kubalska ◽  
Ałła Graban ◽  
Hieronim Jakubowski
Keyword(s):  
Telomere Length ◽  
Copy Number ◽  
Mtdna Copy Number

scholarly journals Mitochondrial Biogenesis, Telomere Length and Cellular Senescence in Parkinson’s Disease and Lewy Body Dementia

2021 ◽  
Author(s):  
Muhammad Asghar ◽  
Amani Odeh ◽  
Ahmad Jouni Fattahi ◽  
Alexandra Edward Henriksson ◽  
Aurelie Miglar ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Telomere Length ◽  
Cellular Senescence ◽  
Mitochondrial Biogenesis ◽  
Copy Number ◽  
Cellular Aging ◽  
Mtdna Copy Number

Abstract Background Progressive age is the single major risk factor for neurodegenerative diseases. Cellular aging markers during the course of Parkinson’s disease (PD) have been implicated in previous studies, however majority of these studies have investigated the association of individual cellular aging hallmarks with PD but not jointly. Method Here, we have studied the association of PD with three aging hallmarks (telomere attrition, mitochondrial dysfunction, and cellular senescence) in blood and the brain tissue. Telomere length and mitochondrial DNA ( mtDNA ) copy number was assessed by qPCR, while mitochondrial function ( PGC-1α and PGC-1β ) and expression of cyclin-dependent kinase inhibitor 2A ( CDKN2A ), cellular senescence marker was measured by RT-qPCR. Results Our results show that patients diagnosed with PD had 20% lower mitochondrial DNA copy number but 26% longer telomeres in blood compared to controls. Moreover, telomere length in blood was positively correlated with medication (Levodopa Equivalent Daily Dose). Similar results were found in brain tissue, where patients with Parkinson’s disease (PD), Parkinson dementia (PDD) and Dementia with Lewy Bodies (DLB) showed (46-95%) depleted mtDNA copy number, but (7-9%) longer telomeres compared to controls. Furthermore, when compared to controls, patients had lower mitochondrial biogenesis ( PGC-1α and PGC-1β ) and higher load of cellular senescent cells in postmortem prefrontal cortex tissue, where DLB showing the highest effect among the patient groups. Conclusion Our results show that mitochondrial dysfunction and cellular senescence but not telomere shortening is associated with PD, PDD and DLB. Our findings suggest that mitochondrial copy number and function could be used as viable biomarker in blood as an early indicator for the risk of neurodegenerative diseases.

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