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https://www.readbyqxmd.com/read/28342615/effect-of-increasing-body-condition-on-oxidative-stress-and-mitochondrial-biogenesis-in-subcutaneous-adipose-tissue-depot-of-nonlactating-dairy-cows
#1
L Laubenthal, L Ruda, N Sultana, J Winkler, J Rehage, U Meyer, S Dänicke, H Sauerwein, S Häussler
With the onset of lactation, dairy cows with a body condition score >3.5 are sensitive to oxidative stress and metabolic disorders. Adipose tissue (AT) can adapt to varying metabolic demands and energy requirements by the plasticity of its size during lactation. In AT, angiogenesis is necessary to guarantee sufficient oxygen and nutrient supply for adipocytes. Cellular energy metabolism is reflected mainly by mitochondria, which can be quantified by the mitochondrial DNA copy number per cell. In the present study, we aimed to investigate the effect of overconditioning on angiogenesis and mitochondrial biogenesis in AT of nonlactating cows, irrespective of the physiological influences of lactation and pregnancy...
March 22, 2017: Journal of Dairy Science
https://www.readbyqxmd.com/read/28340409/mitochondrial-dna-damage-and-oxidative-damage-in-hl-60-cells-exposed-to-900mhz-radiofrequency-fields
#2
Yulong Sun, Lin Zong, Zhen Gao, Shunxing Zhu, Jian Tong, Yi Cao
HL-60 cells, derived from human promyelocytic leukemia, were exposed to continuous wave 900MHz radiofrequency fields (RF) at 120μW/cm(2) power intensity for 4h/day for 5 consecutive days to examine whether such exposure is capable damaging the mitochondrial DNA (mtDNA) mediated through the production of reactive oxygen species (ROS). In addition, the effect of RF exposure was examined on 8-hydroxy-2'-dexoyguanosine (8-OHdG) which is a biomarker for oxidative damage and on the mitochondrial synthesis of adenosine triphosphate (ATP) which is the energy required for cellular functions...
March 7, 2017: Mutation Research
https://www.readbyqxmd.com/read/28340313/linkage-between-mitochondrial-genome-alterations-telomere-length-and-aging-population
#3
Egija Zole, Krista Zadinane, Liana Pliss, Renate Ranka
We studied telomere length (TL) and mitochondrial DNA (mtDNA) copy number variations in individuals from Latvian Caucasian population in different age groups. We showed a positive correlation between TL and mtDNA copy number in individuals of up to 90 years of age; however, this correlation was not observed in the 90-100 years age group. While TL shortened with age and mtDNA content decreased with increasing age, in this study it was observed that mtDNA copy number in nonagenarians was slightly higher than in the 60-89 years age group...
March 24, 2017: Mitochondrial DNA. Part A. DNA Mapping, Sequencing, and Analysis
https://www.readbyqxmd.com/read/28339599/a-single-nucleotide-polymorphism-in-coq9-affects-mitochondrial-and-ovarian-function-and-fertility-in-holstein-cows%C3%A2
#4
M Sofia Ortega, Stephanie Wohlgemuth, Paula Tribulo, Luiz G B Siqueira, Daniel J Null, John B Cole, Marcus V Da Silva, Peter J Hansen
A single missense mutation at position 159 of coenzyme Q9 (COQ9) (G→A; rs109301586) has been associated with genetic variation in fertility in Holstein cattle, with the A allele associated with higher fertility. COQ9 is involved in the synthesis of coenzyme COQ10, a component of the electron transport system of the mitochondria. Here we tested whether reproductive phenotype is associated with the mutation and evaluated functional consequences for cellular oxygen metabolism, body weight changes, and ovarian function...
February 3, 2017: Biology of Reproduction
https://www.readbyqxmd.com/read/28338610/fructose-rich-diet-affects-mitochondrial-dna-damage-and-repair-in-rats
#5
Federica Cioffi, Rosalba Senese, Pasquale Lasala, Angela Ziello, Arianna Mazzoli, Raffaella Crescenzo, Giovanna Liverini, Antonia Lanni, Fernando Goglia, Susanna Iossa
Evidence indicates that many forms of fructose-induced metabolic disturbance are associated with oxidative stress and mitochondrial dysfunction. Mitochondria are prominent targets of oxidative damage; however, it is not clear whether mitochondrial DNA (mtDNA) damage and/or its lack of repair are events involved in metabolic disease resulting from a fructose-rich diet. In the present study, we evaluated the degree of oxidative damage to liver mtDNA and its repair, in addition to the state of oxidative stress and antioxidant defense in the liver of rats fed a high-fructose diet...
March 24, 2017: Nutrients
https://www.readbyqxmd.com/read/28337894/actn3-ace-genotypes-and-mitochondrial-genome-in-professional-soccer-players%C3%A2-performance
#6
V Galeandro, A Notarnicola, A Bianco, S Tafuri, L Russo, V Pesce, B Moretti, V Petruzzella
Two nuclear genes, ACTN3, encoding for the α-actinin skeletal muscle isoform 3, and ACE encoding the angiotensin-converting enzyme, have both been associated with quantitative physical performance traits in the general population. The purpose of our study was to assess the association between the two nuclear gene variants, R577X (rs1815739) in ACTN3 and I/D (rs4340) in ACE, with elite athletes’ performance and the effect of training on the mitochondrial DNA (mtDNA) content in peripheral blood. We evaluated the genotypes and frequencies of ACTN3 R577X and ACE I/D polymorphisms between soccer players (n = 43) and healthy non-athletic controls (n = 128)...
January 2017: Journal of Biological Regulators and Homeostatic Agents
https://www.readbyqxmd.com/read/28336261/methane-rescues-retinal-ganglion-cells-and-limits-retinal-mitochondrial-dysfunction-following-optic-nerve-crush
#7
Ruobing Wang, Qinglei Sun, Fangzhou Xia, Zeli Chen, Jiangchun Wu, Yuelu Zhang, Jiajun Xu, Lin Liu
Secondary degeneration is a common event in traumatic central nervous system disorders, which involves neuronal apoptosis and mitochondrial dysfunction. Exogenous methane exerts the therapeutic effects in many organ injury. Our study aims to investigate the potential neuroprotection of methane in a rat model of optic nerve crush (ONC). Adult male Sprague-Dawley rats were subjected to ONC and administrated intraperitoneally with methane-saturated or normal saline (10 ml/kg) once per day for one week after ONC...
March 20, 2017: Experimental Eye Research
https://www.readbyqxmd.com/read/28329339/interrelations-between-mitochondrial-dna-copy-number-and-inflammation-in-older-adults
#8
I-Chien Wu, Cheng-Chieh Lin, Chin-San Liu, Chih-Cheng Hsu, Ching-Yu Chen, Chao A Hsiung
Background: Interplays between inflammation and mitochondrial biology are reported. Here, we examined the cross-sectional interrelationships of mitochondrial DNA copy number (mtDNACN) and inflammation and their interaction with physical functioning. Methods: A total of 1990 community-dwelling adults aged 65 years and older who were participating in the Healthy Aging Longitudinal Study in Taiwan underwent measurements of peripheral-blood leukocytes MtDNACN, multiple inflammatory markers, grip strength, and gait speed...
March 11, 2017: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/28322835/role-of-mitochondrial-dysfunction-in-renal-fibrosis-promoted-by-hypochlorite-modified-albumin-in-a-remnant-kidney-model-and-protective-effects-of-antioxidant-peptide-ss-31
#9
Hao Zhao, Yan-Jun Liu, Zong-Rui Liu, Dong-Dong Tang, Xiao-Wen Chen, Yi-Hua Chen, Ru-Ning Zhou, Si-Qi Chen, Hong-Xin Niu
Oxidative stress aggravates renal fibrosis, a pathway involved in almost all forms of chronic kidney disease (CKD). However, the underlying mechanism involved in the pathogenesis of renal oxidative stress has not been completely elucidated. In this study, we explored the role and mechanism of hypochlorite-modified albumin (HOCl-alb) in mediating oxidative stress and fibrotic response in a remnant-kidney rat model. Five-sixths nephrectomy (5/6 NX) was performed on the rats and then the animals were randomly assigned to intravenous treatment with either vehicle alone, or HOCl-rat serum albumin (RSA) in the presence or absence of SS-31 (administered intraperitoneally)...
March 18, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28318978/the-mitochondrial-dna-polymerase-promotes-elimination-of-paternal-mitochondrial-genomes
#10
Zhongsheng Yu, Patrick H O'Farrell, Nikita Yakubovich, Steven Z DeLuca
Mitochondrial DNA (mtDNA) is typically inherited from only one parent [1-3]. In animals, this is usually the mother. Maternal inheritance is often presented as the passive outcome of the difference in cytoplasmic content of egg and sperm; however, active programs enforce uniparental inheritance at two levels, eliminating paternal mitochondrial genomes or destroying mitochondria delivered to the zygote by the sperm [4-13]. Both levels operate in Drosophila [8, 12, 13]. As sperm formation begins, hundreds of doomed mitochondrial genomes are visualized within the two huge mitochondria of each spermatid...
March 11, 2017: Current Biology: CB
https://www.readbyqxmd.com/read/28318037/deoxycytidine-and-deoxythymidine-treatment-for-thymidine-kinase-2-deficiency
#11
Carlos Lopez-Gomez, Rebecca J Levy, Maria J Sanchez-Quintero, Marti Juanola-Falgarona, Emanuele Barca, Beatriz Garcia-Diaz, Saba Tadesse, Caterina Garone, Michio Hirano
OBJECTIVE: Thymidine kinase 2 (TK2), a critical enzyme in the mitochondrial pyrimidine salvage pathway, is essential for mitochondrial DNA (mtDNA) maintenance. Mutations in the nuclear gene TK2 cause TK2 deficiency, which manifests predominantly in children as myopathy with mtDNA depletion. Molecular bypass therapy with the TK2 products, dCMP and dTMP, prolongs the lifespan of Tk2-deficient (Tk2(-/-) ) mice by 2-3 fold. Because we observed rapid catabolism of the deoxynucleoside monophosphates to deoxythymidine (dT) and deoxycytidine (dC), we hypothesized that: 1) deoxynucleosides might be the major active agents and 2) inhibition of deoxycytidine deamination might enhance dTMP+dCMP therapy...
March 20, 2017: Annals of Neurology
https://www.readbyqxmd.com/read/28298141/using-multiple-biomarkers-and-determinants-to-obtain-a-better-measurement-of-oxidative-stress-a-latent-variable-structural-equation-model-approach
#12
Ronald C Eldridge, W Dana Flanders, Roberd M Bostick, Veronika Fedirko, Myron Gross, Bharat Thyagarajan, Michael Goodman
PURPOSE: Since oxidative stress involves a variety of cellular changes, no single biomarker can serve as a complete measure of this complex biological process. The analytic technique of structural equation modeling (SEM) provides a possible solution to this problem by modeling a latent (unobserved) variable constructed from the covariance of multiple biomarkers. METHODS: Using three pooled datasets, we modeled a latent oxidative stress variable from five biomarkers related to oxidative stress: F2-isoprostanes (FIP), fluorescent oxidation products, mitochondrial DNA copy number, γ-tocopherol (Gtoc), and C-reactive protein (CRP, an inflammation marker closely linked to oxidative stress)...
March 16, 2017: Biomarkers: Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals
https://www.readbyqxmd.com/read/28297679/integrative-genomic-analysis-of-cholangiocarcinoma-identifies-distinct-idh-mutant-molecular-profiles
#13
Farshad Farshidfar, Siyuan Zheng, Marie-Claude Gingras, Yulia Newton, Juliann Shih, A Gordon Robertson, Toshinori Hinoue, Katherine A Hoadley, Ewan A Gibb, Jason Roszik, Kyle R Covington, Chia-Chin Wu, Eve Shinbrot, Nicolas Stransky, Apurva Hegde, Ju Dong Yang, Ed Reznik, Sara Sadeghi, Chandra Sekhar Pedamallu, Akinyemi I Ojesina, Julian M Hess, J Todd Auman, Suhn K Rhie, Reanne Bowlby, Mitesh J Borad, Andrew X Zhu, Josh M Stuart, Chris Sander, Rehan Akbani, Andrew D Cherniack, Vikram Deshpande, Taofic Mounajjed, Wai Chin Foo, Michael S Torbenson, David E Kleiner, Peter W Laird, David A Wheeler, Autumn J McRee, Oliver F Bathe, Jesper B Andersen, Nabeel Bardeesy, Lewis R Roberts, Lawrence N Kwong
Cholangiocarcinoma (CCA) is an aggressive malignancy of the bile ducts, with poor prognosis and limited treatment options. Here, we describe the integrated analysis of somatic mutations, RNA expression, copy number, and DNA methylation by The Cancer Genome Atlas of a set of predominantly intrahepatic CCA cases and propose a molecular classification scheme. We identified an IDH mutant-enriched subtype with distinct molecular features including low expression of chromatin modifiers, elevated expression of mitochondrial genes, and increased mitochondrial DNA copy number...
March 14, 2017: Cell Reports
https://www.readbyqxmd.com/read/28274239/occupational-exposure-to-particles-and-mitochondrial-dna-relevance-for-blood-pressure
#14
Yiyi Xu, Huiqi Li, Maria Hedmer, Mohammad Bakhtiar Hossain, Håkan Tinnerberg, Karin Broberg, Maria Albin
BACKGROUND: Particle exposure is a risk factor for cardiovascular diseases. Mitochondrial DNA (mtDNA) is a primary target for oxidative stress generated by particle exposure. We aimed to elucidate the effects of occupational exposure to particle-containing welding fumes on different biomarkers of mtDNA function, and in turn, explore if they modify the association between particle exposure and cardiovascular response, measured as blood pressure. METHODS: We investigated 101 welders and 127 controls (all non-smoking males) from southern Sweden...
March 9, 2017: Environmental Health: a Global Access Science Source
https://www.readbyqxmd.com/read/28271444/the-role-of-mitochondria-in-osteogenic-adipogenic-and-chondrogenic-differentiation-of-mesenchymal-stem-cells
#15
REVIEW
Qianqian Li, Zewen Gao, Ye Chen, Min-Xin Guan
Mesenchymal stem cells (MSCs) are progenitors of connective tissues, which have emerged as important tools for tissue engineering due to their differentiation potential along various cell types. In recent years, accumulating evidence has suggested that the regulation of mitochondria dynamics and function is essential for successful differentiation of MSCs. In this paper, we review and provide an integrated view on the role of mitochondria in MSC differentiation. The mitochondria are maintained at a relatively low activity level in MSCs, and upon induction, mtDNA copy number, protein levels of respiratory enzymes, the oxygen consumption rate, mRNA levels of mitochondrial biogenesis-associated genes, and intracellular ATP content are increased...
March 7, 2017: Protein & Cell
https://www.readbyqxmd.com/read/28252199/analysis-of-mtdna-ndna-ratio-in-mice
#16
Pedro M Quiros, Aashima Goyal, Pooja Jha, Johan Auwerx
Mitochondrial DNA (mtDNA) lacks the protection provided by the nucleosomes in the nuclear DNA and does not have a DNA repair mechanism, making it highly susceptible to damage, which can lead to mtDNA depletion. mtDNA depletion compromises the efficient function of cells and tissues and thus impacts negatively on health. Here, we describe a brief and easy protocol to quantify mtDNA copy number by determining the mtDNA/nDNA ratio. The procedure has been validated using a cohort of young and aged mice. © 2017 by John Wiley & Sons, Inc...
March 2, 2017: Current Protocols in Mouse Biology
https://www.readbyqxmd.com/read/28251996/mitochondrial-dna-copy-number-augments-performance-of-a1c-and-oral-glucose-tolerance-testing-in-the-prediction-of-type-2-diabetes
#17
Seong Beom Cho, InSong Koh, Hye-Young Nam, Jae-Pil Jeon, Hong Kyu Lee, Bok-Ghee Han
Here, we tested the performance of the mitochondrial DNA copy number (mtDNA-CN) in predicting future type 2 diabetes (n = 1108). We used the baseline clinical data (age, sex, body mass index, waist-to-hip ratio, systolic and diastolic blood pressure) and the mtDNA-CN, hemoglobin A1c (A1C) levels and results of oral glucose tolerance test (OGTT) including fasting plasma glucose, 1-hour glucose, and 2-hour glucose levels, to predict future diabetes. We built a prediction model using the baseline data and the diabetes status at biannual follow-up of 8 years...
March 2, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28251677/mitochondrial-dna-and-primary-mitochondrial-dysfunction-in-parkinson-s-disease
#18
REVIEW
Maria Pia Giannoccaro, Chiara La Morgia, Giovanni Rizzo, Valerio Carelli
In 1979, it was observed that parkinsonism could be induced by a toxin inhibiting mitochondrial respiratory complex I. This initiated the long-standing hypothesis that mitochondrial dysfunction may play a key role in the pathogenesis of Parkinson's disease (PD). This hypothesis evolved, with accumulating evidence pointing to complex I dysfunction, which could be caused by environmental or genetic factors. Attention was focused on the mitochondrial DNA, considering the occurrence of mutations, polymorphic haplogroup-specific variants, and defective mitochondrial DNA maintenance with the accumulation of multiple deletions and a reduction of copy number...
March 2, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28245802/characterization-of-two-novel-intronic-opa1-mutations-resulting-in-aberrant-pre-mrna-splicing
#19
Ramona Bolognini, Christina Gerth-Kahlert, Mathias Abegg, Deborah Bartholdi, Nicolas Mathis, Veit Sturm, Sabina Gallati, André Schaller
BACKGROUND: We report two novel splice region mutations in OPA1 in two unrelated families presenting with autosomal-dominant optic atrophy type 1 (ADOA1) (ADOA or Kjer type optic atrophy). Mutations in OPA1 encoding a mitochondrial inner membrane protein are a major cause of ADOA. METHODS: We analyzed two unrelated families including four affected individuals clinically suspicious of ADOA. Standard ocular examinations were performed in affected individuals of both families...
February 28, 2017: BMC Medical Genetics
https://www.readbyqxmd.com/read/28242054/effects-of-methyl-and-inorganic-mercury-exposure-on-genome-homeostasis-and-mitochondrial-function-in-caenorhabditis-elegans
#20
Lauren H Wyatt, Anthony L Luz, Xiou Cao, Laura L Maurer, Ashley M Blawas, Alejandro Aballay, William K Y Pan, Joel N Meyer
Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Reported impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans...
February 13, 2017: DNA Repair
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