scholarly journals Pathological Interaction between DNA Repair and Mitochondrial Dysfunction in ALS

2020 ◽  
Author(s):  
Luis Bermúdez-Guzmán ◽  
Alejandro Leal
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction

Skin Abnormalities in Disorders with DNA Repair Defects, Premature Aging, and Mitochondrial Dysfunction

2021 ◽  
Author(s):  
Mansoor Hussain ◽  
Sudarshan Krishnamurthy ◽  
Jaimin Patel ◽  
Edward Kim ◽  
Beverly A. Baptiste ◽  
...  
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction ◽  
Premature Aging ◽  
Skin Abnormalities

Selenite activates the ATM kinase-dependent DNA repair pathway in human osteosarcoma cells with mitochondrial dysfunction

2015 ◽  
Vol 95 (3) ◽  
pp. 170-176 ◽  
Author(s):  
Marta Wojewoda ◽  
Jarosław Walczak ◽  
Jerzy Duszyński ◽  
Joanna Szczepanowska
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction ◽  
Repair Pathway ◽  
Osteosarcoma Cells ◽  
Atm Kinase ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Mitochondrial dysfunction in DNA repair defective disorders: Mechanisms and pathological relevance

2016 ◽  
Vol 258 ◽  
pp. S19
Author(s):  
Eugenia Dogliotti
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction

The interplay between inflammation, oxidative stress, DNA damage, DNA repair and mitochondrial dysfunction in depression

2018 ◽  
Vol 80 ◽  
pp. 309-321 ◽  
Author(s):  
Piotr Czarny ◽  
Paulina Wigner ◽  
Piotr Galecki ◽  
Tomasz Sliwinski
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Mitochondrial Dysfunction

Role of mitochondrial dysfunction in the pathophysiology of DNA repair disorders

2018 ◽  
Vol 42 (6) ◽  
pp. 643-650 ◽  
Author(s):  
Mateus Prates Mori ◽  
Nadja Cristhina de Souza-Pinto
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction

Impaired DNA Repair Systems: Generation of Mitochondrial Dysfunction and Increased Sensitivity to Excitotoxicity

2007 ◽  
pp. 17-21
Author(s):  
Simona Francisconi ◽  
Mara Codenotti ◽  
Erminia Poli ◽  
Daniela Uberti ◽  
Giulia Ferrari-Toninelli ◽  
...  
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction ◽  
Increased Sensitivity ◽  
Repair Systems

scholarly journals Alteration of Mitochondrial Function and Insulin Sensitivity in Primary Mouse Skeletal Muscle Cells Isolated From Transgenic and Knockout Mice: Role of OGG1

Endocrinology ◽  
2013 ◽  
Vol 154 (8) ◽  
pp. 2640-2649 ◽  
Author(s):  
Larysa V. Yuzefovych ◽  
A. Michele Schuler ◽  
Jemimah Chen ◽  
Diego F. Alvarez ◽  
Lars Eide ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Dna Repair ◽  
Insulin Sensitivity ◽  
Transgenic Mice ◽  
Mitochondrial Dysfunction ◽  
Knockout Mice ◽  
Repair Enzyme ◽  
Mitochondrial Mass ◽  
Mtdna Damage

Abstract Recent evidence has linked mitochondrial dysfunction and DNA damage, increased oxidative stress in skeletal muscle, and insulin resistance (IR). The purpose of this study was to determine the role of the DNA repair enzyme, human 8-oxoguanine DNA glycosylase/apurinic/apyrimidinic lyase (hOGG1), on palmitate-induced mitochondrial dysfunction and IR in primary cultures of skeletal muscle derived from hind limb of ogg1−/− knockout mice and transgenic mice, which overexpress human (hOGG1) in mitochondria (transgenic [Tg]/MTS-hOGG1). Following exposure to palmitate, we evaluated mitochondrial DNA (mtDNA) damage, mitochondrial function, production of mitochondrial reactive oxygen species (mtROS), mitochondrial mass, JNK activation, insulin signaling pathways, and glucose uptake. Palmitate-induced mtDNA damage, mtROS, mitochondrial dysfunction, and activation of JNK were all diminished, whereas ATP levels, mitochondrial mass, insulin-stimulated phosphorylation of Akt (Ser 473), and insulin sensitivity were increased in primary myotubes isolated from Tg/MTS-hOGG1 mice compared to myotubes isolated from either knockout or wild-type mice. In addition, both basal and maximal respiratory rates during mitochondrial oxidation on pyruvate showed a variable response, with some animals displaying an increased respiration in muscle fibers isolated from the transgenic mice. Our results support the model that DNA repair enzyme OGG1 plays a pivotal role in repairing mtDNA damage, and consequently, in mtROS production and regulating downstream events leading to IR in skeletal muscle.

scholarly journals Biological sex and DNA repair deficiency drive Alzheimer’s disease via systemic metabolic remodeling and brain mitochondrial dysfunction

2020 ◽  
Vol 140 (1) ◽  
pp. 25-47 ◽  
Author(s):  
Tyler G. Demarest ◽  
Vijay R. Varma ◽  
Darlene Estrada ◽  
Mansi Babbar ◽  
Sambuddha Basu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Repair ◽  
Mitochondrial Dysfunction ◽  
Biological Sex ◽  
Repair Deficiency ◽  
Metabolic Remodeling ◽  
Dna Repair Deficiency

scholarly journals Protection from Palmitate-Induced Mitochondrial DNA Damage Prevents from Mitochondrial Oxidative Stress, Mitochondrial Dysfunction, Apoptosis, and Impaired Insulin Signaling in Rat L6 Skeletal Muscle Cells

Endocrinology ◽  
2012 ◽  
Vol 153 (1) ◽  
pp. 92-100 ◽  
Author(s):  
Larysa V. Yuzefovych ◽  
Viktoriya A. Solodushko ◽  
Glenn L. Wilson ◽  
Lyudmila I. Rachek
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Dna Repair ◽  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Insulin Signaling ◽  
Mtdna Damage ◽  
L6 Myotubes ◽  
Impaired Insulin

Saturated free fatty acids have been implicated in the increase of oxidative stress, mitochondrial dysfunction, apoptosis, and insulin resistance seen in type 2 diabetes. The purpose of this study was to determine whether palmitate-induced mitochondrial DNA (mtDNA) damage contributed to increased oxidative stress, mitochondrial dysfunction, apoptosis, impaired insulin signaling, and reduced glucose uptake in skeletal muscle cells. Adenoviral vectors were used to deliver the DNA repair enzyme human 8-oxoguanine DNA glycosylase/(apurinic/apyrimidinic) lyase (hOGG1) to mitochondria in L6 myotubes. After palmitate exposure, we evaluated mtDNA damage, mitochondrial function, production of mitochondrial reactive oxygen species, apoptosis, insulin signaling pathways, and glucose uptake. Protection of mtDNA from palmitate-induced damage by overexpression of hOGG1 targeted to mitochondria significantly diminished palmitate-induced mitochondrial superoxide production, restored the decline in ATP levels, reduced activation of c-Jun N-terminal kinase (JNK) kinase, prevented cells from entering apoptosis, increased insulin-stimulated phosphorylation of serine-threonine kinase (Akt) (Ser473) and tyrosine phosphorylation of insulin receptor substrate-1, and thereby enhanced glucose transporter 4 translocation to plasma membrane, and restored insulin signaling. Addition of a specific inhibitor of JNK mimicked the effect of mitochondrial overexpression of hOGG1 and partially restored insulin sensitivity, thus confirming the involvement of mtDNA damage and subsequent increase of oxidative stress and JNK activation in insulin signaling in L6 myotubes. Our results are the first to report that mtDNA damage is the proximal cause in palmitate-induced mitochondrial dysfunction and impaired insulin signaling and provide strong evidence that targeting DNA repair enzymes into mitochondria in skeletal muscles could be a potential therapeutic treatment for insulin resistance.

259: Dna-Repair Genetic Polymorphisms and Prostate Cancer Risk

2005 ◽  
Vol 173 (4S) ◽  
pp. 71-71
Author(s):  
Peter E. Clark ◽  
M. Craig Hall ◽  
Kristin L. Lockett ◽  
Jianfeng Xu ◽  
Sigun L. Zheng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Repair ◽  
Cancer Risk ◽  
Genetic Polymorphisms ◽  
Prostate Cancer Risk
Sign in / Sign up

Export Citation Format

Share Document