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https://www.readbyqxmd.com/read/28342966/time-courses-of-post-injury-mitochondrial-oxidative-damage-and-respiratory-dysfunction-and-neuronal-cytoskeletal-degradation-in-a-rat-model-of-focal-traumatic-brain-injury
#1
Rachel L Hill, Indrapal N Singh, Juan A Wang, Edward D Hall
Traumatic brain injury (TBI) results in rapid reactive oxygen species (ROS) production and oxidative damage to essential brain cellular components leading to neuronal dysfunction and cell death. It is increasingly appreciated that a major player in TBI-induced oxidative damage is the reactive nitrogen species (RNS) peroxynitrite (PN) which is produced in large part in injured brain mitochondria. Once formed, PN decomposes into highly reactive free radicals that trigger membrane lipid peroxidation (LP) of polyunsaturated fatty acids (e...
March 23, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28338610/fructose-rich-diet-affects-mitochondrial-dna-damage-and-repair-in-rats
#2
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/28338413/human-tissue-engineered-skeletal-muscle-myobundles-to-measure-oxygen-uptake-and-assess-mitochondrial-toxicity
#3
Brittany N J Davis, Jeffrey W Santoso, Michaela J Walker, Cindy S Cheng, Timothy R Koves, William E Kraus, George A Truskey
Mitochondrial dysfunction is responsible for the toxicity of a number of drugs. Current isolated mitochondria or cellular monoculture mitochondrial respiration measurement systems lack physiological relevance. Using a tissue engineering rather than cell- or mitochondria-based approach enables a more physiologically relevant detection of drug-induced mitochondrial impairment. To probe oxygen consumption and mitochondrial health, we assayed the bioenergetic profile of engineered three-dimensional human skeletal muscle myobundles derived from primary myoblasts...
March 24, 2017: Tissue Engineering. Part C, Methods
https://www.readbyqxmd.com/read/28337707/investigation-of-yeast-mitophagy-with-fluorescence-microscopy-and-western-blotting
#4
Sachiyo Nagumo, Koji Okamoto
Selective clearance of superfluous or dysfunctional mitochondria is a fundamental process that depends on the autophagic membrane trafficking pathways found in many cell types. This catabolic event, called mitophagy, is conserved from yeast to humans and serves to control mitochondrial quality and quantity. In budding yeast, degradation of mitochondria occurs under various physiological conditions, such as respiration at stationary phase, or starvation in a prolonged period. During these events, the transmembrane protein Atg32 localizes to the mitochondrial surface and plays a specific and essential role in yeast mitophagy...
March 24, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28337125/neuronal-mitophagy-in-neurodegenerative-diseases
#5
REVIEW
Marta Martinez-Vicente
Neuronal homeostasis depends on the proper functioning of different quality control systems. All intracellular components are subjected to continuous turnover through the coordinated synthesis, degradation and recycling of their constituent elements. Autophagy is the catabolic mechanism by which intracellular cytosolic components, including proteins, organelles, aggregates and any other intracellular materials, are delivered to lysosomes for degradation. Among the different types of selective autophagy described to date, the process of mitophagy involves the selective autophagic degradation of mitochondria...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28336486/mitochondrial-dysfunction-in-airway-disease
#6
Y S Prakash, Christina M Pabelick, Gary C Sieck
There is increasing appreciation that mitochondria serve cellular functions beyond oxygen sensing and energy production. Accordingly, it has become important to explore non-canonical roles of mitochondria in normal and pathophysiological processes that influence airway structure and function in the context of diseases such as asthma and COPD. Mitochondria can sense upstream processes such as inflammation, infection, tobacco smoke and environmental insults important in these diseases, and in turn can respond to such stimuli via altered mitochondrial protein expression, structure, and resultant dysfunction...
March 21, 2017: Chest
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/28333383/calcium-transport-and-signaling-in-mitochondria
#8
Roberto Bravo-Sagua, Valentina Parra, Camila López-Crisosto, Paula Díaz, Andrew F G Quest, Sergio Lavandero
Calcium (Ca2+) is a key player in the regulation of many cell functions. Just like Ca2+, mitochondria are ubiquitous, versatile, and dynamic players in determining both cell survival and death decisions. Given their ubiquitous nature, the regulation of both is deeply intertwined, whereby Ca2+ regulates mitochondrial functions, while mitochondria shape Ca2+ dynamics. Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies...
March 16, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28333265/improving-oocyte-quality-by-transfer-of-autologous-mitochondria-from-fully-grown-oocytes
#9
Stine Gry Kristensen, Susanne Elisabeth Pors, Claus Yding Andersen
Older women are often the most challenging group of patients in fertility clinics due to a decline in both number and overall quality of oocytes. The quality of oocytes has been linked to mitochondrial dysfunction. In this mini-review, we discuss this hypothesis and suggest alternative treatment options using autologous mitochondria to potentially augment pregnancy potential in ART. Autologous transfer of mitochondria from the patient's own germline cells has attracted much attention as a possible new treatment to revitalize deficient oocytes...
March 2, 2017: Human Reproduction
https://www.readbyqxmd.com/read/28331061/an-intracellular-matrix-metalloproteinase-2-isoform-induces-tubular-regulated-necrosis-implications-for-acute-kidney-injury
#10
Carla S Ceron, Celine Baligand, Sunil K Joshi, Shaynah Wanga, Patrick M Cowley, Joy P Walker, Sang Heon Song, Rajeev Mahimkar, Anthony J Baker, Robert L Raffai, Zhen J Wang, David H Lovett
Acute kidney injury (AKI) causes severe morbidity, mortality, and chronic kidney disease (CKD). Mortality is particularly marked in the elderly and with pre-existing CKD. Oxidative stress is a common theme in models of AKI induced by ischemia/reperfusion (I/R) injury. We recently characterized an intracellular isoform of matrix metalloproteinase-2 (MMP-2) induced by oxidative stress-mediated activation of an alternate promoter in the first intron of the MMP-2 gene. This generates an N-terminal truncated MMP-2 isoform (NTT-MMP-2) that is intracellular and associated with mitochondria...
March 22, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28330953/your-mitochondria-are-what-you-eat-a-high-fat-or-a-high-sucrose-diet-eliminates-metabolic-flexibility-in-isolated-mitochondria-from-rat-skeletal-muscle
#11
Wenche Jørgensen, Kasper A Rud, Ole H Mortensen, Lis Frandsen, Niels Grunnet, Bjørn Quistorff
Extreme diets consisting of either high fat (HF) or high sucrose (HS) may lead to insulin resistance in skeletal muscle, often associated with mitochondrial dysfunction. However, it is not known if these diets alter normal interactions of pyruvate and fatty acid oxidation at the level of the mitochondria. Here, we report that rat muscle mitochondria does show the normal Randle-type fat-carbohydrate interaction seen in vivo. The mechanism behind this metabolic flexibility at the level of the isolated mitochondria is a regulation of the flux-ratio: pyruvate dehydrogenase (PDH)/β-oxidation to suit the actual substrate availability, with the PDH flux as the major point of regulation...
March 2017: Physiological Reports
https://www.readbyqxmd.com/read/28330601/mitochondria-in-cell-senescence-is-mitophagy-the-weakest-link
#12
REVIEW
Viktor I Korolchuk, Satomi Miwa, Bernadette Carroll, Thomas von Zglinicki
Cell senescence is increasingly recognized as a major contributor to the loss of health and fitness associated with aging. Senescent cells accumulate dysfunctional mitochondria; oxidative phosphorylation efficiency is decreased and reactive oxygen species production is increased. In this review we will discuss how the turnover of mitochondria (a term referred to as mitophagy) is perturbed in senescence contributing to mitochondrial accumulation and Senescence-Associated Mitochondrial Dysfunction (SAMD). We will further explore the subsequent cellular consequences; in particular SAMD appears to be necessary for at least part of the specific Senescence-Associated Secretory Phenotype (SASP) and may be responsible for tissue-level metabolic dysfunction that is associated with aging and obesity...
March 14, 2017: EBioMedicine
https://www.readbyqxmd.com/read/28329820/hepatocellular-toxicity-of-imidazole-and-triazole-antimycotic-agents
#13
Patrizia Haegler, Lorenz Joerin, Stephan Krähenbühl, Jamal Bouitbir
Hepatotoxicity has been described for all antimycotic azoles currently marketed. A possible mechanism involving mitochondrial dysfunction has been postulated for ketoconazole, but not for the other azoles. The aim of the current investigations was to study the toxicity of different azoles in human cell models and to find out mechanisms of their toxicity. In HepG2 cells, posaconazole and ketoconazole were cytotoxic starting at 20 and 50 µM and decreased the cellular ATP content starting at 5 and 10 µM, respectively...
January 27, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28324764/enhancing-mitofusin-marf-ameliorates-neuromuscular-dysfunction-in-drosophila-models-of-tdp-43-proteinopathies
#14
Bilal Khalil, Marie-Jeanne Cabirol-Pol, Laetitia Miguel, Alexander J Whitworth, Magalie Lecourtois, Jean-Charles Liévens
Transactive response DNA-binding protein 43 kDa (TDP-43) is considered a major pathological protein in amyotrophic lateral sclerosis and frontotemporal lobar degeneration. The precise mechanisms by which TDP-43 dysregulation leads to toxicity in neurons are not fully understood. Using TDP-43-expressing Drosophila, we examined whether mitochondrial dysfunction is a central determinant in TDP-43 pathogenesis. Expression of human wild-type TDP-43 in Drosophila neurons results in abnormally small mitochondria...
February 27, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28324491/monitoring-mitophagy-during-aging-in-caenorhabditis-elegans
#15
Nikolaos Charmpilas, Konstantinos Kounakis, Nektarios Tavernarakis
Mitochondria constitute the main energy-producing centers of eukaryotic cells. In addition, they are involved in several crucial cellular processes, such as lipid metabolism, calcium buffering, and apoptosis. As such, their malfunction can be detrimental for proper cellular physiology and homeostasis. Mitophagy is a mechanism that protects and maintains cellular function by sequestering harmful or dysfunctional mitochondria to lysosomes for degradation. In this report, we present experimental procedures for quantitative, in vivo monitoring of mitophagy events in the nematode Caenorhabditis elegans...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324201/potential-roles-of-mitochondria-associated-er-membranes-mams-in-traumatic-brain-injury
#16
REVIEW
Dongdong Sun, Xin Chen, Gang Gu, Jianhao Wang, Jianning Zhang
The endoplasmic reticulum (ER) and mitochondria have both been shown to be critical in cellular homeostasis. The functions of the ER and mitochondria are independent but interrelated. These two organelles could form physical interactions, known as MAMs, to regulate physiological functions between ER and mitochondria to maintain Ca(2+), lipid, and metabolite exchange. Several proteins are located in MAMs, including RNA-dependent protein kinase (PKR)-like ER kinase, inositol 1,4,5-trisphosphate receptors, phosphofurin acidic cluster sorting protein-2 and sigma-1 receptor to ensure regulation...
March 21, 2017: Cellular and Molecular Neurobiology
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
#17
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/28322751/neuroprotective-effects-of-2-4-dinitrophenol-in-an-acute-model-of-parkinson-s-disease
#18
Yujeong Lee, Gwangbeom Heo, Kyung Moon Lee, Ah Hyun Kim, Ki Wung Chung, Eunok Im, Hae Young Chung, Jaewon Lee
Neurons depend on mitochondria for homeostasis and survival, and thus, mitochondrial dysfunction has been implicated in neurodegenerative diseases, including Parkinson's disease (PD). Increasing evidence indicates the mitochondrial uncoupler, 2,4-dinitrophenol (DNP), protects neurons against neurodegeneration and enhances neural plasticity. Here, the authors evaluated the protective effects of intraperitoneally (i.p.) administered low dose DNP in an acute mouse model of PD. Mice were administered DNP (1 or 5 mg/kg) for 12 consecutive days, and then on day 13, MPTP (20 mg/kg, i...
March 17, 2017: Brain Research
https://www.readbyqxmd.com/read/28321271/parkin-in-cancer-mitophagy-related-unrelated-tasks
#19
EDITORIAL
Nabil Eid, Yoichi Kondo
Dysfunctional mitochondria may produce excessive reactive oxygen species, thus inducing DNA damage, which may be oncogenic if not repaired. As a major role of the PINK1-Parkin pathway involves selective autophagic clearance of damaged mitochondria via a process termed mitophagy, Parkin-mediated mitophagy may be a tumor-suppressive mechanism. As an alternative mechanism for tumor inhibition beyond mitophagy, Parkin has been reported to have other oncosuppressive functions such as DNA repair, negative regulation of cell proliferation and stimulation of p53 tumor suppressor function...
March 8, 2017: World Journal of Hepatology
https://www.readbyqxmd.com/read/28320896/estrogen-maintains-mitochondrial-content-and-function-in-the-right-ventricle-of-rats-with-pulmonary-hypertension
#20
Aiping Liu, Jennifer Philip, Kalyan C Vinnakota, Francoise Van den Bergh, Diana M Tabima, Timothy Hacker, Daniel A Beard, Naomi C Chesler
The typical cause of death in pulmonary hypertension (PH) is right ventricular (RV) failure, with females showing better survival rates than males. Recently, metabolic shift and mitochondrial dysfunction have been demonstrated in RV failure secondary to PH In light of evidence showing that estrogen protects mitochondrial function and biogenesis in noncardiovascular systems, we hypothesized that the mechanism by which estrogen preserves RV function is via protection of mitochondrial content and oxidative capacity in PH We used a well-established model of PH (Sugen+Hypoxia) in ovariectomized female rats with/without estrogen treatment...
March 2017: Physiological Reports
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