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Mitochondrial dysfunction

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https://www.readbyqxmd.com/read/27922662/metabolic-reprogramming-and-ampk%C3%AE-1-pathway-activation-by-caulerpin-in-colorectal-cancer-cells
#1
Hua Yu, Huiqin Zhang, Mingjun Dong, Zhou Wu, Zhonglei Shen, Yangyang Xie, Zhenfang Kong, Xiaoyu Dai, Binbin Xu
Caulerpin, a secondary metabolite from the marine invasive green algae Caulerpa cylindracea is known to induce mitochondrial dysfunctions. In this study, the anticancer property of caulerpin was assessed in a panel of colorectal cancer cell lines. We demonstrated that caulerpin inhibited oxidative phosphorylation (OXPHOS) and facilitated an early intervention of the mitochondrial function, via inhibiting mitochondrial complex I, accompanied by the dissipation of mitochondrial membrane potential and a surge of reactive oxygen species (ROS) generation...
December 6, 2016: International Journal of Oncology
https://www.readbyqxmd.com/read/27922635/increased-plasma-levels-of-circulating-cell-free-mitochondrial-dna-in-suicide-attempters-associations-with-hpa-axis-hyperactivity
#2
D Lindqvist, J Fernström, C Grudet, L Ljunggren, L Träskman-Bendz, L Ohlsson, Å Westrin
Preclinical data suggest that chronic stress may cause cellular damage and mitochondrial dysfunction, potentially leading to the release of mitochondrial DNA (mtDNA) into the bloodstream. Major depressive disorder has been associated with an increased amount of mtDNA in leukocytes from saliva samples and blood; however, no previous studies have measured plasma levels of free-circulating mtDNA in a clinical psychiatric sample. In this study, free circulating mtDNA was quantified in plasma samples from 37 suicide attempters, who had undergone a dexamethasone suppression test (DST), and 37 healthy controls...
December 6, 2016: Translational Psychiatry
https://www.readbyqxmd.com/read/27922495/toxic-and-endocrine-myopathies
#3
Hans D Katzberg, Charles D Kassardjian
PURPOSE OF REVIEW: This article discusses the clinical features, pathophysiology, and management of toxic and endocrine myopathies. RECENT FINDINGS: Early detection and expeditious correction of metabolic disturbances in endocrinopathies such as Cushing syndrome, thyroid and parathyroid diseases, and acromegaly can minimize and prevent neurologic complications including myopathy. Recently proposed mechanisms of injury in patients with critical illness myopathy include inhibition of protein synthesis, mitochondrial dysfunction, disruption of the ubiquitin-proteasome system, oxidative stress, and disruption of intramuscular calcium homeostasis, which can cause a myosin-loss myopathy...
December 2016: Continuum: Lifelong Learning in Neurology
https://www.readbyqxmd.com/read/27922198/dnmt1-modulation-in-chronic-hepatitis-b-patients-and-hypothetic-influence-on-mitochondrial-dna-methylation-status-during-long-term-nucleo-t-side-analogues-therapy
#4
Giordano Madeddu, Silvia Ortu, Giovanni Garrucciu, Ivana Maida, Michela Melis, Alberto Augusto Muredda, Maria Stella Mura, Sergio Babudieri
Inhibition of viral replication is the most important goal in patients with Hepatitis B virus chronic infection (CHB). Currently, five oral nucleo(t)side analogues (NAs), including Lamivudine, Adefovir, Telbivudine, Entecavir and Tenofovir, have been approved for treatment. The widespread use of NAs has also been linked with a progressive growth of unlikely anomaly attributable to mitochondrial dysfunctions, not previously recognized. Here we explore the hypothesis that NAs may cause persistent epigenetic changes during prolonged NAs therapy in CHB patients...
December 6, 2016: Journal of Medical Virology
https://www.readbyqxmd.com/read/27921261/attempting-to-compensate-for-reduced-neuronal-nitric-oxide-synthase-protein-with-nitrate-supplementation-cannot-overcome-metabolic-dysfunction-but-rather-has-detrimental-effects-in-dystrophin-deficient-mdx-muscle
#5
Cara A Timpani, Adam J Trewin, Vanesa Stojanovska, Ainsley Robinson, Craig A Goodman, Kulmira Nurgali, Andrew C Betik, Nigel Stepto, Alan Hayes, Glenn K McConell, Emma Rybalka
Duchenne muscular dystrophy arises from the loss of dystrophin and is characterized by calcium dysregulation, muscular atrophy, and metabolic dysfunction. The secondary reduction of neuronal nitric oxide synthase (nNOS) from the sarcolemma reduces NO production and bioavailability. As NO modulates glucose uptake, metabolism, and mitochondrial bioenergetics, we investigated whether an 8-week nitrate supplementation regimen could overcome metabolic dysfunction in the mdx mouse. Dystrophin-positive control (C57BL/10) and dystrophin-deficient mdx mice were supplemented with sodium nitrate (85 mg/l) in drinking water...
December 5, 2016: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
https://www.readbyqxmd.com/read/27919073/mitochondrial-replacement-in-human-oocytes-carrying-pathogenic-mitochondrial-dna-mutations
#6
Eunju Kang, Jun Wu, Nuria Marti Gutierrez, Amy Koski, Rebecca Tippner-Hedges, Karen Agaronyan, Aida Platero-Luengo, Paloma Martinez-Redondo, Hong Ma, Yeonmi Lee, Tomonari Hayama, Crystal Van Dyken, Xinjian Wang, Shiyu Luo, Riffat Ahmed, Ying Li, Dongmei Ji, Refik Kayali, Cengiz Cinnioglu, Susan Olson, Jeffrey Jensen, David Battaglia, David Lee, Diana Wu, Taosheng Huang, Don P Wolf, Dmitry Temiakov, Juan Carlos Izpisua Belmonte, Paula Amato, Shoukhrat Mitalipov
Maternally inherited mitochondrial (mt)DNA mutations can cause fatal or severely debilitating syndromes in children, with disease severity dependent on the specific gene mutation and the ratio of mutant to wild-type mtDNA (heteroplasmy) in each cell and tissue. Pathogenic mtDNA mutations are relatively common, with an estimated 778 affected children born each year in the United States. Mitochondrial replacement therapies or techniques (MRT) circumventing mother-to-child mtDNA disease transmission involve replacement of oocyte maternal mtDNA...
November 30, 2016: Nature
https://www.readbyqxmd.com/read/27917127/maternal-high-fat-diet-alters-skeletal-muscle-mitochondrial-catalytic-activity-in-adult-male-rat-offspring
#7
Chantal A Pileggi, Christopher P Hedges, Stephanie A Segovia, James F Markworth, Brenan R Durainayagam, Clint Gray, Xiaoyuan D Zhang, Matthew P G Barnett, Mark H Vickers, Anthony J R Hickey, Clare M Reynolds, David Cameron-Smith
A maternal high-fat (HF) diet during pregnancy can lead to metabolic compromise, such as insulin resistance in adult offspring. Skeletal muscle mitochondrial dysfunction is one mechanism contributing to metabolic impairments in insulin resistant states. Therefore, the present study aimed to investigate whether mitochondrial dysfunction is evident in metabolically compromised offspring born to HF-fed dams. Sprague-Dawley dams were randomly assigned to receive a purified control diet (CD; 10% kcal from fat) or a high fat diet (HFD; 45% kcal from fat) for 10 days prior to mating, throughout pregnancy and during lactation...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/27916650/cardiac-oxidative-stress-in-diabetes-mechanisms-and-therapeutic-potential
#8
REVIEW
Alyssa Faria, Shanta J Persaud
Macrovascular complications of diabetes, including diabetic cardiovascular disease (CVD), occur through a number of hyperglycaemia-induced mechanisms that include generation of oxidative stress, accumulation of advanced glycation end-products (AGE) and activation of protein kinase C (PKC). Cardiac oxidative stress is associated with increased cardiac fibrosis and hypertrophy, and reduced cardiac performance and contractility, leading to severe cardiac dysfunction and potentially fatal cardiac events. It occurs under conditions of excessive synthesis of reactive oxygen species (ROS)...
December 1, 2016: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/27916530/enhanced-respiratory-chain-supercomplex-formation-in-response-to-exercise-in-human-skeletal-muscle
#9
Chiara Greggio, Pooja Jha, Sameer S Kulkarni, Sylviane Lagarrigue, Nicholas T Broskey, Marie Boutant, Xu Wang, Sonia Conde Alonso, Emmanuel Ofori, Johan Auwerx, Carles Cantó, Francesca Amati
Mitochondrial dysfunction is a hallmark of multiple metabolic complications. Physical activity is known to increase mitochondrial content in skeletal muscle, counteracting age-related decline in muscle function and protecting against metabolic and cardiovascular complications. Here, we investigated the effect of 4 months of exercise training on skeletal muscle mitochondria electron transport chain complexes and supercomplexes in 26 healthy, sedentary older adults. Exercise differentially modulated respiratory complexes...
November 28, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27916526/the-mitochondrial-lon-protease-is-required-for-age-specific-and-sex-specific-adaptation-to-oxidative-stress
#10
Laura C D Pomatto, Caroline Carney, Brenda Shen, Sarah Wong, Kelly Halaszynski, Matthew P Salomon, Kelvin J A Davies, John Tower
Multiple human diseases involving chronic oxidative stress show a significant sex bias, including neurodegenerative diseases, cancer, immune dysfunction, diabetes, and cardiovascular disease. However, a possible molecular mechanism for the sex bias in physiological adaptation to oxidative stress remains unclear. Here, we report that Drosophila melanogaster females but not males adapt to hydrogen peroxide stress, whereas males but not females adapt to paraquat (superoxide) stress. Stress adaptation in each sex requires the conserved mitochondrial Lon protease and is associated with sex-specific expression of Lon protein isoforms and proteolytic activity...
November 23, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/27916511/liqustri-lucidi-fructus-inhibits-hepatic-injury-and-functions-as-an-antioxidant-by-activation-of-amp-activated-protein-kinase-in-vivo-and-in-vitro
#11
Hye Lim Seo, Su Youn Baek, Eun Hye Lee, Ju-Hee Lee, Seul-Gi Lee, Kwang-Youn Kim, Mi Hee Jang, Min-Hui Park, Joung-Hee Kim, Keun-Jun Kim, Hyeong Sik Lee, Soon-Cheol Ahn, Jong Rok Lee, Sook Jahr Park, Sang Chan Kim, Young Woo Kim
Medicinal herbs are used to treat or prevent various diseases, and function to regulate protective mechanisms as nutraceuticals. Fructus Ligustri lucidi is the fruit of Ligustrum lucidum and has been used for its tonic effects on the liver. This study was designed to examine the effects of Fructus Ligustri lucidi water extract (FLL) against severe oxidative stress and mitochondrial impairment in vivo and in vitro and to elucidate its cellular mechanisms of action. Treatment of HepG2 cells with arachidonic acid (AA) + iron successfully induced oxidative stress and apoptosis, as indicated by depletion of glutathione, formation of ROS, increases in mitochondrial membrane permeability (MMP), and altered expression of apoptosis-related proteins, such as procaspase-3 and Bcl-xL...
December 1, 2016: Chemico-biological Interactions
https://www.readbyqxmd.com/read/27915046/dna-damage-related-crosstalk-between-the-nucleus-and-mitochondria
#12
Mohammad Saki, Aishwarya Prakash
The electron transport chain is the primary pathway by which a cell generates energy in the form of ATP. Byproducts of this process produce reactive oxygen species that can cause damage to mitochondrial DNA. If not properly repaired, the accumulation of DNA damage can lead to mitochondrial dysfunction linked to several human disorders including neurodegenerative diseases and cancer. Mitochondria are able to combat oxidative DNA damage via repair mechanisms that are analogous to those found in the nucleus. Of the repair pathways currently reported in the mitochondria, the base excision repair pathway is the most comprehensively described...
November 30, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27914013/inhibitory-effect-of-homocysteine-on-rat-neural-stem-cell-growth-in-vitro-is-associated-with-reduced-protein-levels-and-enzymatic-activities-of-aconitase-and-respiratory-complex-iii
#13
Xu-Mei Zhang, Ya-Qian Zhao, Hai Yan, Huan Liu, Guo-Wei Huang
Increased blood plasma concentration of the sulphur amino acid homocysteine (Hcy) is considered as an independent risk factor of the neurodegenerative diseases. However, the detailed molecular mechanisms by which Hcy leads to neurotoxicity have yet to be clarified. Recent research has suggested that neurotoxicity of Hcy may involve negative regulation of neural stem cell (NSC) proliferation. In the current study, primary NSCs were isolated from neonatal rat brain hippocampus and the inhibition in cell growth was observed after exposure to l50 μM and 500 μM L-Hcy...
December 2, 2016: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/27913212/vcp-cooperates-with-ubxd1-to-degrade-mitochondrial-outer-membrane-protein-mcl1-in-model-of-huntington-s-disease
#14
Xing Guo, Xin Qi
Proteasome-dependent turnover of mitochondrial outer membrane (OMM)-associated proteins is one of the mechanisms for maintaining proper mitochondrial quality and function. However, the underlying pathways and their implications in human disease are poorly understood. Huntington's disease (HD) is a fatal, inherited neurodegenerative disorder caused by expanded CAG repeats in the N terminal of the huntingtin gene (mutant Huntingtin, mtHtt). In this study, we show an extensive degradation of the OMM protein MCL1 (Myeloid cell leukemia sequence 1) in both HD mouse striatal cells and HD patient fibroblasts...
November 29, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27912197/rac1-nadph-oxidase-signaling-promotes-cd36-activation-under-glucotoxic-conditions-in-pancreatic-beta-cells
#15
Suma Elumalai, Udayakumar Karunakaran, In Kyu Lee, Jun Sung Moon, Kyu Chang Won
We recently reported that cluster determinant 36 (CD36), a fatty acid transporter, plays a pivotal role in glucotoxicity-induced β-cell dysfunction. However, little is known about how glucotoxicity influences CD36 expression. Emerging evidence suggests that the small GTPase Rac1 is involved in the pathogenesis of beta cell dysfunction in type 2 diabetes (T2D). The primary objective of the current study was to determine the role of Rac1 in CD36 activation and its impact on β-cell dysfunction in diabetes mellitus...
November 23, 2016: Redox Biology
https://www.readbyqxmd.com/read/27912102/toyocamycin-induces-apoptosis-via-the-crosstalk-between-reactive-oxygen-species-and-p38-erk-mapks-signaling-pathway-in-human-prostate-cancer-pc-3-cells
#16
Sul-Gi Park, Sang-Hun Kim, Kwang-Youn Kim, Sun-Nyoung Yu, Hyeun-Deok Choi, Young-Wook Kim, Hyo-Won Nam, Young-Kyo Seo, Soon-Cheol Ahn
BACKGROUND: Toyocamycin, an antibiotic agent isolated from Streptomyces species, has been shown to have anticancer and chemopreventive effects on various cancer cells. Until now, Toyocamycin-induced apoptosis has not been reported to be involved in the regulation between mitogen-activated protein kinases (MAPKs) and reactive oxygen species (ROS) production. METHODS: Cell viability assay, western blot, cell-cycle arrest, annexin V/propidium iodide assay, reactive oxygen species (ROS) production, mitochondrial membrane potential and intracellular Ca(2+) flux were assayed...
October 24, 2016: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/27911893/the-mitochondrial-m-aaa-protease-prevents-demyelination-and-hair-greying
#17
Shuaiyu Wang, Julie Jacquemyn, Sara Murru, Paola Martinelli, Esther Barth, Thomas Langer, Carien M Niessen, Elena I Rugarli
The m-AAA protease preserves proteostasis of the inner mitochondrial membrane. It ensures a functional respiratory chain, by controlling the turnover of respiratory complex subunits and allowing mitochondrial translation, but other functions in mitochondria are conceivable. Mutations in genes encoding subunits of the m-AAA protease have been linked to various neurodegenerative diseases in humans, such as hereditary spastic paraplegia and spinocerebellar ataxia. While essential functions of the m-AAA protease for neuronal survival have been established, its role in adult glial cells remains enigmatic...
December 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27911875/autophagy-flux-induced-by-ginsenoside-rg3-attenuates-human-prion-protein-mediated-neurotoxicity-and-mitochondrial-dysfunction
#18
Ji-Hong Moon, Ju-Hee Lee, You-Jin Lee, Sang-Youel Park
Mitochondrial quality control is a process by which mitochondria undergo successive rounds of fusion and fission with dynamic exchange of components to segregate functional and damaged elements. Removal of mitochondrion that contains damaged components is accomplished via autophagy. In this study, we investigated whether ginsenoside Rg3, an active ingredient of the herbal medicine ginseng that is used as a tonic and restorative agent, could attenuate prion peptide, PrP (106-126)-induced neurotoxicity and mitochondrial damage...
November 30, 2016: Oncotarget
https://www.readbyqxmd.com/read/27911732/the-warburg-effect-80-years-on
#19
REVIEW
Michelle Potter, Emma Newport, Karl J Morten
Influential research by Warburg and Cori in the 1920s ignited interest in how cancer cells' energy generation is different from that of normal cells. They observed high glucose consumption and large amounts of lactate excretion from cancer cells compared with normal cells, which oxidised glucose using mitochondria. It was therefore assumed that cancer cells were generating energy using glycolysis rather than mitochondrial oxidative phosphorylation, and that the mitochondria were dysfunctional. Advances in research techniques since then have shown the mitochondria in cancer cells to be functional across a range of tumour types...
October 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27911731/insights-into-the-post-transcriptional-regulation-of-the-mitochondrial-electron-transport-chain
#20
REVIEW
Tamara M Sirey, Chris P Ponting
The regulation of the mitochondrial electron transport chain is central to the control of cellular homeostasis. There are significant gaps in our understanding of how the expression of the mitochondrial and nuclear genome-encoded components of the electron transport chain are co-ordinated, and how the assembly of the protein complexes that constitute the electron transport chain are regulated. Furthermore, the role post-transcriptional gene regulation may play in modulating these processes needs to be clarified...
October 15, 2016: Biochemical Society Transactions
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